ULCERATIVE COLITIS A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES
J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS
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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright 2004 by ICON Group International, Inc. Copyright 2004 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1
Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Ulcerative Colitis: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-84175-6 1. Ulcerative Colitis-Popular works. I. Title.
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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on ulcerative colitis. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.
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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications. Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.
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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes&Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health
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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON ULCERATIVE COLITIS ................................................................................ 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Ulcerative Colitis ........................................................................ 60 E-Journals: PubMed Central ..................................................................................................... 116 The National Library of Medicine: PubMed .............................................................................. 119 CHAPTER 2. NUTRITION AND ULCERATIVE COLITIS .................................................................... 165 Overview.................................................................................................................................... 165 Finding Nutrition Studies on Ulcerative Colitis ....................................................................... 165 Federal Resources on Nutrition ................................................................................................. 171 Additional Web Resources ......................................................................................................... 172 CHAPTER 3. ALTERNATIVE MEDICINE AND ULCERATIVE COLITIS.............................................. 175 Overview.................................................................................................................................... 175 National Center for Complementary and Alternative Medicine................................................ 175 Additional Web Resources ......................................................................................................... 191 General References ..................................................................................................................... 197 CHAPTER 4. DISSERTATIONS ON ULCERATIVE COLITIS................................................................ 199 Overview.................................................................................................................................... 199 Dissertations on Ulcerative Colitis ............................................................................................ 199 Keeping Current ........................................................................................................................ 200 CHAPTER 5. CLINICAL TRIALS AND ULCERATIVE COLITIS .......................................................... 201 Overview.................................................................................................................................... 201 Recent Trials on Ulcerative Colitis ............................................................................................ 201 Keeping Current on Clinical Trials ........................................................................................... 209 CHAPTER 6. PATENTS ON ULCERATIVE COLITIS .......................................................................... 211 Overview.................................................................................................................................... 211 Patents on Ulcerative Colitis ..................................................................................................... 211 Patent Applications on Ulcerative Colitis ................................................................................. 233 Keeping Current ........................................................................................................................ 266 CHAPTER 7. BOOKS ON ULCERATIVE COLITIS .............................................................................. 267 Overview.................................................................................................................................... 267 Book Summaries: Federal Agencies............................................................................................ 267 Book Summaries: Online Booksellers......................................................................................... 271 The National Library of Medicine Book Index ........................................................................... 274 Chapters on Ulcerative Colitis ................................................................................................... 275 Directories.................................................................................................................................. 309 CHAPTER 8. MULTIMEDIA ON ULCERATIVE COLITIS ................................................................... 311 Overview.................................................................................................................................... 311 Video Recordings ....................................................................................................................... 311 Bibliography: Multimedia on Ulcerative Colitis........................................................................ 313 CHAPTER 9. PERIODICALS AND NEWS ON ULCERATIVE COLITIS ................................................ 315 Overview.................................................................................................................................... 315 News Services and Press Releases.............................................................................................. 315 Newsletters on Ulcerative Colitis .............................................................................................. 319 Newsletter Articles .................................................................................................................... 319 Academic Periodicals covering Ulcerative Colitis...................................................................... 322 CHAPTER 10. RESEARCHING MEDICATIONS................................................................................. 323 Overview.................................................................................................................................... 323 U.S. Pharmacopeia..................................................................................................................... 323 Commercial Databases ............................................................................................................... 325
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Researching Orphan Drugs ....................................................................................................... 326 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 331 Overview.................................................................................................................................... 331 NIH Guidelines.......................................................................................................................... 331 NIH Databases........................................................................................................................... 333 Other Commercial Databases..................................................................................................... 336 The Genome Project and Ulcerative Colitis ............................................................................... 336 APPENDIX B. PATIENT RESOURCES ............................................................................................... 341 Overview.................................................................................................................................... 341 Patient Guideline Sources.......................................................................................................... 341 Finding Associations.................................................................................................................. 357 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 359 Overview.................................................................................................................................... 359 Preparation................................................................................................................................. 359 Finding a Local Medical Library................................................................................................ 359 Medical Libraries in the U.S. and Canada ................................................................................. 359 ONLINE GLOSSARIES................................................................................................................ 365 Online Dictionary Directories ................................................................................................... 367 ULCERATIVE COLITIS DICTIONARY ................................................................................... 369 INDEX .............................................................................................................................................. 477
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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with ulcerative colitis is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to know as much as possible about ulcerative colitis, using the most advanced research tools available and spending the least amount of time doing so. In addition to offering a structured and comprehensive bibliography, the pages that follow will tell you where and how to find reliable information covering virtually all topics related to ulcerative colitis, from the essentials to the most advanced areas of research. Public, academic, government, and peer-reviewed research studies are emphasized. Various abstracts are reproduced to give you some of the latest official information available to date on ulcerative colitis. Abundant guidance is given on how to obtain free-of-charge primary research results via the Internet. While this book focuses on the field of medicine, when some sources provide access to non-medical information relating to ulcerative colitis, these are noted in the text. E-book and electronic versions of this book are fully interactive with each of the Internet sites mentioned (clicking on a hyperlink automatically opens your browser to the site indicated). If you are using the hard copy version of this book, you can access a cited Web site by typing the provided Web address directly into your Internet browser. You may find it useful to refer to synonyms or related terms when accessing these Internet databases. NOTE: At the time of publication, the Web addresses were functional. However, some links may fail due to URL address changes, which is a common occurrence on the Internet. For readers unfamiliar with the Internet, detailed instructions are offered on how to access electronic resources. For readers unfamiliar with medical terminology, a comprehensive glossary is provided. For readers without access to Internet resources, a directory of medical libraries, that have or can locate references cited here, is given. We hope these resources will prove useful to the widest possible audience seeking information on ulcerative colitis. The Editors
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From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.
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CHAPTER 1. STUDIES ON ULCERATIVE COLITIS Overview In this chapter, we will show you how to locate peer-reviewed references and studies on ulcerative colitis.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and ulcerative colitis, you will need to use the advanced search options. First, go to http://chid.nih.gov/index.html. From there, select the “Detailed Search” option (or go directly to that page with the following hyperlink: http://chid.nih.gov/detail/detail.html). The trick in extracting studies is found in the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Journal Article.” At the top of the search form, select the number of records you would like to see (we recommend 100) and check the box to display “whole records.” We recommend that you type “ulcerative colitis” (or synonyms) into the “For these words:” box. Consider using the option “anywhere in record” to make your search as broad as possible. If you want to limit the search to only a particular field, such as the title of the journal, then select this option in the “Search in these fields” drop box. The following is what you can expect from this type of search: •
Biologic Therapy of Inflammatory Bowel Disease Source: Gastroenterology. 122(6): 1592-1608. 2002. Contact: Available from W.B. Saunders Company. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452. Website: www.gastrojournal.org. Summary: Advancing knowledge regarding the biology of chronic inflammation has led to the development of specific biologic therapies that mechanistically target individual inflammatory pathways. This article explores the many biologic therapies that are being evaluated for the treatment of the chronic inflammatory bowel diseases (IBD): Crohn's disease and ulcerative colitis. Biologic compounds proven to be effective for Crohn's disease include monoclonal antibodies to tumor necrosis factor (infliximab and CDP571) and to the leukocyte adhesion molecule alpha 4 integrin (natalizumab). Other biologic
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compounds for which there is insufficient evidence to judge efficacy for IBD include: p55 tumor necrosis factor (TNF) binding protein (onercept); interferon alpha; interferon beta-1a; anti-interferon gamma antibody; anti-interleukin 12 antibody; p65 anti-sense oligonucleotide granulocyte colony stimulating factor, and granulocyte macrophage colony stimulating factor; anti-interleukin 2 receptor antibody; epidermal growth factor; keratinocyte growth factor 2 (repifermin); human growth hormone; anti-CD4 antibody; and anti-alpha4beta7 antibody. Biologic therapies that have been proven ineffective for inflammatory bowel disease include: interleukin 10; interleukin 11; antisense intercellular adhesion molecule 1; and the TNF receptor fusion protein etanercept. The authors conclude that based on the early successes of infliximab, CDP571 and natalizumab, it seems certain that biologic therapy will play an important role in the future treatment of IBD. 4 figures. 2 tables. 144 references. •
Inflammatory Bowel Disease and Cancer Source: Gastroenterology Clinics of North America. 26(1): 129-139. March 1997. Contact: Available from W.B. Saunders Company. Periodicals Fulfillment, 6277 Sea Harbor Drive, Orlando, FL 32887. (800) 654-2452. Summary: Although fewer than 1 percent of all colorectal cancer cases arise in the setting of chronic inflammatory bowel disease (IBD), the development of gastrointestinal (GI) neoplasia presents a formidable problem for both the patient and the physician. This article provides a summary of the problem of colorectal cancer in ulcerative colitis (UC) and Crohn's disease. Topics include risk factors and magnitude of risk; the biology of colon cancer in UC, patient management; surveillance strategy; markers to complement dysplasia; and risk factors for developing colorectal cancer in Crohn's disease. The author concludes that, although the absolute number of colorectal cancers developing in patients with IBD may not seem dramatic to the individual practitioner, the overall relative risk, the fear of this dreaded complication among patients, and the excess mortality among the entire IBD population are all sufficiently high enough to warrant clinical vigilance. To date, the cost-to-benefit ratios of surveillance programs are not yet established. Nonetheless, the availability of new molecular tools to identify the highest-risk groups, together with the pursuit of carefully designed clinical investigations in this area, should provide important new insights into the pathogenesis and prevention of colorectal cancer in IBD. 2 figures. 1 table. 48 references. (AA-M).
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Nutritional Issues in Inflammatory Bowel Disease Source: Gastroenterology Clinics of North America. 27(2): 435-451. June 1998. Contact: Available from W.B. Saunders. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000. Summary: Although significant advances have been made in understanding the pathogenesis and treatment of Crohn's disease and ulcerative colitis, few standards of care exist for using nutrition as primary or adjunctive therapy to treat these diseases. The data concerning its benefits are conflicting, however. Nutritional therapy that has been used in the treatment of inflammatory bowel diseases (IBD) includes total parenteral nutrition (TPN), and elemental, peptide, polymeric, and exclusion diets. This article apprises the clinician of the role of these various forms of nutrition, with emphasis on the results of controlled studies. The most important clinical consequences of malnutrition in IBD are growth retardation in children; weight loss and decreased functional capacity; and, if the association is causative, perioperative morbidity. Protein-
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calorie, folic acid, vitamin B12, niacin, and zinc deficiencies can cause diarrhea and could therefore contribute to disease activity in IBD. Current evidence indicates that patients with IBD, except for patients with lactose intolerance, patients with strictures in the gastrointestinal tract, and patients with extensive ileal resection or disease, should be encouraged to eat a normal, healthy diet. The article concludes with a brief section on the use of alternative therapy, including medicinal herbs. 4 tables. 106 references. •
Medical Treatment of Severe Ulcerative Colitis Source: Alimentary Pharmacology and Therapeutics. 16(Supplement 4): 7-12. July 2002. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com. Summary: Approximately 15 percent of patients with ulcerative colitis (UC, a type of inflammatory bowel disease, or IBD) have a severe attack requiring hospitalization at some time during their illness. This article reviews the medical treatment of severe UC. The authors note that hospitalization leads to a remission in 60 to 80 percent of patients. However, nonresponders may require a total colectomy. Mortality (death) in severe episodes of UC decreased from 31 to 61 percent in the 1950s to 5 to 9 percent in the 1960s, thanks to the introduction of steroids and to a policy of early colectomy. Recently, some new drugs have been shown to be effective in the treatment of severe steroidrefractory (resistant) UC. This review article concludes on the clinical evaluation, prognostic factors, and new developments in medical therapy in severe UC. The authors also report on a retrospective evaluation of a consecutive series of patients with severe UC who were admitted to a Gastroenterology Department in Torino, Italy. 1 figure. 3 tables. 37 references.
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Review Article: The Treatment of Inflammatory Bowel Disease with 6Mercaptopurine or Azathioprine Source: Alimentary Pharmacology and Therapeutics. 15(11): 1699-1708. November 2001. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com. Summary: Azathioprine is a prodrug of 6-mercaptopurine that is further metabolized by various enzymes present in the liver and gut. Azathioprine and 6-mercaptopurine have been used in the treatment of inflammatory bowel disease (IBD, which includes ulcerative colitis and Crohn's disease) for more than 30 years. However, widespread use of these drugs is a more recent phenomenon, due to a long standing debate on the efficacy of these agents in IBD. Both drugs are slow acting, which is why clinical efficacy cannot be expected until several weeks or even months of treatment have elapsed. Consequently, these drugs have no place as monotherapy (single drugs) in the treatment of acute relapsing IBD. This review article suggestions guidelines for the application of azathioprine and 6-mercaptopurine in the treatment of IBD. The clinical effects of these drugs are probably identical, although their exact mode of action is still unknown. In Crohn's disease, these drugs are indicated in chronic active disease that fails to respond to glucocorticoids, or when the prednisolone dosage cannot be reduced below 10 to 15 milligrams, particularly if adverse effects are problematic. The drugs should be used to maintain remission, but only in patients with previous extensive or troublesome chronic active disease. In ulcerative colitis, patient indications for these drugs include chronic
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unresponsive glucocorticoid-dependent disease and frequent relapses (more than three in 2 years). 1 table. 74 references. •
Colonoscopy Plus Biopsy in the Inflammatory Bowel Diseases Source: Gastrointestinal Endoscopy Clinics of North America. 10(4): 755-774. October 2000. Contact: Available from W.B. Saunders Company. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000. Summary: Biopsy of the colon is an important diagnostic tool in the investigation of the inflammatory bowel diseases (IBD). Colon biopsies are critical in helping to diagnose diarrhea, to distinguish different forms of colitis, to determine the extent of disease, and to determine if neoplasia (including cancer) has arisen in the setting of chronic colitis. This article reviews a number of scenarios where colon biopsies are of particular importance, such as biopsies in the patient with undiagnosed diarrhea, distinguishing different forms of inflammatory bowel disease (IBD), assessing disease extent and activity, differential diagnosis of and diagnosing other disorders superimposed on inflammatory bowel disease, neoplasia in patients with IBD, and colonic biopsy as a mirror of generalized gastrointestinal or systemic disease. One table summarizes the recommended locations and numbers of biopsies for different scenarios. The author concludes that to use colon biopsies most appropriately in patient management and to get the most mileage from them usually requires frequent clinician-pathologist interaction, often repeat endoscopy with biopsies at a different time, and the assessment of the biopsies in the clinical context. 1 figure. 3 tables. 94 references.
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Iron and Inflammatory Bowel Disease Source: Alimentary Pharmacology and Therapeutics. 15(4): 429-438. April 2001. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com. Summary: Both anemia of iron deficiency and anemia of chronic disease are frequently encountered in patients with inflammatory bowel disease (IBD, consisting of Crohn's disease or ulcerative colitis). Anemia of iron deficiency is mostly due to inadequate intake or loss of iron. Anemia of chronic disease probably results from decreased erythropoiesis (creation of the hormone erythropoietin, which helps the body use oxygen), secondary to increased levels of proinflammatory cytokines, reactive oxygen metabolites, and nitric oxide. This article reviews the problem of iron in patients with IBD. The authors note that assessment of the iron status in a condition association with inflammation, such as IBD, is difficult. The combination of serum transferrin receptor with ferritin concentrations, however, allows a reliable assessment of the iron deficit. The best treatment for anemia of chronic disease is the cure of the underlying disease. Erythropoietin reportedly may increase hemoglobin levels in some of these patients. The anemia of iron deficiency is usually treated with oral iron supplements. Iron supplementation may lead to an increased inflammatory activity through the generation of reactive oxygen species. To date, data from studies in animal models of IBD support the theoretical disadvantage of iron supplementation in this respect. However, the results cannot be easily generalized to the human situation, because the amount of supplemented iron in these experiments was much higher than the does used in patients with iron deficiency. 2 figures. 97 references.
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Bone Mineral Density Assessment in Children with Inflammatory Bowel Disease Source: Gastroenterology. 114(5): 902-911. May 1998. Contact: Available from W.B. Saunders Company. 6277 Sea Harbor Drive, Orlando, FL 19106-3399. (800) 654-2452 or (407) 345-4000. Summary: Children with inflammatory bowel disease (IBD) are at risk for osteoporosis because of undernutrition, delayed puberty, and prolonged use of corticosteroids. This article reports on a study that compared bone mineral density (BMD) in children with IBD with that in normal children and assessed the effects of nutritional and hormonal factors and corticosteroid dosages on BMD. A total of 162 subjects (99 with IBD and 63 healthy sibling controls) were enrolled in the study. Patients underwent anthropometric assessment, pubertal staging, bone age radiography, and BMD assessment by dual energy x-ray absorptiometry of the lumbar spine, femoral neck, and radius. The study also included laboratory evaluations. BMD Z scores at the lumbar spine and femoral neck were lower in patients with IBD, and lower in those with Crohn's disease in general than in those with ulcerative colitis (UC). Low BMD persisted after correction for bone age in girls with Crohn's disease. Cumulative corticosteroid dose was a significant predictor of reduced BMD. BMD did not correlate with measures of calcium homeostasis, except with elevated serum phosphate and urine calcium levels in girls. The authors conclude that low BMD occurs in children with IBD (more in Crohn's disease than in UC), especially in pubertal and postpubertal girls. Cumulative corticosteroid dose is a predictor of low BMD, but other factors in Crohn's disease remain undetermined. 2 figures. 6 tables. 46 references. (AA-M).
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Perinatal Exposure to Measles Virus and the Risk of Inflammatory Bowel Disease Source: Reproductive Toxicology. 11(5): 647-652. September-October 1997. Contact: Available from Elsevier Science, Inc. 633-3730 P.O. Box 945, New York, NY 10158-0945. (888)437-4636 or (212) 6333730. Fax (212) 633-3680. Summary: Concern about a possible link between perinatal exposure to measles (rubeola) virus and an increased risk of inflammatory bowel disease (IBD, including ulcerative colitis and Crohn's disease) has grown out of histologic investigations that supported a possible role of chronic infection with measles virus as an agent in recurrent attacks of Crohn's disease. This article explores the possible connection between prenatal exposure to the measles virus and the risk of IBD. The authors note that the causative factors in IBD remain unknown and the search to identify a possible infective agent as a causative factor is not new. The authors describe the history of this hypothesis for Crohn's etiology, the measles vaccine and Crohn's disease, and auxiliary data from twin studies. The authors conclude that, at this point, things look 'relatively bleak' for the hypothetical association between measles virus and Crohn's disease, and even more so for a possible role for perinatal exposure to measles and Crohn's disease. It is possible that measles virus does not play a role in most cases of Crohn's disease, but that chronic measles infections do exist in rare cases, producing symptoms indistinguishable from those found in Crohn's disease. The authors conclude by cautioning readers that scientific inquiry takes great amounts of time and should not prematurely affect a program such as measles vaccination, which is a successful health promotion strategy. To some extent, however, this fascination with perinatal risk is good, because it has the potential to improve the public health when genuine risks are identified and controlled. 1 figure. 1 table. 55 references.
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Inflammatory Bowel Disease: Short-and Long-Term Treatments Source: Disease-A-Month. 44(4): 145-172. April 1998. Contact: Available from Mosby, Inc. 11830 Westline Industrial Drive, St. Louis, MO 631446-3318. (800) 453-4351 or (314) 453-4351. Fax (314) 432-1158. E-mail:
[email protected]. Website: www.mosby.com/Mosby/Periodicals. Summary: Crohn's disease (CD) and ulcerative colitis (UC) are chronic inflammatory disorders of the digestive tract, known together as inflammatory bowel disease (IBD). The true cause or causes of IBD are unknown, although abnormal function of the immune system is clearly involved. Proposed causes include chronic infection, genetic abnormality, environmental factors, autoimmunity, and other abnormalities of immunoregulatory mechanisms. Each factor might play a role as a triggering or perpetuating cause. The chronic nature of these diseases and their tendency for spontaneous relapse and flareup have made study and treatment of these diseases complex. This article discusses standard and novel therapies for IBD and includes some review of what is known about the pathophysiology and manifestations of these diseases as a framework for understanding the rationale behind the treatment options. The section on UC discusses short-term therapy, including antibiotics, glucocorticoids, immunosuppressive therapy; nicotine; specialized nutritional therapy, including parenteral nutrition and defined diets; and specific micronutrient supplements, as well as long-term therapy. The section on Crohn's disease defines steroid-refractory and steroid-dependent disease and then discusses short-term therapy, including sulfasalazine, antibiotics, glucocorticoids, budesonide, immunosuppressive therapy, methotrexate, and cyclosporine; specialized nutritional therapy for CD, including defined diets, parenteral nutrition, and specific micronutrient supplements; and longterm therapy for CD, notably drug therapy. The next section of the article considers novel immunomodulatory treatments in IBD, including cytokines and cytokine blockade, T-cell apheresis and T-cell inhibition, and inhibition of adhesion molecules. The final section discusses special considerations in IBD, notably pouchitis in UC, and fistulas in CD. The authors conclude that although surgery should not be considered a failure of medical therapy, the fact that two thirds of patients with CD still require surgery to manage their disease suggests that advances in treatment are needed. 3 figures. 2 tables. 150 references.
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Evolving Treatment Strategies for Inflammatory Bowel Disease Source: in Coggins, C.H.; Hancock, E.W., Eds. Annual Review of Medicine: Selected Topics in the Clinical Sciences, Volume 52. Palo Alto, CA: Annual Reviews Inc. 2001. p. 299-318. Contact: Available from Annual Reviews Inc. 4139 El Camino Way, P.O. Box 10139, Palo Alto, CA 94303-0139. (800) 523-8635. Fax: (415) 855- 9815. PRICE: $47. ISBN: 0824305450. Summary: Crohn's disease and ulcerative colitis (collectively known as inflammatory bowel disease or IBD) are idiopathic (of unknown cause) inflammatory bowel diseases characterized by dysregulated intestinal immune responses in genetically susceptible hosts. This article explains how conventional approaches to the medical therapy of ulcerative colitis and Crohn's disease can now be directed at either induction or maintenance of remission to improve therapeutic efficacy while minimizing complications. Newer approaches have expanded the utility of conventional therapies by improving both safety and efficacy and highlight the importance of specific targets along the immunoinflammatory pathways. Agents discussed include aminosalicylates, corticosteroids, antibiotics, azathioprine, 6 mercaptopurine, methotrexate,
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mycophenolate, cyclosporine, tacrolimus (FK 506), infliximab, and investigational therapies, including CDP571, etanercept, thalidomide, interleukins, adhesion molecules, heparin, probiotics, and nicotine. The combination of conventional and novel approaches now offers the potential of modifying the natural history of these diseases. 2 tables. 143 references. •
Critical Review of Cyclosporine Therapy in Inflammatory Bowel Disease Source: Inflammatory Bowel Diseases. 1(1): 48-63. Spring 1995. Contact: Available from Raven Press, Ltd. 1185 Avenue of the Americas, New York, NY 10036. (800) 777-2836 or (212) 930-9500. Fax (212) 869-3495. Summary: Cyclosporine A (CsA) is a potent inhibitor of cell-mediated immunity; in this article, the author critically reviews the use of CsA in patients with Crohn's disease and ulcerative colitis (UC). Topics covered include the mechanism of action; pharmacology; results in Crohn's disease, in controlled studies, uncontrolled studies, and in patients with fistulous disease; results in UC, including controlled and uncontrolled studies in severe UC, the use in patients with UC associated with primary sclerosing cholangitis, and in refractory left-sided UC; results in the extra-intestinal manifestations of inflammatory bowel disease (IBD); the correlation of clinical response with cyclosporine blood concentrations and with dose; and cyclosporine toxicity. The author concludes that CsA must be used at relatively high (and potentially toxic) dosages to achieve efficacy in IBD. 3 figures. 7 tables. 138 references. (AA-M).
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Long-term Risk of Malignancy After Treatment of Inflammatory Bowel Disease With Azathioprine Source: Alimentary Pharmacology and Therapeutics. 16(7): 1225-1232. July 2002. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com. Summary: Data from renal (kidney) transplant and rheumatoid arthritis (RA) patients suggest that there is an increased risk of malignancy after treatment with azathioprine. Whether this is true for patients with inflammatory bowel disease (IBD) remains uncertain. This article reports on a retrospective review of clinical notes: azathioprine was given to 626 of 2,204 patients (885 with Crohn's disease and 1,349 with ulcerative colitis). The mean total duration of azathioprine was 27 months. The mean follow up from diagnosis was 13.7 years and the mean follow up from the start of azathioprine was 6.9 years. Thirty-one cancers were observed in 30 patients treated with azathioprine (4.5 percent of the population) and 77 cancers were observed in 70 patients not treated with azathioprine (4.5 percent). Logistic regression analysis (including in the model the age, sex, diagnosis, and extent of disease) showed that treatment with azathioprine did not significantly affect the risk of development of cancer. Eight patients had lymphoma; three had been given azathioprine. For patients with ulcerative colitis, the number of colorectal cancers in patients given azathioprine was 8 of 355 (2.2 percent) compared with 28 of 994 (2.8 percent) for patients not given azathioprine (not a significant difference). The authors conclude that no increased risk of cancer diagnosis following azathioprine treatment was observed. 1 figure. 6 tables. 24 references.
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Medical Therapy for Inflammatory Bowel Disease Source: Gastroenterology Clinics of North America. 28(2): 297-321. June 1999.
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Contact: Available from W.B. Saunders. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000. Summary: Despite advances in the understanding of Crohn's disease (CD) and ulcerative colitis (UC), the origins of inflammatory bowel disease (IBD) remain elusive. The therapeutic modalities used to treat CD and UC work at various sites along the immunoinflammatory cascades. This article reviews the pharmacology, mechanisms of action, clinical efficacy, and adverse effects of traditional therapies, such as aminosalicylates and corticosteroids, and examines the expanding number of immunomodulatory agents used in the management of IBD. Traditional therapies, such as aminosalicylates and corticosteroids, continue to be cornerstones in managing of IBD. However, immunomodulators, such as azathioprine and 6 mercaptopurine (6MP), are demonstrating increasing importance in the setting of steroid resistant and steroid dependent disease. Further, postoperative prophylaxis with certain antibiotics (e.g., metronidazole), aminosalicylates, or immunomodulators may be beneficial in preventing recurrence after resection in some patients with CD. In addition, immunosuppressive agents previously reserved for organ transplantation (e.g., cyclosporine) have expanded the number of medical therapies as advances in molecular engineering techniques are already heralding the development of a novel class of biologic therapies available for certain subgroups of patients. 5 tables. 252 references. (AA-M). •
10-Year Survey of Inflammatory Bowel Diseases: Drug Therapy, Costs and Adverse Reactions Source: Alimentary Pharmacology and Therapeutics. 15(4): 475-481. April 2001. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com. Summary: Drug therapy for Crohn's disease and ulcerative colitis (together termed inflammatory bowel disease, or IBD) is based on antiinflammatory and immunomodulating drugs, nutritional support, and surgical resection (removal of part of the intestine). Recently, new drugs have been introduced to combat IBD. This article reports on a study undertaken to consider drug prescriptions, costs, and adverse reactions in IBD patients in Sweden between 1988 and 1997. The annual drug exposure for Crohn's disease was 0.55 million daily doses per million population, mainly supplementation and aminosalicylic acids. Mesalazine and olsalazine had 61 percent within this group. For ulcerative colitis (UC), drug exposure was 0.61 million daily doses per million per year and aminosalicylic acids fell from 70 percent to 65 percent. For IBD patients, corticosteroid use and nutritional supplementation were common. The annual average cost for IBD drugs was $7.0 million (United States dollars). Annually, 32 adverse drug reactions were reported, mainly hematological reactions such as agranulocytosis and pancytopenia (60 percent), followed by skin reactions. Only 2 deaths were reported. Aminosalicylic acids were the most commonly reported compounds. The authors conclude that drug use for IBD in the pre-biologic agent era rested on aminosalicylic acid drugs and corticosteroids with stable levels, proportions, and costs. The level of adverse drug reactions was low, but hematological (blood) reactions support the monitoring of IBD patients. 6 tables. 26 references.
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Dysplasia in Inflammatory Bowel Diseases: Definition and Clinical Impact Source: Canadian Journal of Gastroenterology. 13(8): 671-678. October 1999.
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Contact: Available from Pulsus Group, Inc. 2902 South Sheridan Way, Oakville, Ontario, Canada L6J 7L6. Fax (905) 829-4799. E-mail:
[email protected]. Summary: Dysplasia is a morphological term that means malformation; this article reviews the definition of dysplasia in inflammatory bowel diseases (IBD) and its clinical impact. For the definition of IBD related dysplasia, the nature and origin of the malformation are stressed and the lesion is defined as an epithelial malformation that is unequivocally neoplastic but noninvasive. The use of a precise definition is necessary because of the clinical consequences related to the finding of dysplasia in IBD. The authors note that the microscopic diagnosis of dysplasia, however, remains difficult. Clinically, it is important to make a proper differential diagnosis between polypoid IBD related dysplasia and sporadic adenoma occurring in IBD, and between therapy related pseudodysplasia and genuine dysplasia. When dysplasia is diagnosed, a second opinion may be indicated because of the clinical consequences. Additional techniques to search for genetic defects associated with carcinogenesis can help to support the diagnosis. These techniques can identify changes in DNA content and molecular changes resulting from defects of genes controlling cell proliferation and death or tissue structure. These changes can be absent, appear early or late in the transition from normalcy toward dysplasia and cancer, or appear during repair. Positive findings indicate an increased cancer risk, but the magnitude of the risk remains to be defined. A positive diagnosis of genuine dysplasia necessitates clinical action, either followup of the patient or treatment. The authors conclude that, in practice, treatment means surgery because dysplasia can be a precursor or a marker of malignancy, except for sporadic adenomas, which can be removed locally. 5 figures. 44 references. •
Case-Control Study of Measles Vaccination and Inflammatory Bowel Disease Source: Lancet. 350(9080): 764-766. September 13, 1997. Summary: Evidence has linked measles infection in early childhood with the subsequent risk of developing inflammatory bowel disease (IBD), particularly Crohn's disease. A cohort study had raised the possibility that immunization with live attenuated measles vaccine, which induces active immunity to measles infection, might also predispose to the later development of IBD, provoking concerns about the safety of the vaccine. This article reports on a case-control study of 140 patients with IBD (including 83 with Crohn's disease) born in or after 1968, and 280 controls matched for age, sex, and general practitioner (GP) area. The study was designed to assess the influence of measles vaccination on later development of IBD. Documentary evidence of childhood vaccination history was sought from GP and community health records. Crude measles vaccination rates were 56.4 percent in patients with IBD and 57.1 percent among controls. Matched odds ratios for measles vaccination were 1.09 in patients with Crohn's disease, 0.84 in patients with ulcerative colitis, and 0.97 in all patients with IBD. The authors conclude that their findings provide no support for the hypothesis that measles vaccination in childhood predisposes to the later development of either IBD overall or Crohn's disease in particular. 3 tables. 29 references. (AA-M).
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Neglect of Growth and Development in the Clinical Monitoring of Children and Teenagers with Inflammatory Bowel Disease: Review of Case Records Source: BMJ. 317(7151): 120-121. July 11, 1998. Contact: Available from BMA House. BMJ Fulfillment Department, Tavistock Square, London WC1H 9TD. 44(0)171 383 6270. E-mail:
[email protected].
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Summary: Failure of growth and retarded sexual development are serious and common problems in children and teenagers with inflammatory bowel disease (IBD), particularly those with Crohn's disease. Thus, height, weight, sexual staging, and bone age should be closely monitored in such patients. In 1989, the authors of this article reported serious underrecording of these variables of growth in a group of Scottish children with IBD. This brief article reports on the authors' assessment of the situation a decade later. They studied 28 boys and 13 girls aged less than 16 years at first admission to hospital with ulcerative colitis (n = 14) or Crohn's disease (n = 27). Their results show that, with the exception of one clinicians, few consultants in adult medicine or surgery record the physical development of teenage patients. The authors hypothesize that perhaps the doctor assumes nothing specific can be done about growth failure, or this neglect may simply be an oversight. The authors also consider the impact of various specialties on patient care management. The article concludes by encouraging readers who treat young people with IBD to be more aware of their patients' special nutritional and developmental problems, and should make regular measurements of the variables of growth. 1 table. 2 references. •
Nutritional Therapies for Ulcerative Colitis: Literature Review, Chart Review Study, and Future Research Source: Alternative Therapies in Health and Medicine. 6(1): 55-63. January 2000. Contact: Available from Innovision Communications. 101 Columbia, Aliso Viejo, CA 92656. (800) 899-1712. Fax (949) 362-2022. E-mail:
[email protected]. Website: www.healthonline.com/altther.htm. Summary: Few clinical studies suggest a significant influence of diet or nutritional supplementation on ulcerative colitis (UC). One reason is that UC, like many chronic diseases, is multifactorial. This article describes and reviews the relevant literature on UC, including studies of diet and intravenous therapy; nutritional status and nutritional supplementation; and bowel flora and immune function and their influences. Also, results of a retrospective chart review study that was done at a complementary medicine office are presented. Finally, suggestions for future research are discussed based on a nutritional model of UC. The authors hope that, taken together, these areas will clarify the current status of UC research and promote the types of investigations that are necessary to establish the validity of nutritional influences on UC, as well as the mechanisms that are involved. The authors conclude that their retrospective chart review study suggests that a dietary and nutritional supplementation regimen may significantly benefit UC patients. The study finding is based on significant improvements in symptoms and medication dosage needed to control symptoms. One figure offers a multifactorial model of the use of nutritional therapy in UC. 3 figures. 4 tables. 65 references.
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Effect of Surgery on Health-Related Quality of Life in Patients with Inflammatory Bowel Disease: A Prospective Study Source: Archives of Surgery. 133(8): 826-832. August 1998. Contact: Available from American Medical Association. Subscriber Services Center, P.O. Box 10946, Chicago, IL 60610-0946. (800) 262-2350 or (312) 670-7827. Fax (312) 464-5831. E-mail:
[email protected]. Website: www.ama-assn.org. Summary: Health related quality of life (HRQL) has increasingly become a factor in management decisions in patients with chronic diseases. This article reports on a study undertaken to measure the effect of surgical resection on quality of life in patients with
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inflammatory bowel disease (IBD). A consecutive series of patients undergoing surgery for IBD between June 1994 and December 1997 were prospectively investigated as a cohort outcomes study. Data were obtained for 63 patients (36 with Crohn's disease, and 27 with ulcerative colitis). Patients with Crohn's disease underwent resection with or without stricturoplasty for intractable disease; all but 3 patients with ulcerative colitis underwent ileoanal anastomoses with ileoanal reservoir. Health status was measured using the Health Status Questionnaire preoperatively and every 3 months postoperatively. Preoperative measures of the HRQL of the patients were low, with values well below the general population in all 8 scales of the inventory. Postoperatively, HRQL measures improved significantly both in patients with Crohn's disease and in those with ulcerative colitis, with scores equal to those of the general population on most scales. For example, average raw scores for general health in previously studied patient groups were 59 in patients with asthma, 55 in those with diabetes mellitus, and 74 in the general population; in the present study, scores were 54 preoperatively and 73 postoperatively. The results of this study confirm that HRQL scores are low in many patients with IBD referred for surgery and that scores improve postoperatively to levels comparable to those of the general population. The author conclude that these data justify early surgical intervention in many patients with symptomatic IBD. Appended to the article are comments from other physicians and the authors' response to them. 3 figures. 4 tables. 20 references. (AA-M). •
Crohn's Disease and Ulcerative Colitis Are Associated with the DNA Repair Gene MLH1 Source: Annals of Surgery. 225(6): 718-725. June 1997. Contact: Available from Lippincott-Raven Publishers. 12107 Insurance Way, Hagerstown, MD 21740. (800) 638-3030. Summary: Identification of genes involved in the etiology of inflammatory bowel disease (IBD) may lead to the development of markers that objectively can define disease and permit therapy. The treatment of Crohn's disease of the colon and ulcerative colitis also is complicated by difficulties in differentiating the two conditions. This article reports on a study undertaken to determine whether there is an association between Crohn's disease and ulcerative colitis (two types of IBD) with MLH1, a DNA repair gene. The DNA and clinical data were obtained on 126 unrelated individuals (45 with Crohn's disease, 36 with ulcerative colitis, and 45 control subjects without intestinal disease). Polymerase chain reaction (PCR) products were analyzed. The association between single haplotypes and disease was expressed as relative odds. The authors found that novel associations exist between IBD and two genetic markers within, and one nearby, the DNA mismatch repair gene MLH1. Two categories of haplotypes were associated with the family history of Crohn's disease or ulcerative colitis. The significant association of MLH1 exon 15/D3S1611 haplotype with colonic Crohn's disease, as opposed to ulcerative colitis, may prove to be useful in distinguishing these two diseases. This information may also be helpful in the identification of individuals who are at high risk of developing IBD. Appended to the article is a discussion by three specialists in the field. 2 figures. 3 tables. 24 references.
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Influence of Sex and Disease on Illness-Related Concerns in Inflammatory Bowel Disease Source: Canadian Journal of Gastroenterology. 13(9): 728-732. November 1999.
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Contact: Available from Pulsus Group, Inc. 2902 South Sheridan Way, Oakville, Ontario, Canada L6J 7L6. Fax (905) 829-4799. E-mail:
[email protected]. Summary: Identifying the normal concerns of people with ulcerative colitis (UC) and Crohn's disease (CD) can facilitate a comprehensive approach to their medical care. Clinically, it can be easily appreciated that the concerns of men and women with inflammatory bowel disease (IBD) may differ and that this may have a substantial impact on both coping and treatment decisions. This article reports on a study undertaken to discover the influence of sex and disease on illness related concerns in people with IBD. The 343 subjects in the study answered 25 items on a Rating Form of IBD Patient Concerns (RFIPC). Compared with men, women reported higher levels of IBD symptom severity and higher overall RFIPC scores. Women were more concerned than men about feelings related to their bodies, attractiveness, feeling alone, and having children. There was an interaction between disease and sex regarding concern about sexual performance and intimacy. In both cases, men with CD reported less concern than the other comparison group. The illness concerns that differ between sexes are not the most intense concerns in either sex. These results confirm that gender has a significant influence on a number of illness concerns, particularly concerns related to self image and relationships. The interaction of disease type and sex with respect to concern over sexual performance and intimacy is open to several potential explanations and requires further research. The authors conclude by encouraging clinicians to inquire into these sex specific concerns with which their patients may be struggling. 3 figures. 2 tables. 10 references. •
Is Ileal Pouch-Anal Anastomosis Really the Procedure of Choice for Patients with Ulcerative Colitis? Source: Diseases of the Colon and Rectum. 41(1): 41-45. January 1998. Contact: Available from Williams and Wilkins. 351 West Camden Street, Baltimore, MD 21201-2436. (800) 638-6423 or (410) 528-8555. Summary: Ileal pouch-anal anastomosis is widely claimed to have replaced total proctocolecotomy with ileostomy as the 'procedure of choice' for ulcerative colitis (UC), largely on the basis of a perceived improved quality of life (QOL). There exists relatively little support for this assertion in the literature. This article reports on a study undertaken to determine if informed patients choosing total proctocolectomy with ileostomy have a similar QOL to those who choose ileal pouch-anal anastomosis. All patients with UC referred to a single surgeon and deemed an appropriate surgical candidate were educated about the available surgical options, and then offered a choice between the two options. Age, gender, and complications (including pouchitis) were recorded prospectively, and all patients were questioned regarding functional outcome and level of satisfaction. They were then asked to complete a slightly modified Inflammatory Bowel Disease Questionnaire, which was analyzed by categoric and overall scores. Sixty-seven patients underwent elective surgery for UC during the study period: 55 patients chose ileal pouch-anal anastomosis and 12 had total proctocolectomy with ileostomy. The groups were similar except for younger age and longer followup in the ileal pouch-anal anastomosis group. Patients undergoing the ileal pouch procedure had significantly more short term or long term complications (49 versus 8 percent), with pouchitis being the most frequent complication. There was no difference in level of satisfaction between the two groups, and no patients in either group wished they had undergone the other procedure. Patients who undergo ileal pouch-anal anastomosis can expect a high level of satisfaction, with a good QOL. However, educated patients choosing an ileostomy can achieve the same quality of life, without the higher
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complication rate associated with a pelvic pouch. 2 figures. 4 tables. 10 references. (AAM). •
Historical Basis of the Idiopathic Inflammatory Bowel Diseases Source: Inflammatory Bowel Diseases. 1(1): 2-26. Spring 1995. Contact: Available from Raven Press, Ltd. 1185 Avenue of the Americas, New York, NY 10036. (800) 777-2836 or (212) 930-9500. Fax (212) 869-3495. Summary: In this article, the author presents an historical review of the idiopathic inflammatory bowel diseases (IBDs). He notes that the nonspecific inflammatory bowel diseases (ulcerative colitis and Crohn's disease) initially emerged in single case reports several centuries ago. The author addresses the early history of ulcerative colitis (UC) and Crohn's disease, the initial IBD literature, and early etiologic concepts. The author concludes that the increasing incidence of patients with UC during the first third to onehalf of the 20th century, which has now stabilized, and the increasing numbers of patients with regional enteritis (Crohn's disease) during the second half of the century, are consistent with an epidemiologic pattern reflecting environmental etiologic factors. 1 table. 266 references. (AA-M).
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Supporting the Patient With Inflammatory Bowel Disease Source: Nursing Times. 91(27): 38-39. July 5, 1995. Contact: Available from Mercury Airfreight International Limited, Inc. 2323 Randolph Avenue, Avenel, NJ 07001. Summary: In this article, the authors consider the nurse's role in patient education, information, and support for people with inflammatory bowel disease (IBD), including Crohn's disease, ulcerative colitis, and ulcerative proctitis. Topics include a basic description of IBD; etiologic factors; diagnostic considerations; complications of IBD; drug therapy used to treat IBD and its typical long-term nature; managing and preventing fecal incontinence; and the psychosocial implications of living with IBD. Two sidebars are included: one presents a brief glossary of IBD terms; the second summarizes the three types of IBD: Crohn's disease, ulcerative colitis, and proctitis. 3 figures. 8 references. (AA-M).
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Differential Diagnosis of Inflammatory Bowel Disease: Part One Source: Practical Gastroenterology. 19(2): 10-12, 15-16, 21-22. February 1995. Summary: In this article, the authors provide a comprehensive review of the differential diagnosis of inflammatory bowel disease (IBD), focusing on characteristic features of the history and physical examination and laboratory, endoscopic, and histopathologic findings that can be used to differentiate these disorders. They stress the importance of physicians caring for patients with idiopathic IBD differentiating ulcerative colitis and Crohn's disease from infectious and noninfectious diseases with similar clinical presentations. They also note that colonoscopy is frequently required to obtain the visual and histologic sampling necessary to make the correct diagnosis. 3 tables. (AAM).
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Maintenance Therapy in Ulcerative Colitis and Crohn's Disease Source: Journal of Clinical Gastroenterology. 20(2): 117-122. March 1995.
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Summary: In this review article, the author surveys the current options for maintaining remissions in inflammatory bowel disease. The first section discusses maintenance therapy of ulcerative colitis, including aminosalicylates, corticosteroids, and immunomodulators. The second section addresses Crohn's disease, including management options using aminosalicylates, corticosteroids, immunomodulators, antibiotics, and dietary therapy. The author concludes that, in contrast to aminosalicylates, corticosteroids and cyclosporine are better suited to the induction of rapid remissions of acute disease than to the maintenance of long term remissions. Antimetabolites, especially azathioprine and 6-mercaptopurine, are highly beneficial and relatively safe for long-term steroid sparing therapy in both ulcerative colitis and Crohn's disease, at least for those patients whose initial remissions have already been induced by these agents. 102 references. (AA-M). •
Inflammatory Bowel Disease: Current and Future Therapeutic Options Source: Postgraduate Medicine. 103(5): 86-88, 90, 95-97, 101-102. May 1998. Contact: Available from McGraw-Hill, Inc. 1221 Avenue of the Americas, New York, NY 10020. (612) 832-7869. Summary: Inflammatory bowel disease (IBD) usually presents as a complicated spectrum of flares and remissions, but the underlying course of the disease is chronic. This article, the second of two on IBD, presents an overview of the available treatment options, including both conventional methods and promising investigative approaches. Some of the most commonly used conventional agents used to treat IBD are the 5aminosalicylic acids, sulfasalazine, mesalamine, and olsalazine sodium. Corticosteroids and immunomodulating agents are also often used. The folic acid antagonist methotrexate and the antibiotics metronidazole, ciprofloxacin, and clarithromycin are other familiar components of conventional therapy. The authors also discuss some alternative approaches, including enema therapy (with introduction of a corticosteroid or a short-chain fatty acid) and nutritional therapy (elemental diets or glutamine supplementation). Because of the chronic nature of their condition, patients with IBD often become quite sophisticated in their understanding of treatment methods so they should be told of new options for controlling their disease. 2 tables. 28 references. (AAM).
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Inflammatory Bowel Disease in Minorities: Fiction or Fact? Source: Practical Gastroenterology. 26(3): 54, 56, 59, 60, 62, 64, 66. March 2002. Contact: Available from Shugar Publishing. 12 Moniebogue Lane, Westhampton Beach, NY 11978. (516) 288-4404. Fax (516) 288-4435. Summary: Inflammatory bowel disease (IBD, consisting of ulcerative colitis and Crohn's disease) has traditionally been considered as 'a disease of the whites.' Limited data is available on the racial differences in the occurrence of IBD. Both ulcerative colitis and Crohn's disease are thought to be rare in minorities. This article reviews the emerging evidence suggesting that the incidence in blacks, Asians, and Hispanics, is higher than previously recognized. Studies of immigrants from low incidence to high incidence regions of the world support the hypothesis that environmental factors play a role in the development of IBD, and may account for its low prevalence in countries with predominantly nonwhite populations. There are also data suggesting differences in clinical features and disease outcomes among minority groups. Whether the differences reflect genetic heterogeneity or sociocultural factors is incompletely defined. The authors conclude that it is important to recognize in this new millennium that IBS can
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occur in minority populations, and its incidence in them is higher than previously recognized. 2 tables. 37 references. •
Impact of Diet on Inflammatory Bowel Disease Source: Digestive Health and Nutrition. p. 9-11. January-February 2002. Contact: Available from American Gastroenterological Association. 7910 Woodmont Avenue, 7th Floor, Bethesda, MD 20814. (877) DHN-4YOU or (301) 654-2055, ext. 650. Email:
[email protected]. Summary: Inflammatory bowel disease (IBD, including ulcerative colitis and Crohns disease) can be debilitating, but many people with IBD find ways to manage their illness through a combination of medications and diet. This article describes the impact of diet on the management of IBD. The author begins with two case reports, one of a patient with ulcerative colitis and one of a patient with Crohns disease. The author then reviews several foods that are known to cause aggravating symptoms for IBD patients: high fiber foods, milk and milk products, fried foods, greasy foods, and large meals. Patients are cautioned that because of the intestinal elimination of proteins and other nutrients from the body, people with IBD may lack essential nutrients; in addition, too many dietary restrictions can contribute to dehydration and malnutrition. People with IBD must be sure to compensate the body sufficiently by following the advice of a physician and nutritionist and eating the right foods and multivitamins. Children and teenagers with IBD must be monitored even more closely because inadequate nutrition and loss of essential vitamins may threaten physical growth as well as behavioral and cognitive development. The author also discusses the impact of drug therapy on the symptoms of IBD and possible interactions between drugs and nutrition. One sidebar summarizes the possible indications for surgery for IBD. The article concludes with two web site addresses for additional information.
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Prevalence of Appendectomy Among Ulcerative Colitis Patients and Their Relatives Source: European Journal of Gastroenterology and Hepatology. 13(10): 1231-1233. October 2001. Contact: Available from Lippincott Williams and Wilkins. 241 Borough High Street, London SE1 1GB, UK 44(0)20-7940-7502. Fax: 44(0)20-7940-7574. Website: http://www.eurojgh.com/. Summary: It has been suggested that appendectomy (removal of the appendix) may protect against ulcerative colitis (UC). However, the incidences of appendectomy and UC in developed countries have diverged over the last 50 years, possibly as a consequence of environmental factors. This study was undertaken to determine whether the incidence of appendectomy is lower in patients with UC than in the general population. Patients with UC (n = 153), their relatives (n = 116), and members of the general population (n = 306) that had been matched for age, sex, and educational status were studied. Six percent of UC patients had undergone appendectomy. The corresponding figure for non family controls was 20 percent. The rate of appendectomy within families (cases plus siblings) was 17 of 269 patients (6.3 percent) and was similar to that for UC patients alone. A negative association between appendectomy and UC exists in our patients with UC. In addition, the appendectomy rate in families of UC patients was lower than that in the general population, possibly implying that common environmental and genetic factors could play an important role in the divergent incidences of appendicitis and UC over the last 50 years. 2 tables. 18 references.
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Information for Patients About Inflammatory Bowel Disease Source: Journal of the Royal College of Physicians of London. 31(2): 184-187. MarchApril 1997. Contact: Available from Royal College Of Physicians. Publications Department, 11 St. Andrews Place, Regent's Park, London NW1 4LE. Phone 0171 935 1174. Fax 0171 487 5218. Summary: It is important that inflammatory bowel disease (IBD) patients fully understand their condition since this helps to improve long term management of the disease. This article reports on a study undertaken to assess the information given to patients with IBD about their condition, its treatment, and the National Association for Colitis and Crohn's disease (NACC, a British patient support organization). Two surveys were performed, using anonymous questionnaires. One included all association members in northeast England, and the other was a sample of patients attending medical outpatient clinics. The surveys showed that more patients heard of the NACC from the media than from medical sources. Of patients seen in medical clinics, 75 percent would welcome more information about their disease. In four of the six participating centers, less than half the patients had been told about the existence of a patient's association. There was considerable variation in the instructions on what action to take in the event of a relapse. These findings suggest that the opportunity offered by outpatient clinics to educate and inform patients is often wasted. Clinicians often neglect to mention the NACC, especially to patients with long-standing disease. The authors conclude that a higher priority should be given to providing patients with appropriate information on IBD. The authors also propose three simple audit standards for the organization of outpatient clinic information. 1 figure. 6 references. (AA).
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Quality-of-Life Factors in Adolescent Inflammatory Bowel Disease Source: Inflammatory Bowel Diseases. 4(1): 6-11. February 1998. Contact: Available from Lippincott Raven Publishers. 12107 Insurance Way, P.O. Box 1580, Hagerstown, MD 21741-1580. (800) 777-2295 or (301) 714-2300. Fax (301) 824-7390. E-mail:
[email protected]. Summary: Little is known about the specific psychosocial factors that influence quality of life in adolescents with newly diagnosed inflammatory bowel disease (IBD). This article reports on a study in which the authors used a model to assess adolescent adjustment to recent-onset IBD. Thirty adolescent-parent pairs completed a set of standardized questionnaires. Adolescents were 12 to 18 years of age and had Crohn's disease or ulcerative colitis of less than 5 years duration. Adolescents health-related quality of life scores significantly correlated with satisfaction and degree of closeness with their social support members, such as parents. An unexpected finding was that the adolescents included more extended family than peers in their social support networks. Also of note was that parental coping styles rather than adolescent coping styles significantly correlated with adolescents quality of life health scores. Severity of illness did not correlate with adolescent quality of life health scores. There was significant agreement between adolescent and parental quality of life health scores and stressful event ratings. Adolescents with recent-onset IBD rely more on family members than their peers for emotional support, and they depend more on their parents coping skills than on their own. These findings may indicate lags in normal adolescent development. Adolescents and parents do communicate and share concerns with each other. The authors conclude that support programs for adolescents with IBD should reinforce
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existing coping skills and parent-adolescent communication while promoting development. 4 tables. 25 references. (AA-M). •
Mesalamine in Pediatric Inflammatory Bowel Disease: A 10-Year Experience Source: Inflammatory Bowel Diseases. 2(4): 229-235. Winter 1996. Summary: Mesalamine is an enteric-coated 5-aminosalicylic acid formulation effective in the treatment of ulcerative colitis, and in decreasing the relapse rate in Crohn's disease. However, little data are available regarding its use in children and adolescents. This article reports on a study to determine the modalities of use, safety, and the optimal dose in this age group. Charts of 153 pediatric patients with inflammatory bowel disease (IBD) treated with mesalamine were reviewed, representing more than 150 patient years of use. Among these, more than half of the children diagnosed with Crohn's disease (120 patients) had ileocolonic involvement, and pancolitis predominated in those with ulcerative colitis (33 patients). Patients with ulcerative colitis were diagnosed at a younger age than those with Crohn's disease, and thus mesalamine therapy was initiated earlier. When used as monotherapy, no difference was noted in the average dose used for the treatment of active disease versus maintenance therapy (36 mg per kg per day). However, the average dose used did increase since 1992, for both the treatment of active disease and relapse prevention (43 mg per kg per day). Overall, 18 patients (11.8 percent) were withdrawn from mesalamine therapy; however, only 8 (5.2 percent) had objective side effects. Exacerbation of diarrhea was the most common reason for withdrawal. The authors conclude that this study suggests that mesalamine is a safe and well-tolerated medication in the longterm treatment of pediatric patients with ulcerative colitis and Crohn's disease. 4 tables. 44 references. (AA-M).
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Critical Approach to New Forms of Treatment of Crohn's Disease and Ulcerative Colitis Source: Alimentary Pharmacology and Therapeutics. 16 (Supplement 4): 53-58. July 2002. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com. Summary: Most patient with inflammatory bowel disease (IBD) can be managed with conventional immunosuppressive therapy. However, the recent increase in knowledge of inflammatory mechanisms and the high incidence of toxicity with prolonged steroid use, together with the fact that controlled trials have clearly shown that glucocorticosteroids do not maintain remission, warrants a rational approach to the choice of newer and less well tested therapeutic approaches in those patients who are not responding effectively to the standard treatment. In this review article, the authors offer a critical approach to the newer forms of treatment in the management of severe cases of IBD. 45 references.
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Nutritional Issues and Therapy in Inflammatory Bowel Disease Source: Seminars in Gastrointestinal Disease. 9(1): 21-30. January 1998. Contact: Available from W.B. Saunders Company. 6277 Sea Harbor Drive, Orlando, FL 32887. (800) 654-2452 or (407) 345-4000. Summary: Nutritional issues in inflammatory bowel disease (IBD) often receive inadequate attention both in regard to therapy and nutritionally related complications of
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IBD. This article reviews much of the research that has evaluated the role of diet in the causation, primary treatment, and adjunctive therapy of both ulcerative colitis (UC) and Crohn's disease (CD). Elemental or polymeric diets have proved beneficial for treating acute flareups of CD and maintenance of IBD. A careful team approach can overcome problems in implementing nutritional therapy. Nutrition also has a critical benefit in postoperative CD and perioperative UC. Easily corrected nutritional abnormalities are often overlooked in patients with IBD, which may have significant consequences. Therapeutic nutritional interventions as primary therapy are of some benefit in Crohn's disease but patient selection is tremendously important. Elemental diets appear useful for at least a distinct subset of patients who require an alternative to steroids, and the best response is seen in those with mild to moderate, nonstricturing, predominantly small bowel disease without bloody diarrhea. Polymeric diets are cheaper, better tolerated, and probably as efficacious as elemental diets. Total parenteral nutrition (TPN) has a demonstrated benefit for nutritional improvement and a clear use in active Crohn's disease. The authors conclude that nutritional therapy may have a central place in the hierarchy of treatment in IBD and further research is critical to better define its benefits. Appended to the article is a relevant case history, with commentary by one of the authors and three additional physicians. 1 table. 30 references. (AA-M). •
Inflammatory Bowel Disease in Pediatric and Adolescent Patients Source: Gastroenterology Clinics of North America. 28(2): 445-458. June 1999. Contact: Available from W.B. Saunders. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000. Summary: Once considered rare in pediatric practice, chronic inflammatory bowel disease (IBD) is now being recognized with increasing frequency in children of all ages. This article reviews IBD in pediatric and adolescent patients. In addition to the usual gastrointestinal symptoms of diarrhea, abdominal pain, weight loss, anemia, joint symptoms, and rectal bleeding, children may exhibit prominent extraintestinal manifestations such as growth failure and delayed puberty. Other problems unique to pediatrics include the lack of controlled clinical trials and the lack of medications available for and tested in children, as well as the psychological issues that occur in children and adolescents with IBD. The authors stress that these unique problems necessitate a different medical approach than is used for adult onset IBD. A critical factor in the successful management of this disease is the willingness of the patient to cooperate with the multidisciplinary care team. Parents and patients must be educated and supported to treat these disorders effectively. 1 table. 61 references. (AA-M).
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Surgical Therapy for Ulcerative Colitis and Crohn's Disease Source: Gastroenterology Clinics of North America. 28(2): 371-390. June 1999. Contact: Available from W.B. Saunders. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000. Summary: Over the past two decades, there has been considerable progress in the surgical management of inflammatory bowel disease (IBD). This article reviews the surgical therapy for ulcerative colitis (UC) and Crohn's disease (CD). Crohn's disease is a chronic, nonspecific inflammatory disease of the gastrointestinal tract of unknown cause. It involves mainly the ileum, colon, and rectum, most often producing symptoms of obstruction or localized perforation with fistula. Although surgical treatment is palliative, operative excision in combination with strictureplasty, where appropriate, provides effective symptomatic relief and reasonable long term benefit. Chronic
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ulcerative colitis is a diffuse inflammatory disease of the mucosal lining of the colon and rectum. Total removal of the colon and rectum provides a complete cure. Newer surgical alternatives have eliminated the need for a permanent ileostomy following definitive resection of the involved colon and rectum. 7 figures. 2 tables. 42 references. (AA-M). •
Screening and Surveillance of Ulcerative Colitis Source: Gastrointestinal Endoscopy Clinics of North America. 7(1): 129-145. January 1997. Contact: Available from W.B. Saunders Company. Periodicals Fulfillment, 6277 Sea Harbor Drive, Orlando, FL 32887. (800) 654-2452. Summary: Patients with longstanding ulcerative colitis (UC) are at a higher risk of developing cancer than the normal population. In this article, the author reviews guidelines for the screening and surveillance of cancer risk in people with UC. The relative risk is difficult to assess because published figures vary markedly. A number of centers have instituted annual colonoscopy screening for patients in the at-risk group. No randomized controlled clinical trials have been undertaken using mortality as end point and power calculations suggest that to obtain a useful answer it is necessary to randomize over 4,000. This number is 10 times larger than the largest surveillance study reported to date and it is unlikely that it will ever be undertaken. A critical analysis of the descriptive studies published to date suggests that there may be some benefit from surveillance, but if so it amounts to a saving of perhaps one life for every 200 to 400 colonoscopies. The author concludes that it is better to adopt a flexible and pragmatic approach to the surveillance of patients with UC, providing patients themselves with the information that is available and drawing attention to the advantages and disadvantages of longterm regular colonoscopy. 1 figure. 66 references. (AA-M).
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Presenting Symptoms and Diagnostic Lag in Children with Inflammatory Bowel Disease Source: Inflammatory Bowel Diseases. 5(3): 158-160. August 1999. Contact: Available from Lippincott Williams and Wilkins, Inc. 12107 Insurance Way, Hagerstown, MD 21740. (800) 638-3030. Fax (301) 824-7390. Summary: Presenting symptoms and their duration may affect the time that elapses prior to definitive diagnosis of inflammatory bowel disease (IBD). This article reports on a study undertaken to determine the mean duration of presenting symptoms and diagnostic lag in children with IBD. The medical records of all patients less than 19 years of age diagnosed with IBD at the pediatric gastroenterology clinic of Children's Hospital of Wisconsin between 1990 and 1995 were reviewed. The age at diagnosis, gender, presenting symptoms and duration, disease location, and diagnostic lag were analyzed. There were 91 children (49 male) diagnosed with IBD. Crohn's disease (CD) was diagnosed in 58 children, ulcerative colitis (UC) in 24, and indeterminate colitis in 9. The mean ages at diagnosis were 11.4 years for CD, 9.7 years for UC, and 7.8 years for indeterminate colitis. The most frequent presenting symptoms were abdominal pain, diarrhea, hematochezia, and weight loss. The average lag in diagnosis of CD was 7.1 months, which varied by disease location: small intestine 10.5 months, ileocolonic 7.5 months, and colonic 6.4 months. The average lag in diagnosis was 6.7 months for UC and 14 months for indeterminate colitis. Children presenting with growth failure had the longest diagnostic lag. The authors conclude that the elapsed time between symptom onset and the diagnosis of CD has decreased. The diagnostic lag in CD
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decreases with distal colonic involvement. Following onset of symptoms, UC was diagnosed only slightly more rapidly than CD. 5 tables. 10 references. •
Inflammatory Bowel Disease is Not Associated with an Increased Risk of Lymphoma Source: Gastroenterology. 121(5): 1080-1087. November 2001. Contact: Available from W.B. Saunders Company. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452. Website: www.gastrojournal.org. Summary: Previous studies of the risk of lymphoma in inflammatory bowel disease (IBD) patients have provided conflicting results. This study examines the risk of Hodgkin's and non Hodgkin's lymphoma among patients with inflammatory bowel disease. The authors performed a retrospective cohort study using the General Practice Research Database. Inflammatory bowel disease patients were matched to randomly selected controls on age, sex, and primary care practice. Lymphoma rates were also compared with published age and sex specific rates. The study included 6,605 patients with Crohn's disease; 10,391 with ulcerative colitis (UC); and 60,506 controls followed for an average of 3.7, 3.9, and 4.4 years, respectively. The incidence of lymphoma was not increased in patients with IBD. In subgroup analyses, an increased risk was not observed among patients with Crohn's disease or UC. Compared with IBD patients not treated with azathioprine or 6MP, the relative risk of lymphoma among the 1,465 IBD patients treated with these medications was 1.27. The authors conclude that patients with IBD do not have an increased risk of lymphoma as compared with the general population. Although the authors cannot completely rule out a modest increased risk of lymphoma with azathioprine of 6MP therapy, an increased risk was not observed in this cohort. 4 tables. 48 references.
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Novel Therapies for Inflammatory Bowel Disease Source: Gastroenterology Clinics of North America. 28(2): 323-351. June 1999. Contact: Available from W.B. Saunders. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000. Summary: Recent advances in the understanding of the basic processes that contribute to inflammatory bowel disease (IBD) have led to the identification of new targets for therapy. Agents in development and those newly introduced for clinical use, include both traditional compounds and a growing number of biologic response modifiers. This review article places these novel therapies within a pathophysiologic framework, highlighting completely new targets and therapeutic modalities. Innovations in drug delivery have provided additional benefits from time tested agents such as corticosteroids and 5 aminosalicylic acid in IBD. Newly developed agents, particularly biologic therapies, have begun to assume a prominent role. These include chimeric and humanized monoclonal antibodies, recominant cytokines, recombinant immunoadhesins, oligopeptide receptor agonists and antagonists, and antisense oligonucleotides. The facility with which these agents may be developed, their specificity of action, and their rapid adoption in clinical trials have greatly accelerated the pace of discovery. The author concludes that cell based and gene based therapies will be tested as better vectors for DNA transfer to the gastrointestinal tract are developed and critical targets are pinpointed. 3 figures. 220 references. (AA-M).
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Genetics of Inflammatory Bowel Disease Source: Alimentary Pharmacology and Therapeutics. 15(6): 731-748. June 2001.
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Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com. Summary: Recent epidemiological, clinical and molecular studies have provided strong evidence that inherited predisposition is important in the pathogenesis (development) of chronic inflammatory bowel diseases (IBD). This article reviews these studies on the genetics of IBD. The authors note that the model most consistent with the epidemiological data suggests that Crohn's disease and ulcerative colitis (the two types of IBD) are related polygenic diseases, sharing some but not all susceptibility genes. Investigators throughout the world have applied the complementary techniques of genome wide scanning and candidate gene analysis. Four areas of linkage have been widely replicated on chromosomes 16 (IBD1), 12 (IBD2), 6 (IBD3, the HLA region), and most recently on chromosome 14. Fine mapping of these regions is under way. Of the positional candidate genes, most attention has centered on the genes of the major histocompatibility complex. Genes within this region may determine disease susceptibility, behavior, complications, and response to therapy. A glossary of genetics terms is appended to the article. 1 appendix. 1 figure. 4 tables. 132 references. •
Use of Community Resources Before Inflammatory Bowel Disease Surgery Is Associated with Postsurgical Quality of Life Source: Canadian Journal of Gastroenterology. 14(2): 95-98. February 2000. Contact: Available from Pulsus Group, Inc. 2902 South Sheridan Way, Oakville, Ontario, Canada L6J 7L6. Fax (905) 829-4799. E-mail:
[email protected]. Summary: Research in chronic illness shows that community resources can have a lasting influence on the course of the illness; however, little research has been done to evaluate the community agencies that specifically address the needs of inflammatory bowel disease (IBD) patients. This article reports on a study undertaken to survey awareness of community agency resources among patients who have surgery for IBD, and to analyze the association between using these resources and qualitative postsurgical outcomes. The subjects were 92 patients who had surgery over a 12 month period; each person completed the Inflammatory Bowel Disease Questionnaire (IBDQ), and a self report instrument used to probe awareness and use of local community resources. Community resources were divided into two groups: those involving primarily social and educational participation, and those involving some individualized attention, usually from a professional or a trained lay facilitator. Results showed that almost all subjects were aware of at least one available resource. Participation in resources before surgery was variable, but 50 percent of the sample participated in at least one social or educational resource and 46.9 percent participated in at least one professional or individual support. For the 92 subjects who completed both the IBDQ and a survey of resources, analysis revealed a main effect of professional or individual resource use on postsurgical quality of life but no main effect of social or educational resources and no interaction. The authors conclude that the association between presurgical participation in professional or individualized community resources and better subjective outcome of IBD surgery may be explained by a positive contribution of participation to coping with surgery for IBD. 3 tables. 9 references.
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Inflammatory Bowel Disease in the Elderly Source: Gastroenterology Clinics of North America. 30(2): 409-426. June 2001.
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Contact: Available from W.B. Saunders Company. 6277 Sea Harbor Drive, Orlando, FL 32821-9816. (800) 654-2452. Summary: Roughly 15 percent of all patients with inflammatory bowel disease (IBD) first develop symptoms after age 65. As the number of elderly in the population continues to grow, clinicians should see a greater number of elderly IBD patients. This article, from a special issue on gastrointestinal (GI) disorders in the elderly, addresses IBD in the older patient. In general, the presenting features of IBD are similar to those encountered in younger patients, but the broad differential diagnosis of colitis in the elderly can make definitive diagnosis more challenging. Despite many advances in cellular and molecular biology, the precise cause of IBD is elusive. The elderly are particularly susceptible to GI infection, suggesting a possible compromise of the mucosal immune system with age. The presentation and course of both ulcerative colitis (UC) and Crohn's disease (CD) in older patients is similar to that in younger patients. Differential diagnosis can include infection, ischemic colitis, diverticular disease, microscopic colitis, medications, and other conditions (lymphoma, radiation enterocolitis, vasculitis, amyloidosis). Whereas most therapies for IBD have not been studied specifically in the elderly, as a general rule, medical and surgical treatment options are the same irrespective of age. The authors stress that osteoporosis (abnormal loss of bone density), a condition generally associated with aging, should be managed aggressively in patients with IBD because many older persons already have a substantial baseline risk for accelerated bone loss. 1 figure. 2 tables. 123 references. •
Ulcerative Colitis of the Appendix ('Ulcerative Appendicitis') Mimicking Acute Appendicitis Source: Canadian Journal of Gastroenterology. 15(3): 201-204. March 2001. Contact: Available from Pulsus Group, Inc. 2902 South Sheridan Way, Oakville, Ontario, Canada L6J 7L6. Fax (905) 829-4799. E-mail:
[email protected]. Summary: The appendix may be involved in ulcerative colitis (UC, a type of inflammatory bowel disease), in the setting of either diffuse or distal disease, and is usually diagnosed incidentally at the time of proctocolectomy (surgery to treat the UC). This article describes a patient in whom a rare case of 'ulcerative appendicitis' occurring on a background of clinically quiescent (no active symptoms) UC presented with the signs and symptoms of acute appendicitis. Prior to this presentation, the patient's UC was in remission for over 2 years. The patient was treated with laparotomy and the appendix was removed. Pathology showed acute inflammation confined to the mucosa, with neutrophilic crypt epithelial infiltration (cryptitis) and crypt abscesses consistent with appendix involvement by UC. Following appendectomy, the patient made a rapid and uneventful recovery; he was asymptomatic one day after the operation and was discharged home on day 2. Six months later, the colitis remained in complete clinical remission, and there has been no recurrence of right lower quadrant symptoms. The authors suggest that this patient's acute appendiceal pain syndrome derived from a complex interplay of mucosal immune, vascular, and neurogenic factors, driven by a localized, active focus of UC. Appendectomy provided both the diagnosis and the cure of this acute illness. The authors conclude that although rare (and perhaps underrecognized), acute right lower quadrant pain in the setting of clinically quiescent UC may herald active ulcerative appendicitis, rather than typical suppurative appendicitis. 1 figure. 24 references.
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Sensorineural Hearing Loss and Ulcerative Colitis Source: Journal of Laryngology and Otology. 111(3): 277-278. March 1997. Contact: Available from Headley Brothers Ltd. The Invicta Press, Ashford, Kent, England TN24 8HH. Fax 01483-451874. Summary: The association of sensorineural hearing loss and ulcerative colitis is well documented and it is speculated that this is autoimmune in origin. This article reports the case of a 12 year old boy who developed acute onset asymmetrical hearing loss, at the same time as a diagnosis of ulcerative colitis (UC) was made. He was treated with olsalazine and prednisolone for three months; his bowel symptoms were controlled and his hearing improved almost immediately. Four years after the onset of disease, he experienced bilateral, profound sensorineural hearing loss in spite of good control of his bowel disease. Tests of immune function showed a raised IgA suggestive of chronic immune response, positive anti-nuclear antibodies, and an ESR of 35 mm per hour. The patient's hearing thresholds did not improve following maximal steroid therapy. Treatment with immunosuppressive drugs was offered to the patient but he refused this line of treatment after the potential side effects were explained to him. Immunological tests may provide a clue as to the etiology of suspected cases of autoimmune inner ear disease. The authors stress that immediate treatment with steroids, with or without immunosuppressive therapy, is essential since delay may lead to irreversible hearing loss. 3 figures. 11 references. (AA-M).
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Bone Mineral Metabolism In Pediatric Inflammatory Bowel Disease Source: Inflammatory Bowel Diseases. 5(3): 192-199. August 1999. Contact: Available from Lippincott Williams and Wilkins, Inc. 12107 Insurance Way, Hagerstown, MD 21740. (800) 638-3030. Fax (301) 824-7390. Summary: The development of reliable techniques to measure bone densitometry and evolving effective drug treatment have created great interest in the diagnosis and treatment of osteoporosis in adults with inflammatory disease. This clinical review article considers a number of studies that have examined the prevalence of abnormal bone mineral metabolism in children and adolescents. Studies conducted over the past decade indicate a greater likelihood of clinically significant problems in Crohn's disease than in ulcerative colitis. Corticosteroids have been proven to impair bone mineral status. The author notes that it is increasingly clear that inflammation and other factors play a bigger role than malabsorption of minerals or vitamin D in most patients. As the use of the bisphosphonate class of drugs is limited in pediatric patients, there is a need to emphasize the role of diet and exercise in children and teenagers, particularly in those affected by inflammatory bowel disease (IBD). 5 tables. 86 references.
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Is Maintenance Therapy Always Necessary for Patients with Ulcerative Colitis in Remission? Source: Alimentary Pharmacology and Therapeutics. 13(3): 373-379. March 1999. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com. Summary: The efficacy of sulfasalazine and mesalazine in preventing relapse in patients with ulcerative colitis (UC) is well known. It is less clear how long such maintenance should be continued, and if the duration of disease remission is a factor that affects the
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risk of recurrence. This article reports on a study undertaken to determine whether the duration of remission affects the relapse rate by comparing the efficacy of a delayed release mesalazine against placebo in patients with UC and whose remission is of short or long duration. The study included 112 patients (66 men, 46 women, mean age 35 years) whose intermittent chronic UC in clinical, endoscopic and histologic remission with sulfasalazine or mesalazine for at least 1 year. Patients were stratified according to the length of their remission, prior to randomization into group A (in remission from 1 to 2 years) or group B (in remission for over 2 years, median 4 years). Patients were treated daily with 1.2 grams of oral mesalazine, for a followup period of 1 year. In group A, while no difference was found between the two treatments after 6 months, mesalazine was significantly more effective than placebo in preventing relapse at 12 months. By contrast, in group B, no statistically significant difference was observed between the two treatments, either at 6 or 12 months. Patients in group B were older, and the disease and remission had lasted longer in their case. The authors conclude that mesalazine prophylaxis is necessary for the prevention of relapse by patients with UC in remission for less than 2 years. This study casts doubt on whether continuous maintenance treatment is necessary in patients with prolonged clinical, endoscopic, and histologic remission, and who are at very low risk of relapse. 2 figures. 1 table. 20 references. (AA-M). •
Inflammatory Bowel Disease: Origins, Presentation, and Course Source: Postgraduate Medicine. 103(5): 77-80, 83-84. May 1998. Contact: Available from McGraw-Hill, Inc. 1221 Avenue of the Americas, New York, NY 10020. (612) 832-7869. Summary: The exact cause of inflammatory bowel disease (IBD) remains unknown, but its destructive nature is clearly recognized. This article, the first of two on IBD, summarizes the pathogenesis and epidemiology of ulcerative colitis (UC) and Crohn's disease. Ways to distinguish between these two facets of IBD, both clinically and pathologically, are explained, as are disorders that may mimic IBD. The incidence and prevalence of IBD vary greatly with geographic location and ethnic background. The greatest risk factor is a family history of IBD and immunopathologic alterations culminating in IBD have only recently been described. UC is by definition confined to the colonic mucosa. Inflammation virtually always involves the rectum and is continuous and confluent to its proximal margin. The upper gastrointestinal tract and small bowel are not significantly involved; such involvement suggests Crohn's disease. Common presenting signs of UC include rectal bleeding, diarrhea, abdominal pain, and tenesmus. Crohn's disease is characterized by transmural inflammation. Any part of the gastrointestinal tract can be inflamed, but certain locations are more commonly involved than others. Transmural inflammation can lead to complications not often seen with UC, such as stricture formation, obstruction, fistulas, and abscesses. IBD can have hepatobiliary, rheumatologic, dermatologic, and ocular complications as well. 4 tables. 32 references. (AA-M).
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Induction and Maintenance of Clinical Remission by Interferon-B in Patients with Steroid-Refractory Active Ulcerative Colitis: An Open Long-term Pilot Trial Source: Alimentary Pharmacology and Therapeutics. 16(7): 1233-1239. July 2002. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com.
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Summary: The imbalance of pro and anti-inflammatory cytokines plays an important role in the pathogenesis (development) of inflammatory bowel disease (IBD). Shifting this disturbed ratio by means of TNF antibodies or interferon has been shown to be helpful in treating Crohn's disease (a type of IBD) and multiple sclerosis, respectively. This article reports on a pilot study that investigated whether interferon beta can induce clinical remission in patients with corticoid-refractory ulcerative colitis (UC, another type of IBD, n = 25). Twenty-two of the 25 patients (88 percent) went into remission during induction treatment. Mean time to response was 3.0 weeks (plus or minus 1.3 weeks); mean length of remission was 13.0 months (plus or minus 19.7 months). Only eight of 22 patients in remission relapsed during maintenance treatment. Five of these went into remission again after increasing the dose. Adverse events consisted of slight to moderate flu-like symptoms and slight to moderate hair loss in five of 15 female patients. The authors conclude that, although this open pilot study included only a small number of patients, the high response rate suggests that interferon beta may be a safe and effective treatment for steroid refractory active UC. 31 figure. 4 tables. 33 references. •
Historical Antecedents of Inflammatory Bowel Disease Therapy Source: Inflammatory Bowel Diseases. 2(2): 73-81. Summer 1996. Summary: The increasingly 'scientific' approach to the treatment of inflammatory bowel disease (IBD), i.e., therapeutic interventions based on research, for example, in the development of anti-inflammatory agents to suppress pro-inflammatory molecules, is in sharp contrast to the arbitrary and sometimes bizarre approaches often used in the past. This article provides an historical account of such earlier therapeutic approaches, to emphasize the progress achieved in the treatment of IBD. The author notes that past therapeutic approaches to ulcerative colitis and Crohn's disease reflected prevailing notions and misconceptions of human illness. The author describes unusual discarded treatments, diet therapy, psychotherapy, sulfonamides, antibiotics, adrenocorticotropic hormone (ACTH), steroids, immunosuppressant medications, and the surgical treatment of ulcerative colitis and Crohn's disease. The author concludes that the current treatment of IBD, though improved over earlier programs, remains variable rather than uniform and supportive rather than curative. The differing therapeutic practices result from a variety of factors: obscure etiologies of IBD; limited knowledge of the biological and pharmacological actions of drugs commonly prescribed; inadequate understanding of genetic differences influencing drug metabolism; insufficient awareness of the factors influencing drug efficiency; the variability of the patient groups studied; and incomplete documentation of the clinical status of patients at the time of therapeutic trial. 112 references.
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Bone and Joint Diseases in Inflammatory Bowel Disease Source: Alimentary Pharmacology and Therapeutics. 12(5): 397-404. May 1998. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com. Summary: The intestinal and articular (joints) systems are closely linked in inflammatory bowel disease (IBD). Clinical and immunological studies support an important etiopathogenetic link between intestinal and articular inflammation. There is increasing evidence for a negative link between bone mass density and intestinal inflammation. This article focuses on the prevalence, etio-pathogenesis, and treatment of
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arthritis (peripheral, sacroiliitis, and spondylitis) and osteoporosis in patients with IBD. Peripheral arthritis is most frequently seen in patients with extensive ulcerative colitis (UC) and in patients with Crohn's disease (CD). Especially in UC, a distinct relationship between attacks of arthritis and flareups of bowel disease is observed. One section discusses gut inflammation in spondyloarthropathy, defined as a group of related inflammatory joint diseases that share similar clinical features and a strong association with HLA B27. Entities include not only inflammatory bowel disease but also ankylosing spondylitis, reactive arthritis triggered by a urogenital or enterogenic infection, some form of psoriatic arthritis, and a group of undifferentiated spondyloarthropathies. The latter half of the article addresses bone mass density and IBD, particularly osteoporosis. Osteoporosis is a systemic skeletal disease characterized by a low bone mass and a micro-architectural deterioration leading to increased bone fragility and susceptibility to fracture. The article concludes that identifying the inflammatory mechanisms that reduce bone mass density should help to prevent and treat this IBD-related morbidity. 1 table. 65 references. (AA-M). •
Review Article: The Management of Inflammatory Bowel Disease During Pregnancy Source: Alimentary Pharmacology and Therapeutics. 12(11): 1039-1053. November 1998. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com. Summary: The management of inflammatory bowel disease (IBD) during pregnancy is a particular challenge because adequate disease control before and during gestation is essential for both maternal and fetal health. This review article is designed for the practicing clinician, to guide the management of patients with IBD before and during pregnancy. The authors note that the literature is conflicting at times and that data on some issues are scanty, so recommendations are based on the balance of evidence including extrapolation if necessary. Many of the clinical, biochemical, radiological, and endoscopic investigations used to monitor and assess disease activity are difficult to use and interpret during pregnancy. Furthermore, patients and clinicians are often concerned about the safety of medical and surgical treatments for the fetus. Discussions on fertility and pregnancy should be incorporated into the general education of a patient, because a quarter of patients conceive after their disease is diagnosed. If the IBD is inactive, a patient should expect to be able to conceive, carry a fetus to term, and deliver a healthy baby. At the beginning of a pregnancy, more detailed reassurance should be given about the safety of the drugs and the importance of maintaining good control of disease activity. Most of the drugs for IBD can be used safely during pregnancy, but the benefit must be clear. Relapses should be treated aggressively, because the danger to the fetus results from the active disease and not from the drug regimens. 6 tables. 127 references.
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Palliative Care in Inflammatory Bowel Disease: An Evidence-Based Approach Source: Inflammatory Bowel Diseases. 6(3): 228-243. August 2000. Contact: Available from Lippincott Williams and Wilkins, Inc. 12107 Insurance Way, Hagerstown, MD 21740. (800) 638-3030. Fax (301) 824-7390. Summary: The management of the patient with inflammatory bowel disease (IBD) is challenging for both the physician and the patient. IBD imposes both a physical and emotional burden on patients' lives. Palliative care is important for IBD patients because it focuses on improving quality of life. While palliative care does not change the natural
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history of the disease, it provides relief from pain and other distressing symptoms. This article focuses on various aspects of care for IBD patients, including pain control, management of oral and skin ulcerations, stomal problems in IBD patients, control of nausea and vomiting, management of chronic diarrhea and pruritis ani (itching of the anus), evaluation of anemia, treatment of steroid related bone disease, and treatment of psychological problems associated with IBD. Each of these areas is discussed from an evidence based approach. The authors categorize the evidence discussed in five groups: category A refers to evidence from clinical trials that are randomized and well controlled; category B evidence refers to evidence from cohort or case controlled studies; category C is evidence from case reports or flawed clinical trials; category D evidence is limited to the clinical experience of the authors; evidence labeled as category E refers to situations where there is insufficient evidence available to form an opinion. The authors also present algorithms for the management of pain and nausea in patients with IBD. 2 figures. 2 tables. 193 references. •
Critical Assessment of New Therapies in Inflammatory Bowel Disease Source: Journal of Gastroenterology and Hepatology. 17 (Supplement): S176-S185. February 2002. Contact: Available from Blackwell Science. 54 University Street, Carlton South 3053, Victoria, Australia. +61393470300. Fax +61393475001. E-mail:
[email protected]. Website: www.blackwell-science.com. Summary: The only disease modifying therapy for inflammatory bowel disease (IBD), until recently, was immunosuppression with azathioprine. Other 'standard' therapies for IBD were merely symptomatic. This review article offers a critical assessment of new therapies for IBD. With the advent of biological therapies, especially the chimeric monoclonal anti-TNF antibody infliximab, treatment starts to target specific pathogenic disease mechanisms, which allow thorough suppression of the disease process and healing of the bowel in the long term. Moreover, infliximab is the only drug up to the present that allows short-term healing of fistulizing Crohn's disease (one type of IBD). This therapy is associated with problems of immunogenicity. The formation of antibodies to infliximab jeopardizes the efficacy and is associated with infusion reactions. The author contends that optimization of anti-TNG strategies will occur in the coming years. Another promising therapy is antagonization of alpha4 integrins and hence, of migration of inflammatory cells to the intestine. The author expects that more simple therapies using small molecules that inhibit the key cytokines or proinflammatory processes will take over in the next decade. In the current and future approach to IBD therapy, immunosuppression with azathioprine or 6-MP and methotrexate play a central role. At the present time, the combination of infliximab with azathioprine or methotrexate can be regarded as the new standard for the therapy of refractory Crohn's disease. In ulcerative colitis (UC, another type of IBD), much less progress has been made and the value of biological therapy as well as of long term management with immunosuppression remains controversial. Probiotics are an attractive treatment option for IBD, but studies so far are small and data are not yet convincing. 2 figures. 5 tables. 59 references.
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Inflammatory Bowel Disease: Progress Toward a Gene Source: Canadian Journal of Gastroenterology. 14(3): 207-218. March 2000. Contact: Available from Pulsus Group, Inc. 2902 South Sheridan Way, Oakville, Ontario, Canada L6J 7L6. Fax (905) 829-4799. E-mail:
[email protected].
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Summary: The pathogenesis of ulcerative colitis (UC) and Crohn's disease (CD) is still unknown, but the importance of genetic susceptibility has been clearly shown by epidemiological data from family and twin studies. This article reports on research progress toward identifying the genetic basis of these inflammatory bowel diseases (IBD). Linkage studies have identified two susceptibility loci for IBD on chromosomes 12 and 16. More important, these linkages have been replicated by independent investigators, and studies of positional candidates within these regions continue, together with fine mapping strategies. Regions of 'suggestive' linkage on chromosomes 1, 3, 4, 6, 7, 10, 22, and X have also been reported in individual studies. Other important candidate genes investigated include the interleukin 1 receptor antagonist, MUC3, and genes of the human leukocyte antigen (HLA) system. The apparently conflicting data in different studies from around the world may be explained by ethnic differences, case mix, and genetic heterogeneity. Animal studies have provided insights from targeted mutations and quantitative trait locus analysis. The goals of continuing research include narrowing the regions of linkages and analysis of candidate genes and possibly applying newly developed methods using single nucleotide polymorphisms. Advances in IBD genetics hold the potential to provide knowledge about disease pathogenesis at the molecular level, with ensuing benefits for clinical practice. 2 figures. 2 tables. 144 references. •
Human Colonic Microvascular Endothelial Cells Is a Model of Inflammatory Bowel Disease Source: American Journal of Surgery. 174(3): 247-250. September 1997. Contact: Available from Elsevier Science. 655 Avenue of the Americas, New York, NY 10010-5107. (212) 989-5800 or (212) 633-3730. Fax (212) 633-3990. E-mail:
[email protected]. Website: www.elsevier.nl. Summary: The pathophysiology of inflammatory bowel disease (IBD) remains elusive primarily because of the limitations of the models available for study in the basic science laboratories. IBD is associated with increased vascular permeability seen clinically as mucosal edema (fluid accumulation) and loss of the submucosal vascular pattern. In this article, the author proposes a new model for the study of IBD; data sources include research and review articles published in the English literature. The review focuses on the role of substance P (SP), bradykinin (BK), and vascular endothelial growth factor (VEGF) in the regulation of endothelial cells. Autoradiographic studies of cross sections of human colon involved with ulcerative colitis and Crohn's disease demonstrate increased expression of NK1R binding sites with ectopic expression seen in the endothelium of blood vessels in the submucosa, muscle, and subserosal fat. The author concludes that the human colonic microvascular endothelial cell in culture is a legitimate model for the study of the human colon in the normal and diseased states. This model can be particularly useful because there are no good models in animals that mimic IBD in humans. 1 figure. 40 references.
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Polyunsaturated Fatty Acids and Inflammatory Bowel Disease Source: American Journal of Clinical Nutrition. 71(1 Supplement): 339S-342S. January 2000. Contact: Available from American Journal of Clinical Nutrition. Production Office, 9650 Rockville Pike, Bethesda, MD 20814. (301) 530-7038. Fax (301) 571-8303. Website: www.ajcn.org.
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Summary: The rationale for supplementation with n-3 fatty acids to promote the health of the gastrointestinal (GI) tract lies in the antiinflammatory effects of these lipid (fat) compounds. The first evidence of the importance of dietary intake of n-3 polyunsaturated fatty acids was derived from epidemiological observations of the low incidence of inflammatory bowel disease (IBD) in Eskimos. This article briefly reviews the literature on the use of n-3 fatty acids in IBD (ulcerative colitis and Crohn disease), the results of which are controversial. The discrepancies between studies may reside in the different study designs used as well as in the various formulations and dosages used, some of which may lead to a high incidence of side effects. Choosing a formulation that lowers the incidence of side effects, selecting patients carefully, and paying strict attention to experimental design are critical when investigating further the therapeutic potential of these lipids in inflammatory bowel disease. 1 figure. 27 references. •
'Modern Life' in the Epidemiology of Inflammatory Bowel Disease: A Case-Control Study with Special Emphasis on Nutritional Factors Source: European Journal of Gastroenterology and Hepatology. 10(3): 243-249. March 1998. Contact: Available from Rapid Science Publishers. 400 Market Street, Suite 750, Philadelphia, PA 19106. (800) 552-5866 or (215) 574-2210. Summary: The rising incidence of inflammatory bowel disease (IBD) since the second World War coincides with profound changes in dietary patterns. This article reports on a case control study that investigated the possible pathogenic role of some characteristic modern dietary factors in IBD. The study focused on risk factors in 688 recently diagnosed cases of IBD (290 with Crohn's disease and 398 with ulcerative colitis) compared with 616 population controls. Smoking, age, gender, and education were taken into account by using logistic regression analysis. There was a positive association between the development of Crohn's disease and cola drinks, chewing gum, and chocolate consumption, and a negative association with consumption of citrus fruit. Consumption of cola drinks and chocolate were also positively associated with developing ulcerative colitis. There was a negative association between the intake of citrus fruits and 'having a stuffed pet' for a period longer than 5 years during childhood and developing. No association with the frequency of toothbrushing and developing IBD was found. The authors conclude that these nutritional items may be true risk factors or they might simply be the expression of a modern lifestyle also involving other risk factors for IBD that at present are still unknown. 4 tables. 39 references. (AA-M).
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Update on the Surgical Management of Ulcerative Colitis and Ulcerative Proctitis: Current Controversies and Problems Source: Inflammatory Bowel Diseases. 1(4): 299-312. Winter 1995. Summary: The surgical management of ulcerative colitis (UC) has been revolutionized in recent years by the development of the ileal pouch-anal procedure. Although it is now the operation of choice for most patients, there remain several controversies. This article covers the current controversies and problems associated with the surgical management of UC and ulcerative proctitis. The authors note that a variety of ileal pouch designs are available, each with advantages and disadvantages. The technique used to anastomose the pouch to the anal canal is also open to debate. Some surgeons favor distal mucosectomy with eradication of all disease; others choose to perform a stapled anastomosis to achieve better functional results. The main concern for
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gastroenterologists, however, is the risk of pouchitis. The authors discuss the etiology, diagnosis, and treatment of pouchitis. They also briefly discuss the more classic treatment options for UC, including panproctocolectomy with ileostomy, colectomy with ileorectal anastomosis, and the Kock continent ileostomy. 3 figures. 1 table. 105 references. (AA-M). •
Current Theories on the Causes of Inflammatory Bowel Disease Source: Gastroenterology Clinics of North America. 28(2): 283-296. June 1999. Contact: Available from W.B. Saunders. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000. Summary: The understanding of the pathogenesis of Crohn's disease (CD) and ulcerative colitis (UC) has greatly expanded over the past decade. This review article discusses current theories on the causes of inflammatory bowel disease (IBD), the collective term used for CD and UC. The presence of abnormalities in the immune system, the contribution of nonimmune cells in the intestinal mucosa, a variety of genetic risk determinants, and random environmental factors may all be necessary to induce what clinically presents as IBD. The authors conclude that several agents likely initiate an immune response that finally leads to pathology in the intestinal microenvironment and genetic background of a particular patient. The authors also predict what future directions are most likely to yield useful information and how understanding of these diseases will evolve within the next few years. 1 figure. 96 references. (AA-M).
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Update in Medical Therapy of Ulcerative Colitis: A Practical Approach Source: Journal of Clinical Gastroenterology. 34(4): 397-407. April 2002. Contact: Available from Lippincott Williams and Wilkins, Inc. 12107 Insurance Way, Hagerstown, MD 21740. (800) 638-3030 or (301) 714-2300. Summary: The vast array of medications use in the therapy of inflammatory bowel disease (IBD) often confounds the clinician in the choice of specific agents regarding the balance between safety and efficacy. This review article surveys and evaluates the currently available IBD therapies as well as those used in clinical trials of ulcerative colitis (UC). The author provides the busy clinician with a practical guide to the use of established and newly emerging medical therapies of IBD. The approach to therapy is divided into categories for the treatment of mild to moderate, moderate to severe, and severe disease; maintenance strategies; and pouchitis. The author stresses that the key is to design an individualized program geared to each patient's specific needs. The practitioner must evaluate the patient's response to treatment with each visit, weighing the risks of drug toxicity, cancer surveillance, long-term debility, and surgical candidacy. 9 tables. 129 references.
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Long-Term Aminosalicylate Therapy is Under-used in Patients With Ulcerative Colitis: A Cross-Sectional Survey Source: Alimentary Pharmacology and Therapeutics. 16(11): 1889-1893. November 2002. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com.
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Summary: There is evidence from case-control studies that aminosalicylates drugs can reduce colorectal cancer risk by 75 to 81 percent in patients with ulcerative colitis. Patients may fail to comply with long-term therapies, however, or may have been advised to discontinue treatment once in remission. This article reports on a study undertaken to describe the usage of long-term aminosalicylates therapy in patients with ulcerative colitis (UC). The cross-sectional study was performed using data extracted from general practitioner clinical records on demographic features, extent and duration of disease, use of aminosalicylates therapy, and specialist care. The study included 363 people who had UC and no history of colorectal surgery. Ninety-five of 175 patients (54 percent) with proctitis, 78 of 123 patients (63 percent) with left-sided colitis, and 28 of 45 patients (62 percent) with extensive colitis were currently taking an aminosalicylate drug. Those doing so were more likely to be under specialist care than to be definitely or possibly discharged. The likelihood of current aminosalicylates therapy was not related to gender or the extent of disease, but was negatively related to the duration of disease. The authors conclude that a substantial minority of patients with ulcerative colitis does not take long-term aminosalicylates therapy. Those who do are more likely to be under specialist care, to be older, or to have disease of shorter duration. 2 tables. 23 references. •
Review Article: Insurance Risks for Patients With Ulcerative Colitis or Crohn's Disease Source: Alimentary Pharmacology and Therapeutics. 11(1): 51-59. February 1997. Contact: Available from Mercury Airfreight International, Ltd. 2323 EF, Randolph Avenue, Avenel, NJ 07001. E-mail:
[email protected]. Summary: This article addresses the issue of insurance risks for patients with ulcerative colitis (UC) or Crohn's disease. Prospective population-based studies have allowed a reevaluation of the risks of insuring patients with UC or Crohn's disease. Life expectancy, the risk of cancer, and working capacity are very much better than previously recognized and are normal for many patients. Three population-based studies in UC have shown a mortality similar to or slightly less than the general population except in the first year after diagnosis, while two have shown a slightly higher mortality, except for those with proctitis. In Crohn's disease, two populationbased studies have also shown an increased mortality that is similar to that of unskilled manual laborers from all causes of death. Three other studies have shown no increase in overall mortality, except in the first 5 years after diagnosis, in those with proximal small intestinal disease, and in some patients needing multiple operations. Insurance risks should be evaluated on an individual basis, after details of the extent and pattern of disease have been obtained. Although the 'standard life' in insurance terms differs from that of the general population, because people who seek life insurance are self-selected from a more affluent section of society, many patients can be identified who have a particularly good prognosis. These include patients with ulcerative proctitis, those with leftsided colitis in extended remission (more than 12 months), and patients more than 30 years old with localized ileal or ileocecal Crohn's disease that has responded to treatment. The author concludes that, from the published data, it is difficult to justify increasing the insurance premium in such patients. 6 tables. 23 references. (AA-M).
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Cancer Surveillance in Ulcerative Colitis: A Survey of Patients' Knowledge Source: Endoscopy. 28(9): 761-762. November 1996. Contact: Available from Thieme Medical Publishers, Inc. 381 Park Avenue South, New York, NY 10016. (800) 782-3488 or (212) 683-5088. Fax (212) 683-5118.
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Summary: This article briefly reports on a study undertaken to investigate the level of knowledge of colorectal carcinoma and its screening and treatment in a group of 61 patients with long standing and extensive ulcerative colitis. In a questionnaire mailed to them, they were asked about their risk of carcinoma, about the existence of screening facilities, and about the treatment of colorectal carcinoma. Forty three completed questionnaires were returned, and 86 percent of patients were aware of the increased risk of carcinoma. Only 44 percent knew that it was possible to screen for colorectal carcinoma, and 47 percent did not know that carcinoma detected at screening would require surgical removal. The authors conclude that large numbers of patients are unaware of the existence of screening facilities for colorectal cancer and are ignorant of how the disease is treated. Increased public information is required to improve compliance with screening programs and to enable patients to take part in decisions about their management. 6 references. (AA). •
Effects of Inflammatory Bowel Disease on Adolescents Source: Gastroenterology Nursing. 23(2): 63-66. March-April 2000. Contact: Available from Williams and Wilkins. 351 West Camden Street, Baltimore, MD 21201-2436. (410) 528-8555. Summary: This article considers the effects of inflammatory bowel disease (IBD) on adolescents. Adolescence is a time of profound change for individuals; a time that can witness biologic, social, and psychological change in the individual as well as role changes within the family and peer groups. Compounding these difficult transitions with the onset of inflammatory bowel disease leads to additional problems with adolescence adjustment. In the limited studies that have addressed the adolescent and IBD, several key concepts emerge that point to ways for successfully dealing with these adolescent adjustment problems. The author explains how Roy's Adaptation Model can provide a foundation for identifying and selecting interventions in working with adolescents and chronic illness. This model features three steps: assessment of the client's behavior in each of the adaptive modes; selection of the areas of concern that need reinforcing, either maladaptive or adaptive behaviors; and for each of the behaviors, determination of the focal, contextual, and residual stimuli that shapes the behaviors. The author uses a hypothetical case study to demonstrate the application of this model. 15 references.
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Rare Case of Ulcerative Colitis Complicating Wilson's Disease: Possible Association Between the Two Diseases Source: Journal of Clinical Gastroenterology. 35(1): 43-45. July 2002. Contact: Available from Lippincott Williams and Wilkins, Inc. 12107 Insurance Way, Hagerstown, MD 21740. (800) 638-3030 or (301) 714-2300. Summary: This article describes a rare case of ulcerative colitis (UC, a type of inflammatory bowel disease, or IBD) complicated by Wilson's disease. Wilson's disease is a genetic disorder in which failure of copper excretion causes accumulation of copper in the liver and other organs. In this case, a 24 year old Japanese man, UC occurred 12 years after the diagnosis of Wilson's disease, and the colitis was intractable to prednisolone and salazosulfapyridine. Because copper is one of the trace elements necessary for antioxidant defenses during the inflammatory process, altered copper metabolism may have contributed to the intractability of the UC in this case. 2 figures. 31 references.
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Basis of Current and Future Therapy for Inflammatory Bowel Disease Source: American Journal of Medicine. 100(6): 656-662. June 1996. Summary: This article describes current medical therapy as well as the types and theoretical basis of novel therapies being used for inflammatory bowel disease (IBD). Topics include nonspecific inflammation; the use of 5-aminosalicylates and corticosteroids; new inflammatory therapies; the specific immune phase and the use of immunosuppressives to manage it; and the immune induction phase. The author concludes that the majority of patients with IBD can be managed with available therapy, but the available agents do not seem to alter the natural history of the disease. 4 figures. 3 tables. 26 references. (AA-M).
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Ulcerative Colitis and Crohn's Disease in Children: Diagnosis and Management Source: Gastroenterology Clinics of North America. 24(1): 99-117. March 1995. Contact: Available from W.B. Saunders Company, Periodicals Fulfillment, 6277 Sea Harbor Drive, Orlando, FL 32887. (800) 654-2452. Summary: This article describes many of the special features of inflammatory bowel diseases (IBD) in children. Topics include systemic and extraintestinal features, including weight loss, arthralgias and arthritis, delayed growth and sexual maturation, mucocutaneous lesions, renal disease, hepatobiliary disease, and ocular complications; diagnostic tests; treatment, including medical management, maintenance therapy, immunosuppressive therapy, and surgical intervention; nutritional intervention; and monitoring response to therapy. 109 references. (AA-M).
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Pharmacologic Therapy for Inflammatory Bowel Disease Source: American Family Physician. 51(8): 1971-1975. June 1995. Summary: This article describes pharmacologic therapy for inflammatory bowel disease (IBD), a therapy usually carried out in a stepwise fashion. Initially, oral sulfasalazine or 5-aminosalicylic acid (5-ASA) products are given and, for patients with rectal disease, treatment may include topical therapy with either 5-ASA enemas or hydrocortisone suppositories. Patients with more active inflammatory disorders may also require oral corticosteroid therapy. Patients with fulminant disease may require intravenous steroids and antibiotic therapy. If frequent relapses prevent discontinuation or significant reduction of prednisone therapy, azathioprine or 6-mercaptopurine may offer benefit as steroid-sparing agents. Also, intravenous cyclosporine has proved useful in patients with fulminant IBD that is unresponsive to other therapy. Metronidazole has value in the treatment of perianal disease secondary to Crohn's disease. The authors conclude that balancing the risks and benefits of single or combination therapy is an ongoing challenge in patients with IBD. 1 table. 13 references. (AA-M).
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Genetics of Inflammatory Bowel Disease: A Guide for the Clinician Source: Practical Gastroenterology. 21(9): 25-26, 29-30, 32. September 1998. Contact: Available from Shugar Publishing, Inc. 99B Main Street, Westhampton Beach, NY 11978. (631) 288-4404. Fax (631) 288-4435. E-Mail:
[email protected]. Summary: This article explains why the inflammatory bowel diseases (IBD), including ulcerative colitis and Crohn's disease, are fundamentally genetic disorders. IBD genes are being identified and genetic markers and serum antibodies are being used to define clinical subgroups. IBD disorders have a higher prevalence in certain ethnic groups, are
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inherited within families, and are associated with particular genetic syndromes. To locate IBD genes, researchers have combined two different approaches. The first is a genomewide search, in which the entire human genome is screened for genes linked within IBD families. The second is the candidate gene approach, where immunologically relevant genes are tested for associations within IBD populations and families. These two strategies have led to considerable progress in identifying potential genes, but no single gene has yet been linked to a specific functional defect in IBD. However, candidate genes in combination with serum immunologic markers can be used to stratify patients into clinically important subgroups. In this way; these markers may eventually guide the clinician in diagnosis and treatment. 2 tables. 8 references. (AA-M). •
Surgical Options in Ulcerative Colitis Source: Surgical Clinics of North America. 77(1): 85-94. February 1997. Contact: Available from W.B. Saunders Company. Periodicals Fulfillment, 6277 Sea Harbor Drive, Orlando, FL 32887. (800) 654-2452. Summary: This article outlines controversies in surgical options for ulcerative colitis (UC). The authors review the current literature concerning pouch design, the need for a defunctioning ileostomy after the ileal pouch-anal anastomosis, whether a mucosectomy should be performed, and whether a pouch is safe in the setting of cancer. The J configuration appears to be satisfactory if sufficient length of terminal ileum is used. Functional outcome does not appear to be affected if a mucosectomy is performed. The need for defunction should be based on technical and patient-related considerations. Early cancer does not contraindicate ileal pouch-anal anastomosis. 4 tables. 40 references. (AA).
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Modern Medical Management of Acute, Severe Ulcerative Colitis Source: European Journal of Gastroenterology and Hepatology. 9(9): 831-835. July 1997. Contact: Available from Rapid Science Publishers. 400 Market Street, Suite 750, Philadelphia, PA 19106. (800) 552-5866 or (215) 574-2210. Summary: This article outlines the medical management indicated for patients with acute, severe ulcerative colitis (UC), a condition that the authors stress requires careful in-hospital assessment of the patient and the coordinated treatment of a team of experienced gastroenterologists and surgeons. Complete understanding of the potential complications and their management, especially toxic megacolon, is essential. The authors review the current medical arsenal and advocate a standardized approach to management that includes continuous, high dose intravenous hydrocortisone, more aggressive use of topical steroids as well as feeding the patients and continuing (but not initiating) oral 5-aminosalicylic acid (5-ASA) agents. For those patients whose disease proves refractory to intravenous steroids, intravenous cyclosporin (with an acute response rate of 82 percent) is an essential component of medical management. Antibiotics should be used only when specifically indicated. Total parenteral nutrition has not been shown to be helpful in the acute setting. Air contrast barium enema and colonoscopy have been used to predict response but may be dangerous diagnostic modalities in these acutely ill patients and are no better than good clinical judgment. The authors review and advocate long term management of acute response using 6mercaptopurine or azathioprine. The surgical experience and the postoperative complications of the ileal pouch anal anastomosis, which include acute pouchitis in 50 to 60 percent, chronic pouchitis in 5 to 10 percent, and recent reports of dysplasia among patients with chronic pouchitis, must be considered before colectomy is advised. The
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authors conclude that more than 80 percent of patients with acute severe colitis can be spared colectomy using the current arsenal of drug therapies. 27 references (20 annotated). (AA-M). •
Ulcerative Colitis Practice Guidelines in Adults Source: American Journal of Gastroenterology. 92(2): 204-211. February 1997. Summary: This article presents the ulcerative colitis (UC) practice guidelines in adults from the American College of Gastroenterology. Guidelines for clinical practice are intended to indicate preferred approaches to medical problems as established by scientifically valid research. Guidelines are intended to be flexible and must be distinguished from standards of care, which are inflexible and rarely violated. Ulcerative colitis recommendations are presented for diagnosis and assessment, for management of mild-moderate distal colitis, for maintenance of remission in distal disease, for management of mild-moderate extensive colitis, for management of severe colitis, for surgery, and for cancer surveillance. In a patient presenting with persistent bloody diarrhea, rectal urgency, or tenesmus, stool examinations and sigmoidoscopy and biopsy should be performed to confirm the presence of a colitis and to rule out infectious causes. Characteristic endoscopic and histologic findings with negative evaluation for infectious causes will suggest the diagnosis of UC. Patients with mild to moderate distal colitis may be treated with either oral aminosalicylates, topical mesalamine, or topical steroids. When the acute attack is controlled, a maintenance regimen is usually required, especially in patients with severe, extensive, or relapsing disease. The patient with severe colitis refractory to maximal oral treatment with prednisone, oral aminosalicylate drugs, and topical medications, or the patient who presents with toxicity, should be treated for 7 to 10 days with intravenous steroids. Failure to demonstrate significant improvement within 7 to 10 days is an indication for either colectomy or treatment with intravenous cyclosporine in specialized centers. After 8 to 10 years of colitis, annual surveillance colonoscopy with multiple biopsies at regular intervals should be performed. 119 references. (AA-M).
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Clinical Economics Review: Medical Management of Inflammatory Bowel Disease Source: Alimentary Pharmacology and Therapeutics. 13(1): 15-25. January 1999. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com. Summary: This article provides a clinical economics review of the medical management of inflammatory bowel disease (IBD). Inflammatory bowel diseases, although uncommon and rarely fatal, typically present during the period of economically productive adult life. Patients may require extensive therapeutic intervention as a result of the chronic, relapsing nature of the diseases. Their medical management includes oral and topical 5 amino salicylic acid derivatives and corticosteroids, as well as antibiotics and immunosuppressive therapies. Assessing the cost effectiveness of rival treatments requires valid, reliable, global assessments of outcome that consider quality of life, as well as the usual clinical end points. Macroeconomic studies of the overall impact of IBD on health care systems have so far been largely confined to North America, where the total annual U.S. costs, both direct and indirect, incurred by the estimated 380,000 to 480,000 people with IBD have been put at approximately $2 billion. Drugs were estimated to account for only 10 percent of total costs, whereas surgery and hospitalization account for approximately half. Studies from Europe suggest that the
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proportion of patients with Crohn's disease and ulcerative colitis who are capable of full time work is 75 percent and 90 percent, respectively. However, while only a minority of IBD patients suffer chronic ill health and their life expectancy is normal, obtaining life insurance may be problematic, suggesting a misconception that IBD frequently results in a major impact on an individual's economic productivity. 1 figure. 3 tables. 43 references. (AA). •
Risk Factors of Colorectal Cancer in Inflammatory Bowel Disease Source: American Journal of Gastroenterology. 91(1): 44-48. January 1996. Summary: This article reports on a case-control study that compared colorectal cancer (CRC) in patients with and without underlying inflammatory bowel disease (IBD). Of the 11,446 subjects with IBD in the VA file of hospital discharges, 371 had colon cancer. CRC was diagnosed in 52,243 subjects without IBD. CRC patients with IBD were 7 years younger than those without IBD. The distribution of CRC was not significantly different in the subjects with ulcerative colitis and those without IBD, but in patients with Crohn's disease, more cancers were located in the proximal colon. The study investigated the following risk factors: age, sclerosing cholangitis, use of NSAIDs, sex, race, and type of IBD. Sclerosing cholangitis was associated with a strong risk of developing colon cancer in patients with IBD. 1 figure. 4 tables. 26 references. (AA-M).
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Fertility and Pregnancy in Inflammatory Bowel Disease Source: International Journal of Gynecology and Obstetrics. 58(2): 229-237. August 1997. Contact: Available from Elsevier Science. P.O. Box 945, New York, NY 10159-0945. (888) 437-4636 or (212) 633-3730. E-mail:
[email protected]. Summary: This article reports on a retrospective study of fertility and pregnancy in inflammatory bowel disease (IBD), conducted in women aged 16 to 45 years during 1967 through 1986, and carried out in North East Scotland. Five hundred and three women were identified: 15 patients had died from unrelated causes and 22 had emigrated, but 409 of the remaining 466 patients (88 percent) replied to the study questionnaire. Results showed that women with ulcerative colitis and Crohn's disease (the two subsets of IBD) had normal fertility when compared with the general population of North East Scotland. However, unresolved infertility problems were more frequent in women who had undergone surgery for IBD compared with those who had not (12 percent versus 5 percent for Crohn's disease; 25 percent versus 7 percent for ulcerative colitis). Disease relapse rates did not increase in pregnancy. The authors conclude that, overall, at conception women with active disease were as likely to have a normal full-term pregnancy as those in remission. However, spontaneous abortion occurred in five (36 percent) pregnancies of women who had undergone previous surgery for Crohn's disease and had evidence of recurrent disease. Three of these pregnancies were associated with active disease. This study should encourage women with IBD to proceed with pregnancy if they so desire because they are likely to have normal fertility and their disease is not a contraindication. 5 tables. 27 references. (AA-M).
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Oral Preparation of Mesalamine as Long-Term Maintenance Therapy for Ulcerative Colitis: A Randomized, Placebo-Controlled Trial Source: Annals of Internal Medicine. 124(2): 204-211. January 1996.
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Contact: Available from American College of Physicians. American Society of Internal Medicine. 190 North Independence Mall West, Philadelphia, PA 19106-1572. Website: www.acponline.org. Summary: This article reports on a study that was undertaken to compare the safety and efficacy of a pH sensitive, polymer coated oral formulation of mesalamine with those of placebo in maintaining remission in patients with ulcerative colitis. The study include 264 patients with ulcerative colitis (UC) that had been maintained in remission for at least 1 month while the patients were receiving stable doses of sulfasalazine or any oral mesalamine product. Measurement consisted of treatment success, defined as maintenance of remission after 6 months, and treatment failure, defined as relapse during the study (as indicated by proctosigmoidoscopy) or withdrawal due to adverse events. 189 patients were compliant with the protocol for 6 months or stopped receiving therapy because of relapse or adverse events. Of these 189 patients, 25 of the 63 patients (39.7 percent) in the placebo group had treatment success compared with 40 of the 68 patients (58 percent) in the group receiving mesalamine. Forty-two of the 87 patients (48.3 percent) in the placebo group had treatment success compared with 57 of the 90 patients (63.3 percent) in the group receiving mesalamine (lower dosage, 0.8 grams per day) and 61 of the 87 patients (70.1 percent) in the group receiving mesalamine (higher dosage, 1.6 grams per day). Age, sex, and race were not found to predict treatment success or failure. The mesalamine tablet was well tolerated, and no clinically significant changes were seen in hematologic, hepatic, or renal laboratory profiles. 1 figure. 4 tables. 30 references. •
Transdermal Nicotine for Mildly to Moderately Active Ulcerative Colitis: A Randomized, Double-Blind, Placebo-Controlled Trial Source: Annals of Internal Medicine. 126(5): 364-371. March 1, 1997. Summary: This article reports on a study undertaken to determine the efficacy of transdermal nicotine for controlling clinical disease activity in active ulcerative colitis (UC), a type of inflammatory bowel disease (IBD). The doubleblind, placebo controlled design studied 64 nonsmoking patients with mildly to moderately active UC despite the use of medication. Patients were stratified on the basis of smoking history, extent of disease, and concomitant medical therapy. After stratification, patients were randomly assigned to daily treatment with transdermal nicotine (n = 31) at the highest tolerated dose (11 mg for 1 week and then less than 22 mg for 3 weeks) or placebo (n = 33). Clinical features were assessed at baseline and at 4 weeks by endoscopy, physician assessment, and a patient diary of daily symptoms. At 4 weeks, 12 of 31 patients (39 percent) who received nicotine showed clinical improvement compared with 3 of 33 patients (9 percent) who received placebo. Four patients receiving nicotine discontinued therapy because of side effects (contact dermatitis, nausea, acute pancreatitis). The authors conclude that transdermal nicotine administered at the highest tolerated dosage for 4 weeks is efficacious for controlling clinical manifestations of mildly to moderately active UC. The authors briefly consider the phenomenon of 'opposite effects' wherein smoking adversely affects Crohn's disease (another type of IBD). 2 figures. 4 tables. 21 references. (AA-M).
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Surgery for Ulcerative Colitis: Historical Perspective, A Century of Surgical Innovations and Refinements Source: Diseases of the Colon and Rectum. 42(3): 299-306. March 1999.
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Contact: Available from Williams and Wilkins. 352 West Camden Street, Baltimore, MD 21201-2436. Summary: This article reviews a century of surgical innovations and refinements in the treatment for ulcerative colitis (UC). The authors begin with a discussion of the early role of surgery (1890s) and the Brooke ileostomy, then discuss ileorectal anastomosis, Kock's continent ileostomy, the ileoanal anastomosis, and the evolution and refinements of these techniques. In the early 20th century, UC as a disease entity was largely unknown and almost never resected. Initially, surgeons used cecostomies or appendicostomies to irrigate and put the bowel at rest. Diversion of the fecal stream by ileostomy or colostomy had some proponents, but the inadequacies of stomas and stoma appliances and the risk of surgery limited its use. It was not until Brooke devised and successfully used the everted ileostomy that complete removal of the disease began to be practiced more widely and that surgery became an integral part of therapy. It was the advent of Kock's continent ileostomy that revolutionized the entire surgical approach to UC by eliminating the need for an external appliance and still curing the disease. The ileal pouch anal anastomosis provided patients with a curative resection and a functional outcome that gave them an even better quality of life, without the need for a permanent external appliance or a stoma. 4 figures. 64 references. •
Trends in Inflammatory Bowel Disease Therapy Source: Canadian Journal of Gastroenterology. 13(9): 775-776. November 1999. Contact: Available from Pulsus Group, Inc. 2902 South Sheridan Way, Oakville, Ontario, Canada L6J 7L6. Fax (905) 829-4799. E-mail:
[email protected]. Summary: This article reviews advances in gene therapy for treating inflammatory bowel disease (IBD). The authors contend that it is possible that genetic information may be shown to predict disease behavior and response to targeted therapy. Because of the family incidence of IBD of approximately one person in six, the regions of linkage are being narrowed with the use of studies of affected sibling pairs or multiple affected families and family based association studies. There appears to be a multigene basis of IBD, with multiple pathways leading to inflammation, ranging from intrinsic changes in the immune system to alterations in the intestinal barrier function. IBD is categorized into ulcerative colitis (UC) and Crohn's disease (CD) by its description of disease patterns, prediction of outcomes, and direction of appropriate treatment strategies, but not on pathogenetic mechanisms. The authors review newer investigational methods for IBD, including color Doppler sonography (ultrasound) and assays to detect antibodies. A final section discusses optimizing therapy for IBD. The authors caution that UC in the elderly tends to have a greater tendency for distal involvement, with a more severe initial attack, and with a possibly higher risk of complications due to prolonged steroid use. Mesalamine remains the standard of care for the treatment of mild attacks of UC or CD. IBD itself as well as its therapy with glucocorticosteroids are risk factors for osteopenia and osteoporosis.
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Inflammatory Bowel Disease in Children Source: Radiologic Clinics of North America. 34(4): 885-902. July 1996. Contact: Available from W.B. Saunders Company, Periodicals Fulfillment, 6277 Sea Harbor Drive, Orlando, FL 32887. (800) 654-2452. Summary: This article reviews inflammatory bowel disease (IBD) in children, focusing on issues of interest to pediatric radiologists. Topics include Henoch-Schonlein purpura
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(HSP); Kawasaki syndrome; Behcet's disease; chronic Crohn's disease (CD) and ulcerative colitis (UC); the radiology of chronic IBD; the symptoms and radiology of CD; complications of CD, including toxic megacolon; differential diagnoses of CD; symptoms, radiology, differential diagnoses, and complications of UC; and the extraintestinal manifestations of IBD. 23 figures. 46 references. (AA-M). •
Novel Drug Therapies in Inflammatory Bowel Disease Source: European Journal of Gastroenterology and Hepatology. 7(2): 169-182. February 1995. Summary: This article reviews published data on novel drug treatments for inflammatory bowel disease (IBD). The article provides information about corticosteroids, including fluticasone propionate, budesonide, prednisolone metasulfobenzoate, beclomethasone dipropionate, and tixocortol pivalate; immunosuppressive agents, including methotrexate, cyclosporin, and FK506 and rapamycin; lipoxygenase inhibitors; cytokine modulation, including with interleukin-1, interleukin-2, interferons, and tumour necrosis factor; lymphocyte modification, including the use of plasmophoresis and CD4 antibody; nutritional therapy, including the use of glutamine; antituberculous therapy; ciprofloxacin; the 4 aminoquinalones; nicotine; topical lignocaine; bismuth subsalicylate enema; sodium cromoglycate; immunoglobulin; hyperbaric oxygen; heparin; Factor XIII; free radical scavengers; immune adjuvants; thromboxane synthesis inhibition; platelet activating factor antagonists; nitric oxide; sucralfate; and clonidine. 151 references.
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Medical Treatment of Ulcerative Colitis Source: Current Opinion in Gastroenterology. 12(4): 352-355. July 1996. Contact: Available from Rapid Science Publishers. 400 Market Street, Suite 700, Philadelphia, PA 19106. (215) 574-2266. Fax (215) 574-2292. Summary: This article reviews recent research in the medical treatment of ulcerative colitis. For severe attacks in cases refractory to intravenous steroids, cyclosporine may be of value for short-term control; long-term results, however, are less satisfactory. Anecdotal reports of efficacy of heparin and interferon-alpha are exciting but need to be validated. Mild and moderate attacks are usually well controlled with topical treatment, but may require supplementation with oral salicylates and steroids. Patients with refractory distal colitis, a more widely recognized entity, may benefit from the combined use of topical short-chain fatty acids and 5-aminosalicylic acid. Oral salicylates are the first-line approach for maintenance treatment in distal colitis, while topical salicylates may be useful maintenance therapy. 25 references (19 annotated). (AA-M).
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Maintenance of Remission in Ulcerative Colitis Source: Alimentary Pharmacology and Therapeutics. 16(Supplement 4): 21-24. July 2002. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com. Summary: This article reviews strategies undertaken to maintain remission in patients with ulcerative colitis (UC, a type of inflammatory bowel disease, or IBD). The author notes that 70 percent of patients with UC can expect to experience a relapse over a 12 month period. Sulfasalazine was the first drug demonstrated to reduce this relapse rate to 21 percent. Subsequent studies have demonstrated that 5 aminosalicylic acid (5ASA)
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is the main active component and preparations containing only 5ASA have similar efficacy to sulfasalazine. 5ASA is readily absorbed from the small intestine; special release formulations are indicated. A variety of 5ASA preparations is available, differing in their release mechanisms, efficacy, and side effect profile. Most patients can be maintained in remission using oral 5ASA medication. For patients with distal or left sided disease, the use of rectal 5ASA is also of proven benefit in maintaining remission. Some patients with frequent or severe relapses require stronger immunosuppression, and in those patients, azathioprine or 6 mercaptopurine (6MP) are of proven benefit. Azathioprine is also of great use for maintaining remission in patients who have been treated with cyclosporine for a fulminant acute episode of colitis. The author concludes by commenting that the area of natural therapies (probiotics) deserves further exploration. 14 references. •
Current Medical Therapy of Inflammatory Bowel Disease Source: Practical Gastroenterology. 22(12): 19-20, 24-28, 30. December 1998. Contact: Available from Shugar Publishing. 12 Moniebogue Lane, Westhampton Beach, NY 11978. (516) 288-4404. Fax (516) 288-4435. Summary: This article reviews the current medical therapy of inflammatory bowel disease (IBD). The current established drugs used to treat IBD include glucocorticoids (including the newer agent budesonide), sulfasalazine and 5ASA compounds (Asacol, Pentasa, Dipentum, and Balsalazide), and immunomodulatory agents such as azathioprine and 6 mercaptopurine. Additional drugs that have been found to be useful, particularly in refractory cases of Crohn's disease (including fistulizing type of Crohn's disease) include cyclosporine A, methotrexate, humanized antibody against TNFa (cA2), FK506, and IL 10. Various agents, whether used alone or in combination, have to be tailored for each patient and none are ideal. The authors discuss ulcerative colitis (UC) and Crohn's disease separately; they also consider the role of nutrition in managing these diseases. The authors conclude that exciting new developments directed against proinflammatory pathways, cytokines, free oxygen radicals, and cell surface related immune targets are areas of intense recent investigations and many new therapeutic agents are expected to be available in the near future for the medical treatment of IBD. 2 figures. 1 table. 55 references.
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Early Diagnosis of Inflammatory Bowel Disease: Article Five in the Series Source: Practical Gastroenterology. 23(1): 22, 24, 26-28, 31-33, 37-38. January 1999. Contact: Available from Shugar Publishing, Inc. 99B Main Street, Westhampton Beach, NY 11978. (631) 288-4404. Fax (631) 288-4435. E-Mail:
[email protected]. Summary: This article reviews the early diagnosis of inflammatory bowel disease (IBD), the collective term for Crohn's disease (CD) and ulcerative colitis (UC). The cause is incompletely understood. IBD usually develops in the second or third decades of life, but may affect all age groups. Although patients with IBD usually present with diarrhea and crampy abdominal pain, constitutional symptoms such as weight loss and extraintestinal symptoms involving the eye, hepatobiliary (liver) system, joints, skin, and other organ systems are common. Many of the extraintestinal manifestations may predate intestinal involvement by years. Diagnosing IBD can be challenging because of this broad array of possible presentations. However, radiologic, serologic (blood), microbiologic, and endoscopic testing should help the physician make an early diagnosis when IBD is suspected. 5 tables. 27 references. (AA).
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Hepatobiliary Manifestations of Inflammatory Bowel Disease Source: Gastroenterology Clinics of North America. 28(2): 491-513. June 1999. Contact: Available from W.B. Saunders. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000. Summary: This article reviews the hepatobiliary manifestations of inflammatory bowel disease (IBD). A large number of hepatobiliary abnormalities have been described in association with IBD, including primary sclerosing cholangitis (PSC), pericholangitis, chronic hepatitis, cryptogenic cirrhosis, cholangiocarcinoma (gallbladder cancer), and cholelithiasis (gallstones). PSC is the most common of these hepatobiliary diseases. This high degree of association with IBD suggests a common pathogenic mechanism; however, no causal relationship has been established. Medical therapy has not proven successful in slowing disease progression or prolonging survival. PSC usually progresses insidiously and eventually leads to cirrhosis. Endoscopic manipulation is recommended for treating complications of recurrent cholangitis or worsening jaundice in the setting of a dominant stricture, but endoscopic approaches have not been shown to improve survival or decrease the need for liver transplantation. Liver transplantation is life saving for patients with advanced PSC. Pericholangitis, gallstones, and chronic hepatitis are additional disorders noted in association with IBD, but they are much less common and easier to manage than PSC. 3 figures. 6 tables. 140 references. (AA-M).
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Inflammatory Bowel Disease and Pregnancy Source: Gastroenterology Clinics of North America. 27(1): 213-224. March 1998. Contact: Available from W.B. Saunders. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000. Summary: This article reviews the interplay of inflammatory bowel disease (IBD) and pregnancy. The author begins by cautioning that many of the research studies are somewhat dated and often did not distinguish between the subtypes of IBD. However, general implications for practice can be ascertained. Topics include fertility, inheritance and IBD, the influence of ulcerative colitis (UC) on fetal outcome, the influence of Crohn's disease on fetal outcome, the influence of pregnancy on the course of UC and of Crohn's disease, episiotomy in IBD, the influence of drug therapy on the pregnant woman and the fetus, smoking, the effect of surgery for IBD on subsequent pregnancies, and the management of IBD during pregnancy. Drugs discussed include 5aminosalicylic acid agents (mesalamine, olsalazine), corticosteroids, immunosuppressives, cyclosporine, methotrexate, and antibiotics. Rates of healthy babies, congenital abnormalities, stillbirths, and spontaneous abortions are roughly the same in women with UC and Crohn's disease as in the normal population. The presence of UC did not influence the mode of delivery (vaginal versus cesarean section) or the incidence of preeclampsia during gestation. However, if a severe exacerbation requiring surgery occurs during pregnancy, the fetal mortality is high. 71 references.
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Methotrexate for Inflammatory Bowel Disease: Pharmacology and Preliminary Results Source: Mayo Clinic Proceedings. 71(1): 69-80. January 1996. Summary: This article reviews the limited published experience with methotrexate treatment for inflammatory bowel disease (IBD). The authors examine the proposed anti-inflammatory and immune-modifying mechanism of action and pharmacologic properties of methotrexate, and detail its limiting toxicities. Long-term low-dose
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methotrexate therapy (25 mg or less once a week) inhibits production of thymidylate, purines, and methionine, and leads to accumulation of adenosine, a potent antiinflammatory substance. These actions inhibit cellular proliferation, decrease formation of antibodies, and decrease production of mediators of inflammation such as interleukins and eicosanoids. Three uncontrolled trials and two controlled trials have demonstrated efficacy of low-dose methotrexate therapy for inducing remission in Crohn's disease and possibly in ulcerative colitis. Methotrexate may also help maintain remission for both diseases. Although methotrexate is generally well tolerated for longterm use at low dose, several serious toxicities potentially limit its use. •
Review Article: The Management of Severe Ulcerative Colitis Source: Alimentary Pharmacology and Therapeutics. 11(3): 419-424. June 1997. Contact: Available from Mercury Airfreight International, Ltd. 2323 EF, Randolph Avenue, Avenel, NJ 07001. E-mail:
[email protected]. Summary: This article reviews the management of severe ulcerative colitis (UC), a potentially life threatening condition. The authors note that the mortality has fallen dramatically over the past 4 decades to less than 2 percent, including surgical mortality. Early recognition of the severity of the colitis, intensive medical therapy, close liaison between physician and surgeon, and prompt surgery when necessary have all contributed to this improved outcome. Despite the use of high-dose intravenous corticosteroids, 20 to 30 percent of patients will make a poor response and will require urgent surgery. The use of intravenous cyclosporin has proved effective at reducing the immediate surgical rate in this group of unresponsive patients and appears safe. Whether cyclosporin reduces the need for surgery in the longer term is much less uncertain. The authors describe how clinical, radiological, endoscopic, and laboratory parameters can now be used to predict the course of a severe attack. These help in the timing of urgent surgery and are potentially helpful in determining when to begin other therapies such as cyclosporin. 1 table. 36 references. (AA-M).
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Muscoloskeletal Manifestations in Inflammatory Bowel Disease Source: Canadian Journal of Gastroenterology. 15(6): 399-403. June 2001. Contact: Available from Pulsus Group, Inc. 2902 South Sheridan Way, Oakville, Ontario, Canada L6J 7L6. Fax (905) 829-4799. E-mail:
[email protected]. Summary: This article reviews the musculoskeletal manifestations of inflammatory bowel disease (IBD), the most common extraintestinal complications of the condition. Wide ranges in prevalence have been reported, depending on the criteria used to define spondylarthropathy. In 1991, the European Spondylarthropathy Study Group developed classification criteria that included previously neglected cases of undifferentiated spondylarthropathies, which had been ignored in most of the oldest epidemiological studies on IBD. The spectrum of musculoskeletal manifestations in IBD patients includes all of the clinical features of spondylarthropathies: peripheral arthritis, inflammatory spinal pain, dactylitis, enthesitis (Achilles tendinitis and plantar fasciitis), buttock pain, and anterior chest wall pain. Radiological evidence of sacroiliitis is common, but not obligatory. The articular manifestations begin either at the same time or subsequent to the bowel disease; however, the onset of spinal disease often precedes the diagnosis of IBD. The prevalence of the different musculoskeletal manifestations is similar in ulcerative colitis and Crohn's disease (the two categories of IBD). Symptoms usually disappear after proctocolectomy (removal of the affected portion of the colon). The pathogenetic mechanisms (how the disease causes the complications) that produce
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the musculoskeletal manifestations in IBD are unclear. Several arguments favor an important role of the intestinal mucosa in the development of spondylarthropathy. The natural history of the disease is characterized by periods of flares and remission; therefore, the efficacy of treatment is difficult to establish. Most patients respond to rest, physical therapy, and nonsteroidal antiinflammatory drugs (NSAIDs), but these drugs may activate the bowel disease. Sulfasalazine may be recommended in some patients; however, there is no indication for the systemic use of steroids. 6 tables. 43 references. •
Nutrition and Inflammatory Bowel Disease Source: Gastroenterology Clinics of North America. 28(2): 423-443. June 1999. Contact: Available from W.B. Saunders. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000. Summary: This article reviews the nutritional aspects of inflammatory bowel disease (IBD), including the mechanisms and manifestations of malnutrition and the efficacy of nutritional therapies. Nutrient deficiencies in patients with IBD occur via several mechanisms and may complicate the course of the disease. Up to 85 percent of patients hospitalized with exacerbations of IBD have protein energy malnutrition. This form of malnutrition also occurs between flareups of the disease, particularly in patients with Crohn's disease (CD), in whom the development of nutrient deficiencies is often insidious. Nutritional status is assessed by clinical examination and the use of nutritional indices such as the Subjective Global Assessment of nutritional status. Nutritional intervention may improve outcomes in certain people; however, because of the costs and complications of such therapy, careful selection is warranted, especially in patients presumed to need parenteral nutrition. Clinical trials have established the efficacy of enteral formulations in nutritional repletion and reduction of disease activity in CD. Studies have shown the efficacy of nutrients with trophic effects, such as short chain fatty acids, glutamine, epidermal growth factor, nucleotides, and nutrients with immunomodulatory properties, such as omega 3 fatty acids and gamma linoleic acids, as therapy for IBD. 1 figure. 6 tables. 160 references. (AA-M).
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Inflammatory Bowel Disease and Intestinal Cancer Source: Practical Gastroenterology. 22(11): 20, 23-26, 59. November 1998. Contact: Available from Shugar Publishing, Inc. 99B Main Street, Westhampton Beach, NY 11978. (631) 288-4404. Fax (631) 288-4435. E-Mail:
[email protected]. Summary: This article reviews the recommended monitoring and diagnostic techniques to use in patients with inflammatory bowel disease (IBD) who are at higher risk for intestinal cancer. The authors note that the approach to cancer surveillance for patients with longstanding IBD is in question. However, identifying patients at the greatest risk of malignancy for surveillance will allow the clinician to make the largest impact in lowering cancer-related mortality in IBD. Further research in the area of molecular genetics to find a complementary test for dysplasia to assist the gastroenterologist in the early detection of premalignant lesions is underway. The authors recommend that patients with ulcerative colitis have surveillance colonoscopy every 1 to 3 years with colectomy for dysplasia detected in any biopsy specimen. Surveillance in Crohn's disease is recommended only if patients and physicians are aware of the limitations of surveillance and its relatively low effectiveness. Surveillance of Crohn's disease is difficult because of the inaccessibility of the small bowel to endoscopic examination, the difficulty of evaluating segments of bowel that are either bypassed or strictured, and the
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confusion of cancer symptoms associated with those of the underlying IBD. 41 references. •
Safety of Drug Therapy for Inflammatory Bowel Disease in Pregnant and Nursing Women Source: Inflammatory Bowel Diseases. 2(1): 33-47. Spring 1995. Summary: This article reviews the safety of drug therapy for inflammatory bowel disease (IBD) in pregnant and nursing women. The author stresses that drug therapy is justified in pregnant patients with active IBD. Selection of medical treatment depends on disease severity and the potential for fetal toxicity. Preferably, pregnancy should be planned to coincide with periods of disease quiescence, so that drug requirements can be minimized. Sulphasalazine and prednisolone are clearly safe in pregnancy and lactation. Preliminary studies suggest that low to moderate doses of mesalamine are well tolerated in pregnant and nursing mothers. Immunosuppressive therapy during pregnancy in transplant and nontransplant recipients may be associated with an increased risk of fetal growth retardation and prematurity. The risk of congenital malformations from azathioprine and cyclosporin is not markedly increased, although exposure to methotrexate during the first trimester may cause fetal loss and characteristic anomalies. Shortterm therapy with metronidazole in the first trimester is not associated with an increased risk of teratogenicity, although the safety of this drug in pregnancy using higher doses for prolonged periods has not been confirmed. 171 references. (AA-M).
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Ulcerative Colitis: Surgical Indications and Treatment Source: Alimentary Pharmacology and Therapeutics. 16(Supplement 4): 25-28. July 2002. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com. Summary: This article reviews the treatment options for ulcerative colitis (UC, a type of inflammatory bowel disease, or IBD), including the surgical indications. The author notes that the indication for surgery is a balance between the severity of the disease despite full medical treatment and the potential disadvantages of surgery. The decision requires cooperation between the gastroenterologist and surgeon. Colectomy with ileostomy and preservation of the rectum in the emergency setting is the accepted procedure and can rapidly restore the patient to normal health, allowing withdrawal of anti-inflammatory medication. After recovery, all surgical possibilities are then open for the future. The elective indications for surgery include failure of medical treatment, retardation of growth in a child or adolescent, and neoplastic (precancerous) transformation. The choice of operation includes conventional proctocolectomy, restorative proctocolectomy (RPC), and colectomy with ileo-rectal anastomosis. Causes of failure include sepsis (50 percent), dysfunction (30 percent), and pouchitis (10 percent). In selected cases, salvage surgery to avoid failure can be successful with rates of around 70 percent for outlet obstruction and fistulation and 50 percent for pelvic sepsis. 26 references.
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New Steroids for Inflammatory Bowel Disease Source: Inflammatory Bowel Diseases. 1(2): 135-141. Summer 1995.
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Summary: This article reviews the use of glucocorticosteroids (GCS) in inflammatory bowel disease (IBD). The author notes that the antiinflammatory effects of GCS are unsurpassed by those of any other type of drug, but the beneficial effects are often offset by troublesome, and sometimes irreversible, systemic side effects. Improved GCS have been developed with the aim of obtaining improved topical action, with reduced systemic side effects. A high tissue uptake and a high affinity for the GCS-receptor, in combination with a rapid and extensive biotransformation in the liver, are key prerequisites. Budesonide appears to be the most promising of the new topical GCS for IBD. In enema form, it is already in clinical use for active distal ulcerative colitis (UC). Oral, slow release preparations of budesonide are efficacious in the treatment of active ileocecal Crohn's disease (CD), causing less suppression of endogenous plasma cortisol levels than does oral prednisolone, and giving rise to fewer and less severe side effects. Budesonide may also have a role in preventing clinical relapse in certain groups of patients with CD, and is currently under evaluation for extensive and left-side UC. The author concludes that future development of GCS for IBD includes factors such as improved topical delivery systems, enhanced tissue uptake, and even more extensive first pass metabolism. 1 table. 63 references. (AA-M). •
Monitoring Activity in Ulcerative Colitis Source: Alimentary Pharmacology and Therapeutics. 16(Supplement 4): 3-6. July 2002. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com. Summary: This article reviews therapeutic strategies and the monitoring of patients with ulcerative colitis (UC, a type of inflammatory bowel disease, or IBD). The authors note that monitoring is easier in these patients than in patients with Crohn's disease (another type of IBD) for several reasons. The severity of symptoms and activity of inflammation tend to run parallel in UC when involvement of the large bowel is more extensive. The easy accessibility of the colonic mucosa by endoscopic and histologic examination provides further information concerning the degree of inflammation. In severe attacks, the patients must be admitted to the hospital and monitored carefully. Clinical and laboratory parameters (such as daily stools, CRP, fever, hemoglobin, albumin, etc) and plain abdominal x-ray are useful in monitoring the activity of the disease and to predict the outcome. In mild to moderate attacks, endoscopic and histologic evaluation are the best methods for choosing the appropriate treatment and for assessing response. 2 tables. 18 references.
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Is the Appendix a Vestigial Organ? Its Role in Ulcerative Colitis Source: Gastroenterology 121(3): 730-737. September 2001. Contact: Available from W.B. Saunders Company. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452. Website: www.gastrojournal.org. Summary: This article summarizes a research study that considers the role of the appendix in ulcerative colitis (UC, a type of inflammatory bowel disease), including the possible role of appendectomy (removal of the appendix) in protecting against UC. The author briefly reviews the research in this area, then focuses on one particular study that was reported in the New England Journal of Medicine in 2001 (Andersson, R.E., et al, Volume 344). The investigators in that study conclude that the inflammatory response leading to an appendectomy rather than the removal of the appendix was the significant clinical factor negatively associated with developing UC at a later date. The absence of
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this protective effect in older patients with appendicitis also suggests that the immune mechanisms resulting in appendicitis in these patients may differ from those resulting in appendicitis before the third decade. The author then appends a lengthy commentary exploring the ramifications of these results. The author concludes that in the absence of evidence supporting a more causal role for the appendix, adoption of therapeutic appendectomy as a strategy to affect the incidence or clinical course of UC is premature, despite recent case reports suggesting clinical improvement and reduction in mucosal inflammatory mediators after appendectomy. Numerous studies are referred to in the text of this article. •
Ulcerative Colitis in Adults: Summary of the Latest Practice Guidelines Source: Consultant. 37(4): 1085-1086. April 1997. Contact: Available from Cliggott Publishing Company. 55 Holly Hill Lane, Box 4010, Greenwich, CT 06831-0010. Summary: This article summarizes the latest practice guidelines (developed by the American College of Gastroenterology) for the assessment and treatment of ulcerative colitis (UC) in adults. Stool examinations, sigmoidoscopy, and biopsy are indicated to confirm the presence of colitis and to rule out infectious causes in patients who have persistent bloody diarrhea, rectal urgency, or tenesmus. The mucosal changes characteristic of UC, as detected by proctosigmoidoscopy or colonoscopy, include loss of the typical vascular pattern, granularity, friability, and ulceration. Once the diagnosis is confirmed, it is necessary to establish whether the inflammation is distal or extensive. Oral aminosalicylates, topical mesalamine, or topical corticosteroids are appropriate for patients with mild to moderate distal colitis. Oral corticosteroids should be reserved for patients whose disease is refractory to oral aminosalicylates. Mercaptopurine or azathioprine is effective in patients who do not respond to oral prednisone, provided they are not so acutely ill that they require intravenous therapy. A maintenance regimen is usually required for patients with mild to moderate extensive colitis, particularly those who have severe or relapsing disease. In adults with UC, the absolute indications for surgery are exsanguinating hemorrhage, perforation, and documented or strongly suggested carcinoma. Surgery is also indicated in patients with severe colitis (with or without toxic megacolon) that is unresponsive to conventional maximal medical therapy and in patients with less severe but medically intractable symptoms or intolerable corticosteroid side effects. Annual cancer surveillance colonoscopy with multiple biopsies at regular intervals is warranted after 8 to 10 years of colitis. 1 table. 4 references.
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Surgical Outcomes in Ulcerative Colitis and Crohn's Disease Source: Canadian Journal of Gastroenterology. 13(10): 804-805. December 1999. Contact: Available from Pulsus Group, Inc. 2902 South Sheridan Way, Oakville, Ontario, Canada L6J 7L6. Fax (905) 829-4799. E-mail:
[email protected]. Summary: This article summarizes two descriptive studies that provide information on the postoperative aspects of patients who have undergone colonic resective surgery for ulcerative colitis (UC) or Crohn's disease (the two types of inflammatory bowel disease, or IBD). For UC, colonic resection usually results in amelioration of the morbid effects of the disease and substantially eliminates the risk of later malignancy. For Crohn's disease, especially with extensive colonic involvement, resection of the colon and rectum may also be required. For most patients, the early short term results of these surgical therapies have been generally quite satisfactory, with the goal being that the patient may
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return to a normal life as soon as possible following treatment. For patients with UC, operative treatment is performed during the most sexually active and reproductive years. Thus, most patients faced with restorative proctocolectomy (removal of the colon) may have significant concerns related to sexual function and fertility following surgical treatment. Sexual dysfunction may develop in males, but with variable frequency. In the second study, of Crohn's disease patients undergoing total colectomy and ileostomy, preoperative steroid therapy and associated perforating disease were associated with a high incidence of postoperative complications. The author stresses that convincing data on the effectiveness of antibiotic regimens, immunosuppressive agents or biological therapies (e.g., antitumor necrosis factor) are simply not available, particularly data that may demonstrate a more transient benefit. Until truly effective medical therapies for anorectal disease becomes available, proctocolectomy may well be the surgical treatment of choice. •
Considerations Regarding Fertility and Pregnancy in the Management of Inflammatory Bowel Disease Source: Practical Gastroenterology. 20(1): 12, 14, 17-20, 23. January 1996. Contact: Available from Shugar Publishing, Inc. 99B Main Street, Westhampton Beach, NY 11978. (631) 288-4404. Fax (631) 288-4435. E-Mail:
[email protected]. Summary: This article, one in a series on gastrointestinal (GI) disorders during pregnancy, addresses considerations regarding fertility and pregnancy in the management of patients with inflammatory bowel disease (IBD). Although the gravid woman with IBD possesses a greater potential for complications (more so with Crohn's disease than with ulcerative colitis), the majority of patients will experience an uneventful, normal pregnancy. The authors stress that understanding the interaction between pregnancy and the state of the IBD as well as the relative safety and potential risks of treatments is paramount in family planning and patient education. Conception at a time when IBD is under control offers the greatest likelihood of an uncomplicated pregnancy. Physicians caring for patients with IBD must recognize, and inform their patients, that most medications needed to suppress the disease should be continued throughout pregnancy. Drugs discussed include sulfasalazine, corticosteroids, antibiotics, immunosuppressive agents, and oral contraceptives. The article concludes with a brief discussion of breastfeeding by a woman with IBD and the correlation between smoking and Crohn's disease. 45 references. (AA-M).
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Ulcerative Duodenitis with Ulcerative Colitis: Is It Crohn's Disease Or Really Ulcerative Colitis? (editorial) Source: Journal of Clinical Gastroenterology. 32(2): 97. February 2001. Contact: Available from Lippincott Williams and Wilkins, Inc. 12107 Insurance Way, Hagerstown, MD 21740. (800) 638-3030 or (301) 714-2300. Summary: This editorial comments on an accompanying article in which two patients present the dilemma in differentiating between Crohn's disease and ulcerative colitis (the two subtypes of inflammatory bowel disease, IBD). The first case was that of a man, 31, with a history of left sided colitis who subsequently developed erosive duodenitis responsive to methylprednisolone. The second case was that of a woman, 30, with pancolitis who was admitted for closure of an ileostomy after a staged subtotal proctocolectomy with ileoproctostomy and diverting ileostomy. Her hospital course was complicated by the development of ulcerative duodenitis, again responsive to methylprednisolone. Crohn's disease may involve the stomach, the duodenum, or both,
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usually in conjunction with a more distal disease, although this is not always the case. Ulcerative colitis, on the other hand, is a disease of the colon almost always involving the rectum. The authors conclude that upper gastrointestinal tract inflammation (such as duodenitis) warrants further observation and maximum documentation to sustain the issue of whether ulcerative colitis can involve the upper gastrointestinal tract. They note that there might be a third type of IBD, whether occurring from a separate origin or arising from conversion of one type of IBD to the other. 8 references. •
Watching for and Managing Joint Problems in Inflammatory Bowel Disease Source: Journal of Musculoskeletal Medicine. 13(11):28-30,33-34; November 1996. Summary: This journal article for health professionals discusses the nature and prevalence of peripheral joint arthritis and of spondylitis and sacroiliitis in ulcerative colitis and Crohn's disease. These rheumatic manifestations are the most common ones to accompany inflammatory bowel disease. The bowel and joint symptoms may or may not occur at the same time. Similarly, bowel and joint symptoms may or may not respond to the same treatment. Treatment of peripheral joint arthritis is directed toward controlling the bowel disease, and it includes corticosteroids and immunosuppressives. Joint injections and analgesics may provide symptomatic relief. The course of sacroiliitis and spondylitis is independent of the bowel disease. Treatment is aimed at limiting joint damage, and aggressive physical therapy and exercise are the mainstays. 8 references, 1 figure, and 3 tables. (AA-M).
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Explaining Ulcerative Colitis to Friends and Family Source: Insights and Answers. 7-8. Summer 1999. Contact: Available from Insights and Answers. P.O. Box 3217, Cincinnati, OH 452738266. (800) 663-6698. Website: www.living-better.com. Summary: This newsletter article, written by a man with ulcerative colitis (UC, one of the types of inflammatory bowel disease) considers the issues involved in explaining UC to friends and family members. The author underscores the need of letting family and friends be supportive, help the patient through everyday trials and tribulations, comply with the recommended treatment schedule, and stay focused on recovery. The author lists the benefits of telling loved ones about UC, and then offers strategies for exactly how to go about telling them about the disease. These strategies include gather general information, practice what is going to be said, pick out an appropriate time and place to talk, and explain why it is important for them to learn about the disease. The author concludes by reminding readers that even the smallest efforts of support and words of encouragement can go a long way toward helping others who are coping with inflammatory bowel disease.
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Interactions Between Chronic Liver Disease and Inflammatory Bowel Disease Source: Inflammatory Bowel Diseases. 3(4): 288-302. Winter 1997. Contact: Available from Raven Press, Ltd. 1185 Avenue of the Americas, New York, NY 10036. (800) 777-2836 or (212) 930-9500. Fax (212) 869-3495. Summary: This review article considers the interactions between chronic liver disease and inflammatory bowel disease (IBD). The authors review the epidemiology, clinical features, treatment, and prognosis of hepatobiliary disease associated with IBD, as well as the unique clinical features of IBD associated with primary sclerosing cholangitis (PSC). Persistent hepatobiliary dysfunction is seen in 5 to 15 percent of all patients with
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IBD. The most important form of liver disease is PSC, a chronic progressive cholestatic liver disease characterized by inflammation and fibrosis of the biliary tree. Immunology and genetic factors appear to play a role in pathogenesis, although environmental factors such as cigarette smoking may modify the presentation of disease. Sclerosing cholangitis leads to recurrent acute cholangitis, liver failure, cholangiocarcinoma, or death. Liver transplantation is the only effective treatment option. Other hepatobiliary conditions seen in IBD include pericholangitis or small duct PSC, autoimmune hepatitis, cholelithiasis, and fatty infiltration of the liver. 3 tables. 200 references. •
Sulphasalazine Use as a Preventive Factor for Colorectal Cancer in Ulcerative Colitis Patients: A Review Source: Inflammatory Bowel Diseases. 2(4): 276-278. Winter 1996. Summary: This review article considers the use of sulphasalazine in the prevention of colorectal cancer in ulcerative colitis (UC) patients. There is an increased risk of colorectal cancer among patients with UC. This increased risk is obvious for morbidity as well as mortality from colorectal cancer, thus ruling out surveillance bias as an explanation. Duration of disease, extent at diagnosis, and age at diagnosis are the only recognized risk factors for a malignant transformation. The authors consider expected increases in the rates of colorectal cancer (increases that did not materialize) and the possibility that the use of a more aggressive drug therapy could at least partly explain the decrease in the occurrence of colorectal cancer in these patients. The authors describe ecological studies and then analytic studies. They conclude that sulphasalazine should be regarded as a possible chemoprotective agent for colorectal cancer in UC patients. 25 references.
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Activity Scores and Quality of Life Indices in Inflammatory Bowel Disease Source: Current Opinion in Gastroenterology. 11(4): 331-336. July 1995. Contact: Available from Rapid Science Publishers. 400 Market Street, Suite 700, Philadelphia, PA 19106. (215) 574-2266. Fax (215) 574-2292. Summary: This review article examines the types of indices used to evaluate the impact of inflammatory bowel disease (IBD) on patient quality of life or functional status. The clinical course of IBD and the impact of therapies on the disease process have traditionally been assessed using composite activity indices. These indices are variably composed of subjective symptoms, endoscopic appearance, histology of mucosal biopsy specimens, and other laboratory measures of inflammation. More recently, healthrelated quality of life (HRQOL, also called functional status), a subjective measure of physical, emotional, and social function and perception, has become a key element in the assessment of health status in IBD. The author stresses that each index assessing disease activity or HRQOL should be tailored to the study population (e.g., Crohn's disease, ulcerative colitis, pouchitis, pediatric patients) and research questions of the study. The author calls for both cross-sectional and prospective studies in order to adequately gauge disease severity and health status. 25 references (18 annotated). (AAM).
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Surveillance Issues in Inflammatory Bowel Disease: Ulcerative Colitis Source: Journal of Clinical Gastroenterology. 32(2): 99-105. February 2001. Contact: Available from Lippincott Williams and Wilkins, Inc. 12107 Insurance Way, Hagerstown, MD 21740. (800) 638-3030 or (301) 714-2300.
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Summary: This review article on the surveillance of patients with ulcerative colitis (UC) provides an overview of the criteria for evaluating screening and surveillance programs and applies the criteria to the available evidence to determine the effectiveness of the surveillance of patients with UC. The authors examine the clinical outcomes associated with surveillance, the additional clinical time required to confirm the diagnosis of dysplasia and cancer, compliance with surveillance and followup, and the effectiveness of the individual components of a surveillance program, including colonoscopy and pathologist's interpretation. The disability associated with colectomy is considered, as are the cost and acceptability of surveillance programs. Patients with longstanding UC are at risk for developing colorectal cancer, therefore recommended surveillance colonoscopy should be supported. The diagnosis of cancer at an early stage in this group is associated with a good prognosis. The authors conclude that new endoscopic and histopathologic techniques used to improve the identification of high risk patients may enhance the effectiveness and cost effectiveness of surveillance practices. 2 figures. 5 tables. 44 references. •
Therapy for Ulcerative Colitis Source: Current Opinion in Gastroenterology. 14(4): 312-316. July 1998. Contact: Available from Lippincott-Raven Publishers. 227 East Washington Square, Philadelphia, PA 19106. (800) 638-3030. Summary: This review article presents the 1997 literature on the medical therapy of ulcerative colitis (UC). Several recent studies have addressed aspects of this topic, including optimization of current therapies, pilot studies, definitive placebo-controlled trials of newer novel therapies, and reports of associated complications. Combination therapy with rectal and oral 5-aminosalicylate may be more effective than either formulation alone, and the renal safety of high-dose oral 5-aminosalicylate has been confirmed. Rectal 5-aminosalicylate is more effective than conventional rectal corticosteroids, and delayed release oral budesonide may also be beneficial for patients with active UC. Treatment with intravenous cyclosporine is only required in 22 percent of patients with severe UC, and cyclosporine may be associated with severe toxicity, including death. Transdermal nicotine is effective in treating active UC but results in side effects, which may be overcome by administering nicotine directly to the colon. Preliminary studies suggest that both anti-tumor necrosis factor-alpha antibody and heparin may benefit patients with UC. Also, 5-Lipoxygenase inhibitors, short chain fatty-acid enemas, olestra, and ciprofloxacin are not effective therapies for UC. Oral therapy with a probiotic bacterial preparation may maintain remission in patients with UC. Finally, folate or folinic acid may decrease rectal cell proliferation and subsequent development of neoplasia (cancer) in patients with longstanding UC. 60 references (13 annotated). (AA).
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Review Article: Bone and Joint Diseases in Inflammatory Bowel Disease Source: Alimentary Pharmacology and Therapeutics. 12(5): 397-404. May 1998. Summary: This review article provides health professionals with information on the prevalence, etiopathogenesis, and treatment of arthritis and osteoporosis in inflammatory bowel disease. The intestinal and articular systems are closely linked in inflammatory bowel disease. Spondyloarthropathy is the most common extraintestinal manifestation of inflammatory bowel disease. Either a peripheral arthritis or a spondylitis may occur. The peripheral arthritis is pauciarticular and asymmetrical and mainly involves the large and small joints of the lower limbs. Peripheral arthritis is most
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frequently seen in patients with extensive ulcerative colitis or Crohn's colitis. The axial involvement includes sacroiliitis and spondylitis. Clinical and immunologic studies support an important etiopathogenetic link between intestinal and articular inflammation. Treatment options for patients with a spondyloarthropathy include a short course of nonsteroidal anti-inflammatory drugs, sulfasalazine, azathioprine-6mercaptopurine, and methotrexate. Osteoporosis is a systemic skeletal disease characterized by a low bone mass and microarchitectural deterioration leading to increased bone fragility and susceptibility to fracture. Bone mass density can be measured by several methods, including dual energy x-ray absorptiometry. Bone turnover can also be estimated by biochemical markers. The pathogenesis of osteoporosis in inflammatory bowel disease is likely to be multifactorial. There is increasing evidence of a negative link between bone mass density and intestinal inflammation. Treatment options include hormones and biphosphonates. The article concludes that further elucidation of the mechanisms of recirculation, adhesion, and disease inducing features will help in understanding the etiopathogenesis of extraintestinal manifestations of inflammatory bowel disease. 1 table and 65 references. (AA-M) •
Current Medical Therapy for Inflammatory Bowel Disease Source: Southern Medical Journal. 89(6): 556-566. June 1996. Summary: This review article summarizes current medical therapy for inflammatory bowel disease (IBD), with an emphasis on newer therapies. Traditional medical therapy for IBD includes corticosteroids and sulfasalazine. In recent years, several mesalamine derivatives of sulfasalazine have become available. These allow delivery of increased dosages of active medication with minimal side effects. Newer steroid preparations, all investigational at this point, will likely be as effective as prednisone, but with improved side effects. Immunosuppressive agents, including 6-mercaptopurine, azathioprine, and possibly methotrexate, are beneficial in treating refractory IBD, particularly in patients with chronic steroid dependence. Cyclosporine has been shown to be remarkably effective in delaying colectomy for severe ulcerative colitis, but its long-term role remains uncertain. 5 tables. 143 references. (AA).
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Assessment of Disease Activity in Ulcerative Colitis and Crohn's Disease Source: Inflammatory Bowel Diseases. 1(2): 117-134. Summer 1995. Summary: This review article surveys techniques for assessing the clinical state of patients with inflammatory bowel disease (IBD). The authors stress that the presence or absence of active inflammation in the gastrointestinal tract is of central importance, but is not the sole determinant of illness. The secondary consequences of inflammation (which may be anatomical (stricture, fistula, abscesses) or physiological (nutritional)), psychological features, and the consequences of therapy all affect the individual. The authors describe why it is substantially easier to assess patients with ulcerative colitis compared with Crohn's disease. The authors then consider both clinical and laboratory approaches to assessing IBD. The authors also discuss how these approaches to assessment can be useful in conducting drug trials for treating IBD. 7 tables. 119 references. (AA-M).
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Ulcerative Colitis in Children Source: Pediatric Clinics of North America. 43(1): 235-254. February 1996.
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Contact: Available from W.B. Saunders Company. Periodicals Fulfillment, 6277 Sea Harbor Drive, Orlando, FL 32887. (800) 654-2452. Summary: This review article, from an issue on pediatric gastroenterology, describes recent advances in the field and summarizes the clinical presentation, diagnostic evaluation, and management of children with chronic ulcerative colitis (UC). The author notes that chronic nonspecific UC remains a disease of unknown etiology, although much new information continues to be gleaned from basic research and clinical trials. Topics include genetic studies, the etiopathogenesis of UC in children, clinical features of inflammatory bowel disease in childhood, immunosuppressive therapy in children, nutritional intervention, infectious agents as triggers of relapse, and surgical intervention. In most instances, UC responds to medical therapy. Selecting appropriate drug therapy for a specific child depends on the extent and severity of the colitis. 2 tables. 115 references. (AA-M). •
Emerging Perspectives on the Pathophysiology and Treatment of Inflammatory Bowel Disease Source: American Journal of Gastroenterology. 92(12): 1S-24S. December Supplement 1997. Contact: Available from Williams and Wilkins. 351 West Camden Street, Baltimore, MD 21201-2436. (800) 638-6423 or (410) 528-8555. Summary: This supplement provides a series of peer-reviewed articles on the pathophysiology and treatment of inflammatory bowel disease (IBD), developed from a symposium presented in conjunction with Digestive Diseases Week, 1996. Topics explored include the current thinking with regard to the pathogenesis of chronic intestinal inflammation and the possibilities for targeting therapies toward specific key regulatory pathways, factors influencing relapse of disease, and optimal therapies for induction and maintenance of remission. Many factors contribute to relapse of IBD, and the proper identification of the cause of each case may influence disease management. Three theories of IBD etiology are currently under consideration: reaction to a persistent intestinal infection, existence of a defective mucosal barrier to luminal antigens, and a dysregulated host immune response to ubiquitous antigens. The emerging role of quality of life assessment in tailoring individual therapies, programs, and interventions to patient-identified needs is also addressed. Each article includes extensive references.
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Inflammatory Bowel Disease: Immunodiagnostics, Immunotherapeutics, and Ecotherapeutics Source: Gastroenterology. 120(3): 622-635. February 2001. Contact: Available from W.B. Saunders Company. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452. Website: www.gastrojournal.org. Summary: Treatment options for inflammatory bowel disease (IBD) reflect a continuing shift from empiricism to strategies based on improved understanding of the pathophysiology of disease. This article reviews the use of immunodiagnostics, immunotherapeutics, and ecotherapeutics for managing inflammatory bowel disease (Crohn's disease and ulcerative colitis). In susceptible individuals, IBD appears to be the result of defective regulation of mucosal immune interactions with the enteric microflora. This has prompted research directed at the interface of the traditional disciplines of immunology, microbiology, and epithelial cell biology. Whereas immunodiagnostics have been of limited clinical value in IBD, assessments of mucosal
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rather than systemic immune function are promising. For therapy, there is an increasing trend toward more aggressive and earlier use of immunomodulatory agents, particularly for prevention of relapse, with cytokine manipulation as a bridge therapy to achieve remission in patients with acute severe disease. Although most drug treatments are directed toward altering the host response, the rational for manipulating the enteric flora (i.e., the resident bacteria in the intestinal tract) appears sound and will be the basis of additional future therapeutic strategies. The author concludes that notwithstanding the widening range of options for drug therapy in IBD, other outcome modifiers and well established principles of managing chronic disease are as important as ever. 1 figure. 4 tables. 124 references. •
Epidemiology and the Natural Course of Inflammatory Bowel Disease Source: Gastroenterology Clinics of North America. 28(2): 255-281. June 1999. Contact: Available from W.B. Saunders. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000. Summary: Ulcerative colitis (UC) and Crohn's disease (CD) are inflammatory disorders of the gastrointestinal tract that are distributed unevenly within populations and throughout the world. This review article considers epidemiology and the natural course of inflammatory bowel disease (IBD). Although its exact causes remain unknown, epidemiology has provided insight into its pathogenesis. The authors examine geographic, ethnic, and other trends in IBD; risk factors (including genetic and environmental factors); and its natural history. The authors caution that performance of epidemiologic studies of IBD that are similar and easily compared has been hampered by lack of universally adopted diagnostic criteria for these disorders. A study from Baltimore has suggested that the incidence of IBD in African Americans is lower than in American whites. Studies of the incidence of IBD in populations that emigrate to high risk geographic areas suggest that the rate rises in these groups. Several studies have suggested that within a specified geographic area, the incidence of IBD is two to fourfold higher in Jews than in other ethnic groups. Several studies have found a trend toward increased rates of IBD in urban communities compared to rural ones. Both ulcerative colitis and Crohn disease are more frequent in high socioeconomic and white collar populations than in lower socioeconomic and blue collar populations. The authors review the extent and severity of disease, disease course, complications, cancer risks, survival (prognosis), and quality of life in UC and CD. The article concludes with a brief description of IBD in the pediatric population and in the elderly. 4 figures. 3 tables. 125 references. (AA-M).
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Surgical Therapy for Ulcerative Colitis Source: Ostomy Quarterly. 34(1): 36-40. January 1997. Contact: Available from Ostomy Quarterly. 36 Executive Park, Suite 120, Irvine, CA 92614-6744. (800) 826-0826 or (714) 660-8624. Fax (714) 660-9262. Summary: Ulcerative colitis (UC) is a disease that involves the inner lining (mucosa) of the colon and rectum. While the cause of UC remains elusive, surgical removal of the entire colon and rectum is curative. The authors of this article describe surgical therapy for UC. They note that the indications for surgery can be divided into three categories: immediately life threatening, chronically disabling, and an increased cancer risk. They discuss each of these indications and then describe the advantages and disadvantages of each of five surgical alternatives for managing UC. Those alternatives are subtotal colectomy with ileostomy, colectomy with ileorectal anastomosis, proctocolectomy with
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Brooke ileostomy, proctocolectomy with continent ileostomy, and proctocolectomy with ileal pouch anal anastomosis. The authors stress that, as in all operations, the risks of surgical therapy must be balanced against the benefits to the patient. The risks of surgery include the morbidity and mortality associated with the procedure itself and the alteration in lifestyle resulting from the removal and reconstruction of the colon and rectum. The benefits include a cure of UC if the entire colon and rectal mucosa is removed, removing the risk of developing cancer, and improving an individual's lifestyle. Limitations in social activities such as work, as well as the lack of well-being and a reduced energy level, are often significantly improved after surgery. 5 figures. 2 tables. 9 references. •
Avoiding Common Errors in Maintenance Therapy for Ulcerative Colitis Source: Practical Gastroenterology. 22(4): 49-50, 52, 54-56, 58. April 1998. Contact: Available from Shugar Publishing, Inc. 99B Main Street, Westhampton Beach, NY 11978. (631) 288-4404. Fax (631) 288-4435. E-Mail:
[email protected]. Summary: Ulcerative colitis (UC) is a medically incurable chronic disease in which the mucosal lining of the colon becomes inflamed. The goal of medical therapy is to quickly induce remission and maintain it for as long as possible, without creating side effects or adversely affecting quality of life. This article outlines strategies to avoid common errors in maintenance therapy for UC. The authors note that, since therapy is often lifelong, the chance for treatment errors is greatly increased. Aminosalicylates are usually the best choice for long term maintenance of mild to moderate disease. Corticosteroids can quell acute flares in moderate to severe disease, but are contraindicated as maintenance therapy. Immunomodulators are safe and effective as maintenance therapy in more severe cases of steroid resistance and steroid dependence. All of these drugs are safe during pregnancy. Antibiotics are rarely helpful, but resumption of cigarette smoking may sometimes be recommended in lieu of surgery (the potentially life threatening adverse effects associated with smoking must be weighed heavily against the benefits). The only cure for UC is colectomy, which can significantly increase the quality of life for patients who have chronically active symptoms despite optimal medical management. 3 tables. 31 references. (AA-M).
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Ulcerative Colitis in Young Adults: Complexities of Diagnosis and Management Source: Postgraduate Medicine. 103(1): 45-49, 53-54, 56, 59. January 1998. Contact: Available from McGraw-Hill, Inc. 1221 Avenue of the Americas, New York, NY 10020. (612) 832-7869. Summary: Ulcerative colitis (UC) is difficult to differentiate from other inflammatory bowel diseases or to treat with precision. This article discusses the characteristics of UC, the medications used to treat it, and the challenge of recognizing and managing UC. The intestinal inflammation associated with UC may involve the entire colon (36 percent of the patients), or be limited to distal areas such as the left colon (17 percent) or rectum (46 percent). Patients with active disease commonly present with bloody diarrhea, abdominal pain, and rectal urgency. However, symptoms may differ depending on the extent of the colonic inflammation. The diagnosis of UC depends on a combination of findings from the history, physical examination, laboratory evaluation, and endoscopic and histopathologic studies, as well as exclusion of other causes of colitis. Response to therapy and continued observation of the patient over time help to confirm the diagnosis. The author reviews the medical treatment of ulcerative colitis and summarizes factors related to ulcerative colitis, including smoking status, nutritional
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therapy, and cancer. The mainstays of treatment are sulfasalazine for mild to moderate disease and corticosteroids for moderate to severe disease. Side effects of sulfasalazine limit its use in some patients. Refractory UC is best treated surgically. 1 figure. 2 tables. 23 references. (AA-M). •
Ulcerative Colitis: A Rational Approach to Management Source: Consultant. 41(4): 541-548. April 1, 2001. Contact: Available from Cliggott Publishing Company. 330 Boston Post Road, Darien, CT 06820-4027. (203) 661-0600. Summary: Ulcerative colitis (UC), a type of inflammatory bowel disease can manifest as proctitis or proctosigmoiditis, left sided colitoss, or pancolitis. This article offers a rational approach to the management of patients with UC. Frequent low volume bowel movements, urgency, rectal bleeding, and tenesmus (ineffective spasms of the rectum) alone suggest proctitis. Prostration, fever, tachycardia (racing heartbeat), dehydration, and complications of blood loss (which may or may not be accompanied by symptoms of proctitis) suggest more severe disease or more extensive bowel involvement. For patients with mild to moderate disease, mesalamine is recommended to induce and maintain remission. Systemic corticosteroids can induce remission in patients with moderate to severe disease but are not useful for maintenance therapy. Azathioprine or 6 mercaptopurine can be used to wean patients with moderate to severe colitis from corticosteroids and to maintain remission. If severe colitis does not respond to corticosteroids, immunosuppressive therapy or colectomy may be needed. Other indications for surgery include development of acute complications related to disease activity and chronic complications, such as dysplasia, carcinoma, recurrent hemorrhage, or growth retardation in children. Annual surveillance colonoscopy with biopsy is recommended for patients with pancolitis and left sided colitis.
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Review Article: Potential Therapeutic Applications and Mechanisms of Action of Heparin in Inflammatory Bowel Disease Source: Alimentary Pharmacology and Therapeutics. 14(11): 1403-1409. November 2000. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com. Summary: Unfractioned heparin was recently reported to be beneficial in the treatment of inflammatory bowel disease (IBD). This article reviews the potential therapeutic applications and mechanisms of action of heparin in IBD. The available uncontrolled data show that the drug may be effective in steroid resistant ulcerative colitis (UC) with a percent of complete clinical remission of over 70 percent, after an average of 4 to 6 weeks of therapy. The administration of unfractioned heparin is not currently justified by the very limited available data. The worsening of rectal bleeding is infrequent in treated UC patients and only rarely does it require blood transfusion or a colectomy (removal of part of the colon). Low molecular weight heparin was used in a single trial in patients with steroid refractory UC, with results similar to those observed with unfractioned heparin. Since a prothrombotic state has been described in IBD, and microvascular intestinal occlusion (blockage of the smallest blood vessels in the intestine) seems to play a role in the pathogenesis of IBD, it is reasonable that part of the beneficial effects of unfractioned heparin in IBD may result from its anticoagulant properties. However, beyond its well known anticoagulant activity, unfractioned heparin also exhibits a broad spectrum of immunomodulating and anti inflammatory
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properties, by inhibiting the recruitment of neutrophils and reducing pro inflammatory cytokines. Moreover, heparin can restore the high affinity receptor binding of basic fibroblast growth factor; this would aid healing of the ulcerated mucosa. The authors conclude that unfractioned heparin may represent a safe therapeutic option for severe, steroid resistant UC, although randomized, controlled trials are needed to confirm this data. 1 figure. 2 tables. 71 references. •
Increase in Colorectal Epithelial Apoptotic Cells in Patients with Ulcerative Colitis Ultimately Requiring Surgery Source: Journal of Gastroenterology and Hepatology. 17(7): 758-764. July 2002. Contact: Available from Blackwell Science. 54 University Street, Carlton South 3053, Victoria, Australia. +61393470300. Fax +61393475001. E-mail:
[email protected]. Website: www.blackwell-science.com. Summary: Up to one-third of patients with ulcerative colitis (UC) need to undergo surgery, but the factors that exacerbate inflammation (and thus lead to surgery) remain unclear. The authors of this study hypothesize that excessive apoptosis (sloughing of skin crust) reported in active UC may disrupt epithelial defenses and exacerbate the disease. The present study was undertaken to clarify whether apoptotic epithelial cells and histiocytes engulfing them increased in patients with active UC who ultimately require surgery (UC-S) rather than those receiving medication alone (UC-M). The study included 29 patients with UC-S, 35 patients with UC-M, 18 with infectious colitis, and 16 healthy controls. The apoptotic indices in UC-M patients were significantly higher than those in controls but almost equal to those in infectious colitis patients. In the upper and lower halves of the mucosa, both apoptotic indices and histiocyte densities were significantly higher for UC-S than in UC-M. The results suggest that epithelial apoptosis is a non-specific phenomenon and that an increased number of apoptotic cells exceeding histiocyte phagocytic capacity may play a part in the disruption of epithelial defenses and further accelerate mucosal inflammation. 2 figures. 2 tables. 38 references.
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Oxidative Stress as Pathogenic Factor in Inflammatory Bowel Disease: Radicals or Ridiculous? Source: Alimentary Pharmacology and Therapeutics. 16(12): 1997-2015. December 2002. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email:
[email protected]. Website: www.blackwell-science.com. Summary: Virtually all inflammatory mediators investigated to date seem to be dysregulated in the inflamed intestinal mucosa of patients with inflammatory bowel disease (IBD). However, which of these are actually involved in the initiation and perpetuation of intestinal tissue damage is still not fully understood. Among these mediators are the reactive oxygen metabolites, produced in large amounts by the massively infiltrating leucocytes. These reactive oxygen metabolites are believed to constitute a major tissue-destructive force and may contribute significantly to the pathogenesis (development) of IBD. This article provides a concise overview of reactive oxygen metabolite biochemistry, the types of cell and tissue damage potentially inflicted by them, and the endogenous antioxidants which should prevent these harmful effects. The authors note that reactive oxygen metabolite-mediated injury is important in both the primary and downstream secondary pathophysiological mechanisms underlying intestinal inflammation. Nonetheless, how the individual components of the mucosal
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antioxidant enzymatic cascade respond to inflammatory conditions is a neglected area of research. 1 figure. 1 table. 264 references. •
Use of Cytotoxic Agents and Cyclosporine in the Treatment of Autoimmune Disease. Part 2: Inflammatory Bowel Disease, Systemic Vasculitis, and Therapeutic Toxicity Source: Annals of Internal Medicine. 129(1): 49-58. July 1, 1998. Summary: When cytotoxic (cell-damaging) agents were introduced, their ability to disrupt nucleic acid and protein synthesis led to their effective use for the treatment of neoplastic disease (cancer). It then became apparent that these agents also suppress the immune system. This usually unwelcome effect was subsequently studied and beneficially directed toward treating non-neoplastic diseases in which autoimmune mechanisms play a role. This article discusses the use of cytotoxic agents and cyclosporine in the treatment of inflammatory bowel disease (IBD) and systemic vasculitis, and reviews the toxic effects of these agents. The authors caution that because these medications can cause treatment-induced illness or even death, it is imperative to weigh the benefits and risks of cytotoxic therapy when treating a non-neoplastic disease. The authors review research studies that investigated the use of these drugs. Drugs used for IBD include azathioprine and 6-mercaptopurine, methotrexate, and cyclosporine. These drugs are frequently used in combination with other agents and require careful monitoring. The authors stress that the optimal use of various drug combinations requires not only a knowledge of appropriate indications and dosage but also a thorough assessment of patient expectations and quality of life, a careful weighing of the various risks of medical and surgical therapies, the judicious use of other supportive measures, and extensive patient education. The section on toxicity discusses cyclophosphamide, chlorambucil, methotrexate, azathioprine, 6-mercaptopurine, and cyclosporine. The authors caution that infection is still an important cause of illness and death that is largely related to the nonspecific actions of these agents on the immune response. 3 tables. 75 references.
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Immunosuppressive Drugs in the Treatment of Inflammatory Bowel Disease Source: Seminars in Gastrointestinal Disease. 9(1): 2-9. January 1998. Contact: Available from W.B. Saunders Company. 6277 Sea Harbor Drive, Orlando, FL 32887. (800) 654-2452 or (407) 345-4000. Summary: With increasing experience, the threshold for using immunosuppressive drugs in inflammatory bowel disease (IBD) has fallen. There is a tendency now to use them in a greater proportion of patients and at an earlier stage of the disease. This article provides an overview of the agents in common use and highlights their role in the management of IBD. The principal drugs used in clinical practice at this time include: azathioprine (AZA) and its metabolite 6-mercaptopurine (6-MP), methotrexate, and cyclopsporin A. AZA and 6-MP are generally considered the first line immunosuppressive agents. These drugs are effective and generally well tolerated by most patients and enable many patients to avoid the predictable side effects of steroid therapy. The major concerns associated with IS therapy, malignancy, and opportunistic infection have not been significant problems with either AZA or 6-MP in the context of IBD treatment. The toxicities associated with AZA and 6-MP can be divided into allergic-type reactions that are dose-independent (pancreatitis, fever, rash, arthralgias, malaise, nausea, and diarrhea) and non-allergic type reactions that are dose dependent (leukopenia, thrombocytopenia, and hepatitis). Because of the extensive use of immunosuppressive drugs, it is important that clinicians involved in caring for patients
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with IBD be familiar with them. Appended to the article are two relevant case histories, with commentary by one of the authors and three additional physicians. 38 references. (AA-M). •
Menstrual Cycle and Its Effect on Inflammatory Bowel Disease and Irritable Bowel Syndrome: A Prevalence Study Source: American Journal of Gastroenterology. 93(10): 1867-1872. October 1998. Contact: Available from Williams and Wilkins. 351 West Camden Street, Baltimore, MD 21201-2436. (800) 638-6423 or (410) 528-8555. Summary: Women with bowel disease commonly report that their symptoms worsen in relation to their menstrual cycle. This article reports on a study undertaken to determine the nature of gastrointestinal (GI) symptoms correlating with the menstrual cycle in women with inflammatory bowel disease and irritable bowel syndrome (IBS). This retrospective study involved 49 women with ulcerative colitis, 49 women with Crohn's disease (CD), 46 women with IBS, and 90 healthy community controls. Participants were interviewed using a questionnaire that included information on general health, medication history, pregnancy, and premenstrual and menstrual symptoms. Premenstrual symptoms were reported by 93 percent of all women but statistically more often by patients with CD. Patients with CD were also more likely to report increased GI symptoms during menstruation; diarrhea was the symptom reported most often. All disease groups had a cyclical pattern to their bowel habits significantly more than controls. Cyclical symptoms included diarrhea, abdominal pain, and constipation. The authors conclude that the prevalence of menstruation related symptoms is high and appears to affect bowel patterns. The physiological and clinical effects of the menstrual cycle should be taken into consideration when assessing disease activity. 3 figures. 2 tables. 13 references. (AA-M).
Federally Funded Research on Ulcerative Colitis The U.S. Government supports a variety of research studies relating to ulcerative colitis. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to ulcerative colitis. For most of the studies, the agencies reporting into CRISP provide summaries or abstracts. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore ulcerative colitis. The following is typical of the type of information found when searching the CRISP database for ulcerative colitis:
2 Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
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Project Title: 2CDA TREATMENT OF REFRACTORY ULCERATIVE COLITITS Principal Investigator & Institution: Rodgers, Vance D.; Scripps Research Institute Tpc7 La Jolla, Ca 92037 Timing: Fiscal Year 2002 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: 5ASA REGULATION OF MNSOD IN INTESTINAL CELLS Principal Investigator & Institution: Valentine, John F.; Associate Professor; Medicine; University of Florida Gainesville, Fl 32611 Timing: Fiscal Year 2002; Project Start 01-MAY-1998; Project End 30-APR-2003 Summary: Inflammatory bowel disease (ulcerative colitis and Crohn's disease) are chronic inflammatory disease of the gut for which there is no known cause or cure. It has been estimated that 2 million people in the United States have IBD. The peak onset of IBD is between 15 and 25 years of age and the majority of patients with IBD are under age 40. Mesalamine (5-ASA) is the active ingredient in sulfasalazine and is one of the major therapies use to treat active disease and for the maintenance of remission. The mechanism of action of 5-ASA remains unclear, however, we have found that 5-ASA induces a cytoprotective enzyme, manganese superoxide dismutase (MnSOD), at concentrations obtained in the colon of patients taking sulfasalazine orally. MnSOD is the only known 5-ASA regulated gene. The induction of MnSOD by 5-ASA may highlight a new therapeutic mechanism. MnSOD may serve a protective role in the bowel and prevent or reduce cytokine and oxygen radical mediated damage. This may be particularly important in the bowel as it contains low levels of antioxidants. The goal of this research project is to define the mechanisms that control the 5-ASA regulation of MnSOD gene expression in intestinal epithelial cells. The specific aims are designed to answer precise questions on the molecular mechanisms involved in the regulation of MnSOD gene expression by 5-ASA. In this proposal, we are using antisense MnSOD to document the role of MnSOD in 5-ASA induced cytoprotection in cell culture. We will determine how 5-ASA induces MnSOD by defining the sequences involved in the protein-DNA interactions that are responsible for the enhanced transcription of MnSOD. In addition to defining the cis-acting regulatory elements in the promoter region, we will identify and define enhancer elements involved in the regulation of MnSOD. Our studies will involve Dnase I hypersensitivity analysis, promoter deletion analysis, and evaluation of enhancer elements using transient transfection. Although the induction of MnSOD is transcriptional as determined by nuclear run-on experiments, we will also evaluate the role of MnSOD mRNA stabilization as a contributor to the induction of MnSOD mRNA levels. It is our premise that by understanding the mechanisms by which 5-ASA induces MnSOD, we will be able to identify and clone the transcription factors involved as well as design other therapeutic agents and 5-ASA derivatives to act as more potent inducers of MnSOD and possibly other yet to be defined 5-ASA regulated genes. By determining how therapeutic agents such as 5-ASA exert a beneficial influence on the disease activity of IBD, we may gain a further understanding of the pathogenesis of IBD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ANTI CD40L THERAPY IN INFLAMMATORY BOWEL DISEASE Principal Investigator & Institution: Blumberg, Richard S.; Associate Professor of Medicine; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115
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Timing: Fiscal Year 2002 Summary: Inflammatory bowel diseases (IBD), categorized as Crohn's disease (CD) or ulcerative colitis (UC), are complex disorders of unknown etiology with a spectrum of clinical features which exhibit great variation among affected subjects. The majority of patients, however, will required immunosuppressive and/or immunomodulatory agents which are not universally successful in effective maintaining remission and preventing disease relapse. Recent insights into the basic mechanisms of immune responses and the extension of these concepts to CD and UC have led to the identification of new therapeutic targets which may be more efficacious in IBD therapy by focusing on critical biologic pathways. More recently, it has been suggested that costimulatory signals involved in antigen presentation appear to affect immune responses through the up- regulation of an accessory molecule named CD40 ligand (CD40L) on T cells. The interaction between the molecule CD40 and CD40L appears to play a role in CD4 T cell-mediated responses that characterize a variety of autoimmune-mediated disease states including inflammatory bowel disease. Based upon these biologic considerations of CD40-CD40L activity, we believe that human. IBD, both CD and UC, may be diseases which would benefit clinically from therapy directed at the CD40CD40L pathway. We therefore propose a clinical trial of a humanized anti- CD40L antibody in study subjects with inflammatory bowel disease with the following specific aims: 1) To determine any toxicity and potential benefit from anti-CD40L antibody therapy in patients with steroid-resistant or refractory CD and UC. 2) To determine the incidence of clinical and histologic disease remission in patients with steroid-resistant or refractory CD and UC treated with anti-CD40L antibody therapy. 3) To determine the proportion of patients who remain in sustained clinical remission 12 months after antiCD40L antibody therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ANTI-BACTERIAL MUCOSAL IMMUNE RESPONSES IN HUMAN IBD Principal Investigator & Institution: Cohavy, Offer; Cedars-Sinai Medical Center Box 48750, 8700 Beverly Blvd Los Angeles, Ca 90048 Timing: Fiscal Year 2002; Project Start 01-JUL-2002 Summary: Accumulating evidence implicates a significant contribution of intestinal bacteria in IBD pathogenesis. We hypothesize that an antigen-specific immune activation by bacterially expressed proteins mediates the aberrant immune response in the inflamed mucosa. Accordingly, the overall goal of this proposal is to define the antigenic target of the immune response in IBD. Our group recently identified E. coli OmpC, Bacteroides OmpW, and Mycobacterial HupB as candidate targets for the pathogenic immune response underlying human IBD, using the UC associated marker antibody, pANCA. Here, we propose to evaluate these candidate pANCA antigens as targets for a mucosal T cell response in the IBD gut. Aim I will correlate the mucosal T cell response to candidate antigens with serum pANCA levels in an IBD patient cohort. Aim 2 will evaluate T cell responses in relation with disease activity or location. Primary T lymphocytes from lamina propria or peripheral blood T will be isolated and cocultured with antigen-pulsed autologous antigen presenting cells (APC). Proliferation as well as activation marker expression and cytokine secretion profiles will be assessed as an indication of antigen specific response. For a more refined analysis of a response, we will rigorously analyze the cytokine secretion profiles to ascertain the nature of the identified T cell specificity in the context of Th1 vs. Th2 or suppressor cell response. Reactivity profiles across a broad UC patient cohort will be statistically analyzed for
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correlation between antigen specificity and serum pANCA levels or disease- state. Findings from this investigation will define a patient subset expressing a pANCArelated T cell response, and will characterize the pANCA reactive T cell population. In addition, specific microorganisms involved in UC pathogenesis may be identified. And finally, at the molecular level, this study will determine which of the suggested pANCA reactive proteins constitutes a significant antigenic target of the mucosal immune compartment in human IBD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ANTI-INFLAMMATORY INFLAMMATION
LIPIDS
IN
ACUTE
MUCOSAL
Principal Investigator & Institution: Gronert, Karsten; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 15-FEB-2002; Project End 31-DEC-2004 Summary: (provided by applicant) Inflammatory bowel diseases (IBD) that are associate with a dramatic increase in colorectal cancer occur throughout the world with an annual incidence of approximately 12/100,000 people. Aberrant activation of neutrophils and a profound increase in lipid and peptide mediators are cardinal signs of these inflammatory diseases as well as for ischemia reperfusion injury, a known complication of surgical procedures. How acute inflammatory responses switch from vital host defense to aberrant inflammation and neutrophil mediated tissue injury remains to be completely elucidated. Therefore, endogenous mechanisms that disrupt proinflammatory circuits are of interest. Aspirin and omega-3 polyunsaturated fatty acids (PUFA) are therapeutic agents that demonstrate benefits in inflammatory diseases as well as prevention of colon cancer. However, their mechanisms of action still needs to be clearly defined but targets the formation of lipid mediators namely eicosanoids. Both therapeutic agents trigger the formation of novel classes of anti-inflammatory lipids, namely 15R-lipoxins and omega-3 PUFA derived 15R-and 18R-series eicosanoids. This study shall test the hypothesis that acute inflammation induces a regulated and temporal generation of anti-inflammatory lipid signals and that omega-3 fatty acid and aspirin augment these protective lipid mediator circuits. The specific aims of this application will employ a combined approach of structural elucidation, molecular biology and transgenics to delineate three main aspect of the role of lipid signals in neutrophil mediated intestinal injury: i) Establish the temporal relationship of pro- and anti-inflammatory eicosanoids. ii) Determine the impact of aspirin and omega-3 PUFA on eicosanoid profiles and elucidate novel protective lipid mediators. iii) Determine if novel aspirin and omega-3 PUFA triggered lipid mediators are protective against aberrant PMN activation and if changes in expression of receptors for lipid mediators are markers for aberrant intestinal inflammation. The broad and long-term objectives of this application are to elucidate endogenous pathways that block PMN mediated injury to promote resolution of inflammation. Results from this project may provide novel anti-inflammatory tools for controlling inflammatory diseases such as Ulcerative Colitis and Chron's Disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: AZATHIOPRINE /SULFASALAZINE /PENTASA INTERACTIONS IN INFLAMMATORY BOWEL DISEASE Principal Investigator & Institution: Sandborn, William J.; Professor of Medicine; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905
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Timing: Fiscal Year 2002 Summary: A pharmacodynamic and pharmacokinetic study to determine the clinical significance of drug interactions between azathioprine and sulfasalazine, Balsalazide or Pentasa in patients with inflammatory bowel disease. The specific aims of the study are to estimate the proportion of clinically important leukopenia, defined as a total white blood cell (WBC) count $1 billion. The worldwide market in IBD (developed countries only) is four times larger. Given the absence of a specific and completely effective therapy, Inotek anticipates market acceptance to be achieved rapidly, at high levels of penetration, and with a high sustained price point ($1000 per patient per year). Estimated worldwide gross sales revenues after market entry and maturation (ca. 4 years after FDA approval) equal $800 million (anual). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PHASE II STUDY OF BXT 51072 IN PATIENTS W/ ULCERATIVE COLITIS Principal Investigator & Institution: Hanauer, Stephen B.; Professor of Medicine; University of Chicago 5801 S Ellis Ave Chicago, Il 60637 Timing: Fiscal Year 2002 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: QUALITY OF LIFE IN PEDIATRIC INFLAMMATORY BOWEL DISEASE Principal Investigator & Institution: Perrin, James M.; Massachusetts General Hospital 55 Fruit St Boston, Ma 02114 Timing: Fiscal Year 2003; Project Start 01-JAN-2003; Project End 31-DEC-2004 Summary: (provided by applicant): Measurement of the quality of life (QoL) of children and adolescents with inflammatory bowel diseases (IBD) has had little attention, despite the importance of understanding key factors affecting QoL, especially for measuring the effects of clinical trials to improve IBD outcomes. The main purpose of this pilot study is to examine the impact of clinical severity and treatment social factors on the quality of life (QoL) of a diverse population of children and adolescents with inflammatory bowel disease (IBD). Secondary purposes include determining the effects of sociodemographic factors on QoL and exploring the concordance of views of parents and children of QoL. The study aims are to 1) determine the associations of of clinical characteristics (condition type, activity/severity, and treatment) with specific components of general health-related quality of life and IBD-specific QoL; 2) describe the effects of sociodemographic characteristics (SES, age, and gender) on these measures; and 3) compare the views of different observers (parent and child with IBD) of the child's QoL. The study will apply both general and condition-specific QoL measures among a random sample of 250 children and adolescents with IBD, ages 5-18 years, in six clinical sites. We will obtain measures of QoL from both the child and a parent in each case. The study will obtain additional data regarding the subjects' clinical condition (condition type, severity/activity, treatment [including surgery], age of onset) and socioeconomic status (household structure and income). Main analyses will compare general and specific measures of QoL and examine the influence of clinical and sociodemographic variables on QoL, through multivariate regression techniques. We will also examine the differences in child and parent assessments of QoL. The information from this study will provide a stronger base for future studies of treatment and natural history of IBD. It will help to clarify the life domains that are affected by IBD and will inform interventions to improve QoL for children with IBD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RANDOMIZED TRIAL OF ROSIGLITAZONE FOR ULCERATIVE COLITIS Principal Investigator & Institution: Lewis, James D.; Medicine; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002; Project Start 01-SEP-2001; Project End 31-AUG-2006 Summary: (provided by applicant): Ulcerative colitis (UC) is a chronic inflammatory disease involving all or a portion of the colon. Currently, there are few effective medical therapies for UC. Furthermore, because of the potential toxicity of the currently
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available agents, there is a great need for alternative therapies to treat patients with UC refractory to therapy with 5-ASA agents. Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily of transcription factors whose activities are regulated by high affinity binding of small lipophilic ligands such as steroid hormones. A new class of diabetic drugs, the thiazolidinediones, has been developed to bind to the gamma (g) subtype of the PPARs. Colonic epithelial cells express high levels of PPARg protein and have the ability to produce inflammatory cytokines that may contribute to the inflammatory process in UC. We have previously demonstrated that PPARg ligands significantly attenuate cytokine gene expression related to the inflammatory cascade in colon cancer cell lines. Furthermore, we and others have demonstrated that thiazolidinedione ligands for PPARg markedly reduce colonic inflammation in murine models of ulcerative colitis. In addition, we have shown in a pilot study that more than 50% of patients with mild to moderately active UC despite therapy with 5-ASA agents (and corticosteroids or imunomodulator medications for most patients) experienced improved symptoms within 12 weeks of therapy with rosiglitazone 4 mg twice daily. As such, we believe that PPARg may represent a novel target for modulating colonic inflammation in UC. The proposed study is a multi-center, double-blind, randomized controlled trial of rosiglitazone versus placebo for mild to moderately active ulcerative colitis refractory to standard therapy with oral 5-ASA agents. 176 subjects will be randomized to rosiglitazone 4mg bid or placebo for 12 weeks of therapy. The primary outcome will be improvement in disease activity as measured by the Disease Activity Index first described by Sutherland. Secondary outcomes will include clinical remission and quality of life. We will use the techniques of immunohistochemistry to detect expression of PPARg receptors in human colon tissue. We will also use the technique of immunohistochemistry to examine the change in NF-KB activation prior to and following therapy with either placebo or rosiglitazone. Specifically, we will compare expression of p65 and phosphorylated IKBalpha, in colonic tissue prior to and following exposure to rosiglitazone and placebo. If our hypothesis is correct, this study will serve to establish that ligands for PPARg possess biological activity necessary to modulate the inflammatory response in the intact human colon. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: RANDOMIZED, ULCERATIVE COLITIS
CONTROLLED
TRIAL
OF
HEPARIN
IN
Principal Investigator & Institution: Korzenik, Joshua; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2002 Summary: There is no text on file for this abstract. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGULATION OF GUT SUBSTANCE P RECEPTORS Principal Investigator & Institution: Vigna, Steven R.; Associate Professor; Medicine; Duke University Durham, Nc 27706 Timing: Fiscal Year 2002; Project Start 01-APR-1996; Project End 31-DEC-2006 Summary: (provided by applicant): Substance P (SP) is a neuropeptide involved in physiological regulation and has also been implicated in the pathway resulting in pain and inflammation. In the previous funding period we showed that the SP neurokinin-1 receptor (NK-1R) desensitizes more rapidly and extensively than may other G protein-
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coupled receptor and that this is caused by receptor phosphorylation and is correlated with receptor-mediated physiological responses. In addition, we showed that the NK-1R undergoes vigorous agonist-dependent endocytosis and recycling as a primary mechanism of resensitization. We also showed that the NK-1R in the rat intestine mediates Clostridium difficile toxin A-induced inflammation, secretion, and tissue damage. These observations suggest that the NK-1R is highly regulated and plays a major role in intestinal inflammation, but the mechanisms of NK-1R regulation are incompletely understood. The current proposal describes studies designed to reveal additional mechanisms of NK-1R regulation. The proposed specific aims are to 1) test the hypothesis that the N-terminus of SP plays a role in homologous desensitization of the NK-1R even though the C-terminus contains all of the agonist activity of the peptide, 2) test the hypothesis that the cytoplasmic microfilament component of the cytoskeleton in NK-1R-expressing cells plays a role in SP-mediated signaling, and 3) test several hypotheses concerning the mechanisms of SP-stimulation of MAP Kinase activity via the NK-1R. These hypotheses will be tested by multiple approaches including assessment of NK-1R signaling and desensitization after site-directed NK-1R mutagenesis. These studies will lead to insight into the normal mechanisms of SP NK-1R regulation and will suggest possible mechanisms of abnormal NK-1R regulation in intestinal inflammatory diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGULATION OF INTESTINAL EPITHELIAL CELL MIGRATION Principal Investigator & Institution: Polk, D Brent.; Associate Professor; Pediatrics; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2002; Project Start 01-JUL-2001; Project End 30-JUN-2006 Summary: (Adapted from the Applicant's Abstract): Maintenance of an intact intestinal epithelium is critical for intestinal growth, development, wound healing and prevention of disease. Restitution, the initial phase of epithelial wound repair, is regulated by a number of peptides, including epidermal growth factor (EGF). Altered mucosal reepithelialization is a significant component of a number of diseases primarily affecting the gastrointestinal tract, such as ulcerative colitis and peptic ulcer disease. Surprisingly, little information is known about the initial signaling events in the process of basal or stimulated intestinal cell migration. Preliminary data in intestinal epithelial cells from our laboratory and reports on fibroblast migration have permitted the development of the proposed hypothesis that: Epidermal growth factor receptor regulates intestinal epithelial cell migration via integrated signaling pathways requiring tyrosine kinase and the enhanced activities of specific target molecules during the earliest phases of cellular movement. The objective of this proposal is to understand the cellular and molecular mechanisms of growth factor regulated intestinal cell migration through a series of questions comprising the following Specific Aims: 1) What are the principal mechanisms of EGF receptor regulation of intestinal epithelial cell migration? 2) What are the roles of phosphatidylinositol phospholipase C (PLC) gamma 1, protein kinase (PK) C epsilon, and other signal transduction molecules in EGF receptorregulated cellular migration? and 3) How does the EGF receptor mediate cytoskeletal rearrangement during intestinal cell migration? To address the mechanisms of EGF receptor regulation of migration in aim 1, we will express various EGF receptor constructs in a mouse colon cell line derived from the EGF receptor null mouse. In aims 2 and 3, we will express constitutively active and dominant negative forms of PLC gamma 1, PKC epsilon and the Rho small GTPase proteins to establish a molecular ordering of signal transduction from the EGF receptor to cytoskeletal rearrangement
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regulating motility. We will use expression based cloning and coprecipitation assays to identify interacting proteins in the pathway leading to cellular migration. These studies should enhance our understanding of the initial signaling events required for growth factor-regulated intestinal epithelial restitution and provide a mechanistic basis for potential development of novel therapeutic targets. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF CHEMOKINES IN T CELL MEDIATED COLITIS Principal Investigator & Institution: Lillard, James W.; Assistant Professor; Microbiology, Biochemistry & Immunology; Morehouse School of Medicine Atlanta, Ga 30310 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-AUG-2004 Summary: Inflammatory bowel diseases (IBD) are chronic, relapsing and tissue destructive diseases. T helper type l (Thl) cells secreting TNF-alpha and IFN-gamma have been emphasized in ulcerative colitis, while Th2 cells may be more closely associated with Crohn's disease. However, either Thl or Th2 cells can induce colitis in several mouse models; hence the precise causes of these two forms of IBD are incompletely understood. It has recently been shown that the mechanisms of IBD involve antigen- dependent interactions between CD4+ T cells and antigen-presenting cells (APCs) as well as genetic factors. A major deficiency in understanding the steps responsible for IBD, is the lack of comprehension for the role innate and early acting factors play in mucosal immune responses. Chemokines are a family of proteins that are resistant to inactivation by pH or proteolysis as well as affect the chemotaxis and angiogenesis of leukocytes and endothelial cells. Therefore, chemokines no doubt play a pivotal role in the regulation (i.e., initiation, maintenance, and suppression) of mucosal inflammation and tissue destruction. In fact, human interleukin-8 (IL-8), IFN-gamma inducible protein - l0 (IP-l0), CXCR3 (the receptor for IP-10), RANTES (Regulated upon Activation, Normal T cell Expressed and Secreted), and MCP-l/JE (monocyte chemotactic protein-1) have been shown to be unregulated at the sites of mucosal inflammation (IBD). The current proposal stems from our recent findings that RANTES, IP-10, IL- 8, lymphotactin (Lptn), but not MCP-l/JE, can enhance mucosal adaptive immune responses. Since these chemolcines act at several levels, four Specific Aims will be addressed to elucidate the precise role of these chemokines and their corresponding receptors in IBD. The first aim will define the regulatory role of chemokines that are secreted by CD45RBHI CD4+ T cells subsets, which cause experimental IBD after adoptive transfer. The second aim will assess the role of mIL-8Rh (murine IL- 8/GCP2 receptor), CCR5 (a RANTES receptor), CXCR3, and XCRl (Lptn receptor) interactions in the CD45RBHI CD4+ T cell transfer model of murine IBD. The third aim will evaluate the chemokines, cytokines, and corresponding receptors that are expressed by the IBD inducers (CD45RBHI) and IBD suppressors (CDRB45LO) CD4+ T cells subsets. The fourth aim will ascertain the angiogenic or angiostatic factors and cell signaling molecules that are expressed or activated, respectively, by chemokines that regulate IBD. These proposed studies will provide important and novel information regarding the cellular and molecular mechanisms that chemokines use to induce, maintain, and suppress mucosal inflammation and angiogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ROLE OF IL 18 IN CROHN'S DISEASE Principal Investigator & Institution: Pizarro, Theresa T.; Assistant Professor of Medicine; Internal Medicine; University of Virginia Charlottesville Box 400195 Charlottesville, Va 22904 Timing: Fiscal Year 2002; Project Start 01-JUL-2000; Project End 30-JUN-2004 Summary: (Adapted from the applicant's abstract): Inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), affects more than one million people in North America. Increasing evidence suggests that an imbalance of Th1 / Th2 polarization, in favor of Th1 cell subsets, may be a key pathogenic mechanism in a variety of organ-specific autoimmune disease, such as IBD. In CD, evidence has accumulated from both animal models and human studies to indicate that Th1 cytokines are involved in the pathogenesis of this disorder. However, identification of the specific initiating factor(s) driving Th1-mediated immune responses represents an important issue. The present proposal focuses on IL-18, a newly described cytokine, primarily produced by macrophages and other non-immune cell types. Recent studies suggest that IL-18 may function as a "classic" proinflammatory cytokine by playing a primary role in Th1-mediated immune responses and strongly implicates IL-18 as a possible mediator of organ-specific autoimmune disease(s), including CD. Therefore, the central hypothesis of this proposal is that IL-18, having the ability to elicit Th1-polarized T cell responses, may play a crucial pathogenic role in CD, as well-defined prototypic Th1 disorder. The following four specific aims will be investigated to: 1) Characterize the expression of IL-18 in the intestinal mucosa of IBD patients. Using various techniques and at multiple levels, IL-18 mRNA and protein levels will be determined in tissues isolated from the intestines of IBD patients as well as inflammatory and normal controls (IC and NC, respectively). The results obtained from these studies will be compared to those from freshly isolated intestinal mucosal cells, including intestinal epithelial cells (IEC), lamina propria mononuclear cells (LPMC) and various mesenchymal cell populations. Finally, IL-18 expression will be correlated with disease severity as well as clinical phenotype of IBD subgroups. These studies, although descriptive, represent a fundamental step before pursuing more mechanistic studies described in the subsequent specific aims. 2) Determine the factor(s) regulating IL-18 production in, as well as the effects of IL-18 on, intestinal mucosal cells. The regulation of IL-18, in general, and in the context of intestinal inflammation, in particular, will be assessed by investigating the effects of several "classic" proinflammatory and Th1 cytokines on IL-18 expression in different gut mucosal cells. Furthermore, the effects of IL-18, itself, will be evaluated for its ability to activate the inflammatory response typical of CD in IEC, LPMC and intestinal mesenchymal cells by determining IL-18-induced transcription factor activation and subsequent cytokine profile expression. These experiments will reveal critical functions of IL-18 in regulating gut immune responses. 3) Determine the transcriptional regulation of the human IL-18 gene in different intestinal mucosal cell populations. Isolation of the human IL-18 gene, characterization of its structure and mapping of its transcriptional start sites(s) will be initially achieved in order to perform the analyses of IL-18 promoter activity. Promoter function studies will achieved the creation of reporter constructs, site mutagenesis experiments and transfection assays in different intestinal cells lines. These studies will define how the human IL-18 gene is regulated, particularly during gut inflammation, and if transcriptional control varies among different intestinal cell types. 4) Identify, and characterize the properties of, the 31 kD putative IL-18 homologue predominantly found in intestinal epithelial cells. In order to identify the true nature of this putative IL-18 related protein, an expression cDNA phage library will be derived from IEC and immunoscreened for IL-18+ phage plaques. Purified isolates will be subsequently characterized for their unique features.
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These experiments will allow the discovery of novel IL-18 homologues and determine if they are differentially expressed in various cell types within the intestinal mucosa. The ultimate goal of the present research proposal is to define the precise role of IL-18 in CD in order to develop specific treatment modalities aimed at modifying the natural course of this devastating disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF LEPTIN IN MURINE MODELES OF IBD Principal Investigator & Institution: Fantuzzi, Giamila; Medicine; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, Co 800450508 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-AUG-2008 Summary: (provided by applicant): The goal of this project is to investigate the mechanisms by which leptin deficiency regulates susceptibility to intestinal inflammation in mice. In addition to act as a regulator of food intake and energy expenditure, leptin also modulates the immune and inflammatory response. Preliminary data indicate that leptin-deficient (ob/ob) and leptin receptor-deficient (db/db) mice are resistant to colitis induced by chronic administration of DSS or TNBS. The current application will attempt to identify the cell populations responsible for the observed effects. In Specific Aim 1, to evaluate the relative role played by neuronal leptin receptors (Ob-R) in regulation of intestinal inflammation. DSS and TNBS will be administered to mice with a selective deficiency of Ob-R in neurons and their response compared with that of WF mice. To analyze in more detail the role of hypothalamic ObR, DSS- and TNBS-induced intestinal inflammation will be studied in mice in which ObR have been specifically deleted in the arcuate and ventromedial nuclei of the hypothalamus by injecting a vector expressing cre recombinase into Ob-Rflox/flox mice. Because the effects of leptin on both bone marrow- and non-bone marrow-derived cells could contribute to modulation of colitis in the models of DSS and TNBS administration, in Specific Aim 2 the relative contribution of Ob-R expression in these two cell populations will be investigated using bone marrow chimeras for Ob-R. WT bone marrow will be transplanted into db/db mice, while WT mice will receive db/db bone marrow and colitis development will be studied. Furthermore, the direct effects of leptin on T lymphocytes. Preliminary data indicate that Ob-R expression on donor T lymphocytes regulates induction of colitis in the model of CD4+ CD45RBhigh cells transfer into SCID mice. The transfer model will be employed in the attempt to dissect the relative role played by Ob-R expression in donor T lymphocytes versus cells in the recipient mouse. To investigate the direct role of Ob-R expression in T lymphocytes in the modulation of colitis induced by DSS or TNBS, mice with a selective deletion of ObR in T lymphocytes will be employed. Finally, in Specific Aim 3 production of leptin by immune cells at the site of intestinal inflammation will be evaluated in murine models and in biopsies of patients with IBD. The possible participation of immune-derived leptin in the local inflammatory network will also be investigated. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ROLE OF THE ALPHA 1 BETA 1 INTEGRIN IN CHRONIC COLITIS Principal Investigator & Institution: Pavlick, Kevin P.; Molecular and Cellular Physio; Louisiana State Univ Hsc Shreveport P. O. Box 33932 Shreveport, La 71103 Timing: Fiscal Year 2003; Project Start 31-MAR-2003; Project End 28-FEB-2005 Summary: (provided by applicant): The inflammatory bowel diseases (Crohn's disease, ulcerative colitis; IBD) are chronic idiopathic inflammatory disorders of the intestinal
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tract. IBD is characterized by the infiltration of large numbers of monocytes, lymphocytes, and neutrophils into the intestinal interstitium accompanied by extensive mucosal and/or transmural injury. Recent evidence suggests that interaction between collagen-binding integrins (e.g. alpha-1-beta-1) and the extracellular matrix promotes the migration and/or activation of leukocytes in different models of inflammation. However, relatively little information is available describing the importance of leukocyte-interstitial matrix interactions in chronic gut inflammation. Therefore, the overall objective of this study is to better understand the role of the alpha-1-beta-1 collagen-binding integrin in the pathophysiology of chronic gut inflammation in an immune-based murine model of chronic colitis. Hypothesis: We propose that T-cell and/or granulocyte-associated integrin alpha-1-beta-1 interacts with interstitial collagen in the colonic interstitium resulting in the activation of these cells with the upregulation of certain proinflammatory cytokines that may initiate and/or perpetuate chronic gut inflammation. In order to test this hypothesis we propose the following specific aims: 1) Evaluate the importance of T-lymphocyte alpha-1-beta-1 surface expression on the promotion of chronic gut inflammation using donor T-cells from alpha-1-deficient (alpha1-/-) mice. 2) Determine the importance of granulocyte (e.g. monocyte/macrophage, PMNs) alpha-1-beta-1 surface expression on the initiation and/or perpetuation of chronic gut inflammation using RAG-2-/- x alpha-1-/- doubledeficient recipient animals. Understanding the importance of this integrin in an immune-based model of IBD may provide new insights into the pathogenesis of chronic gut inflammation and provide new therapeutic approaches for the treatment of human IBD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF THE CO-STIMULATOR MOLECULAR SLAM IN COLITIS Principal Investigator & Institution: Faubion, William A.; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 30-JUN-2008 Summary: (provided by applicant): Dysregulation of activated T cells leading to a chronic inflammatory state is a central feature of inflammatory boweI disease (ulcerative colitis and Crohn's disease). Co-stimulatory molecules expressed on activated T cells and antigen presenting cells (i.e. macrophages and dendritic ceils) orchestrate T cell((antigen presenting cell interaction and define the type of T cell response (i.e. activation vs. anergy). SLAM (signaling leukocytic activation molecule, CD150) is a costimulatory molecule highly expressed on both activated T cells and macrophages. Through augmentation of pro-inflammatory cytokines, SLAM co-stimulation potentiates the inflammatory state. Preliminary data suggest that disruption of SLAM signaling on activated T cells protects against colitis and SLAM deficient (SLAM-/-) macrophages have a profound defect in pro-inflammatory function. Based on this work we generate the novel hypothesis that SLAM co-stimulation is critical to the function of both macrophages and activated T cells that mediate chronic inflammation in colitis. In specific aim #1, we will use SLAM -/- mice crossed to the Rag-/- background (no T or B cells) to test the hypothesis that SLAM expression on antigen presenting cells is critical to the induction and maintenance of experimental colitis. In specific aim #2, the potential of SLAM-/- T cells to cause colitis will be studied. The ability of anti-SLAM antibodies to prevent colitis will be tested in vivo in two models of experimental colitis in specific aim #3. The studies will test activation states of different T cell subsets and macrophages in vitro by cytokine assay (ELISA). Assessment of colitis in vivo will be made by clinical parameters (i.e. weight loss, diarrhea) as well as histologic scoring of
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the colon at autopsy. This work will establish the role for SLAM in the initiation and maintenance of colitis and has the potential of identifying a new therapeutic target for the immune modulation of human inflammatory bowel disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SAFE FOCUSED DELIVERY OF GENE THERAPEUTICS TO COLON Principal Investigator & Institution: Sano, Takeshi; Beth Israel Deaconess Medical Center St 1005 Boston, Ma 02215 Timing: Fiscal Year 2003; Project Start 19-SEP-2003; Project End 31-AUG-2005 Summary: (provided by applicant): The long-term goal of this project is to develop a safe, efficient gene transfer technology that can be used for gene therapy of diseases in the colorectal system. The R21 phase of this project will focus on the development of a gene transfer technology that allows safe, efficient, and focused delivery of transgenes to the colorectal system. During this technology development phase, we will use inflammatory bowel disease (IBD), which consists of Crohn's disease and ulcerative colitis, as a first target to assess the efficacy of the gene transfer technology. We have recently developed a novel gene transfer technology, in which viral particles (adenoviral vectors and adeno-associated viral vectors) are delivered to target sites in a microbeadassociated form. These virus-microbead conjugates can infect target cells at efficiencies much greater than the same viral vectors used free in solution. A key feature of this gene transfer technology is that the infection sites by viral vectors are equal to the contact sites between target cells and virus-microbead conjugates. This allows focused delivery of transgenes to target sites with high transduction efficiencies by placing virusmicrobead conjugates at the site of interest. Since each viral particle on the microbeads either mediates infection of a cell or stays on the microbeads, no free viral particles should be present. Thus, uncontrolled transduction of other non-target tissues or organs by viral vectors can be eliminated, and immune responses to viral vectors can be minimized. These and other characteristics suggest that this technology could allow for the efficient, safe delivery of transgenes to the colorectal system. In particular, it could be very useful for the development of effective gene therapy protocols for IBD, since a potentially efficacious gene therapy strategy for IBD is to repress intense inflammation in the colon by local, high-level expression of anti-inflammatory cytokines at inflamed lesions. We will investigate the potential of this gene transfer technology for the safe, focused delivery of the gene for a potent anti-inflammatory cytokine, interleukin-10 (IL10), to inflamed lesions in the colon for the amelioration of established colitis. We hypothesize that this technology will allow for safe, efficient, and focused delivery of the IL-10 gene to inflamed lesions in the colon, resulting in the local expression and secretion of IL-10 in the inflamed lesions for the amelioration of established colitis with minimal detrimental effects on other tissues and organs. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SCREENING MARKERS FOR COLORECTAL CANCER Principal Investigator & Institution: Potter, John D.; Member & Program Head; Fred Hutchinson Cancer Research Center Box 19024, 1100 Fairview Ave N Seattle, Wa 98109 Timing: Fiscal Year 2002 Summary: Current colorectal cancer screening modalities are not universally acceptable, and, for reasons of cost and low specificity, unlikely to be widely applied. To address the exigent need for further screening strategies, we propose to evaluate a biologically based screening approach that will incorporate a variety of cellular and molecular
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pathways to neoplasia. The focus of this project-and the entire P01- is on oxidative damage and apoptosis. Additionally, several pathways that are unique to colorectal carcinogenesis will be evaluated as possible targets for early detection efforts. Both human and animal studies will be conducted. To identify markers that discriminate patients with adenomas, hyperplastic polyps, ulcerative colitis, and adenocarcinomas from healthy controls, we propose to collect a variety of biologic materials (blood, colonic biopsies, primary lesions, rectal brushings, stool) and risk factor information on Group Health Cooperative of Puget Sound patients (n=800) undergoing clinically indicated colonoscopy. Specimens from individuals in each of the diagnostic categories will be evaluated for: specific markers of oxidative damage; aberrations in apoptosis proteins (bcl-2, bcl-x, bax); glutathione and GST expression; hypermethylation of the estrogen receptor gene; abnormalities in cell proliferation (Ki-67); and aspects of cell-cell interaction (connexins and E-cadherin). Analyses will explore the sensitivity and specificity of each of this group of biologically relevant markers that represent several pathways to carcinogens, with the goal of establishing an ensemble of markers that can facilitate the identification of individuals carrying neoplastic and pre-neoplastic lesions. Ultimately, we plan to evaluate the efficacy of screening using these markers in a prospective screening trial, which we will plan for the P01 renewal. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: STUDIES IN CHILDREN WITH DIGESTIVE DISORDERS Principal Investigator & Institution: Heyman, Melvin B.; Professor of Pediatrics; Pediatrics; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 94122 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2007 Summary: Clinical research in pediatric disorders is essential to ensure advances in the management, prognosis and quality of life of infants, children and adolescents with these problems. The goals are (1) to foster a program in hypothesis-driven, expert clinical research in pediatric gastroenterology and nutrition, (2) to mentor young clinicians in pediatric gastroenterology and nutrition research, and (3) to promote ongoing interactions and collaborations with clinical investigators. To achieve these goals, current projects and future investigations of gastrointestinal and nutrition problems in pediatric patients will be conducted by trainees at various levels under the guidance and supervision of Dr. Heyman and his collaborators. Studies involving pediatric patients with inflammatory bowel disease (Crohn's disease and ulcerative colitis), HIV infection, familial adenomatous polyposis syndrome (with FAP gene mutations), ichthyosis erythrodermas with poor nutrition, and gastroesophageal reflux disease are currently ongoing or planned utilizing the facilities and staffs of the Pediatric Gastroenterology/Nutrition Clinics and the Pediatric Clinical Research Center at the University of California, San Francisco (UCSF). A cohort study is in the planning stage to determine whether nutrition advice promotes improved long-term outcomes in eating behaviors and health status (e.g., micronutrient adequacy; and growth parameters). The overriding objective of this proposal is to motivate and inspire young clinicians embarking on careers focused on clinically oriented research. Pediatric gastroenterology trainees will be instructed in the proper conduct of perspective randomized controlled clinical trials in infants, children, and adolescents. Trainees will also participate in didactic courses covering clinical trial design and procedure, protocol writing, data management, and ethical considerations. This award will enhance the applicant's ability to devote more time to research- related activities, and to provide guidance and instruction for trainees advancing towards productive scientific careers.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TH2 CELLS DIRECT THE GENESIS OF COLONIC PATCHES AND IBD Principal Investigator & Institution: Mcghee, Jerry R.; Professor; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2002 Summary: Inflammatory bowel disease (IBD) are chronic, relapsing, tissue destructive disease. Recent advances in experimental models for IBD in mice have contributed to a better understand of the mechanisms of intestinal inflammation involving dysfunction of T cells and dysregulation of cytokine production. Notably, a central role for interferon-gamma (IFN-gamma) produced by T helper type 1 (Th1)-T cells and for inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) have been emphasized in these murine models. However, the immunological events which occur in human IBD are not always accommodated by these models. In ulcerative colitis, it is generally recognized that a role for TH1-type responses are not as evident as in Crohn's disease. In our recent investigation, we have obtained evidence that Th2-type responses are also much involved in a murine hapten-induced IBD model which is accompanied by expansion of colonic patches, which are the gut associated lymphoreticular tissues in the colon. Since inflammatory lesions were induced in a condition deficient in Th1 type cells producing IFN-gamma, and were distinct from the lesions seen in mice deficient in Th2 cytokines, we hypothesize that cytokine-phenotypes may explain the different pathological findings in ulcerative colitis and Crohn's disease. The major goal of this grant is to show that Th2-type responses can induce distinct types of lesions from those caused by Th1-type responses. Further, we will define colonic patches as inductive sites of chronic intestinal inflammation that occur through Th2 immune responses. To address this goal, the first aim will be to study the specific roles of Th2-type cells in murine intestinal inflammation through an adoptive transfer system of CD4+ CD45RB/Hi T cells. This study will be done with interactions with project 1 (Dr. Elson) in which adoptive transfer of Th1- or Th2-skewed T cells derived from C3H/HeJBir mice will also be investigated. In the second aim, we will define specific functions for colonic patches by comparing them with Peyer's patches for immune responses to defined antigens and delivery vectors/adjuvants which induced mucosal immunity via Th1- or Th2-type T cells. This study will interact with Project 2 (Dr. Weaver) for studies of antigen (OVA)-specific responses. The third aim will determine if colonic patches are necessary to induce intestinal inflammation by using mice deficient in organized colonic patches. Finally our last aim will define novel molecules which are specifically expressed in colonic patches using 2 dimensional gel analysis and differential display of mRNA between Peyer's and colonic patches. These latter techniques will also be applied to Project 4 (Dr. Leiter) to compare congenic stocks of mice which are done to develop inflammation. These proposed studies will provide new information for understanding the pathogenesis of non-Th1 type intestinal inflammation and the role of organized colonic patch lymphoid tissues in IBD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: TRANSITION FROM EARLY TO LATE COLITIS--IL 12 REGULATION Principal Investigator & Institution: Levine, Alan David.; Professor; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2002
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Summary: Inflammatory bowel disease (IBD) is a chronic and relapsing disease of unknown etiology. The regulatory and environmental events that modulate inflammation or trigger a new round of symptoms are completely uncharacterized. The majority of information about factors which perpetuate inflammation in IBD is obtained from chronically inflamed human tissue, while the data from animal models of IBD derives overwhelmingly from early immune responses. In this project we propose to bridge that gap by contrasting the regulation and expression of inflammatory mediators by mucosal immune cells during early and late enterocolitis in murine models. In a healthy individual exposure to a pathogen results in a highly regulated immune response that first clears the organism and then returns to a controlled state. It is our premise that the chronic inflammation observed in ulcerative colitis and Crohn's disease results from an inability of the mucosal immune response to return to this controlled state. Thus, we present the following central hypothesis: Inflammation in experimental murine models of IBD is initiated by mucosal T cell responses to enterobacterial antigens, and it is perpetuated during the late chronic phase by a proinflammatory response maintained by mucosal immune and non-immune cells. A corollary of this hypothesis is that the immune response generated in early IBD and toward an infectious pathogen are similar and that the characterize and immune mediator profile of early immunity is distinct from the immune response that causes chronic inflammation. In support of this premise we have demonstrated in a T celldependent animal model of enterocolitis (i.e., the IL-10 deficient (IL-10-/-) strain of mice) that the mucosal cytokine profile and anti-cytokine therapeutic efficacy are remarkably different during the early and late phases of intestinal inflammation. We will test this hypothesis with four specific aims: (1) Define the molecular events that regulate mucosal synthesis of IL-12 and IFN-gamma in the early phase of experimental colitis in IL-10-/- mice; 2) Characterize the inflammatory mediators that down-regulate IL-12 synthesis and orchestrate the transition to the late phase of gut inflammation; (3) Investigate the ability of commensal bacterial flora, in general, and Helicobacter species, in particular, to initiate and sustain inflammation in early and late disease; and (4) Identify components of the immune response that support the chronicity of inflammation in the absence of IL- 12 and IFN-gamma production. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: VASCULAR INFLAMMATION
ENDOTHELIAL
CADHERIN
FUNCTION
IN
Principal Investigator & Institution: Shaw, Sunil K.; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 15-MAR-2000; Project End 31-DEC-2003 Summary: Candidate: The applicant has researched mucosal lymphocyte homing and recirculation for the past 8 years. Accomplishments include contributions at both molecular and cell biological levels to interaction of intra- epithelial lymphocytes with epithelial cells. Environment: Brigham and Women's hospital, affiliated with Harvard University, is recognized as a leader in medical research, and will provide a supportive and stimulating environment. The mentor's lab at the Vascular Research Division has access to specialized equipment and tissues necessary for this research. Research: Gastritis, ulceration, celiac sprue, Crohn disease and ulcerative colitis, glomerulonephritis, interstitial nephritis and pyelonephritis are all characterized by the activation of inflammatory cells leading to tissue injury. Leukocyte transmigration and accompanying increased vascular permeability are critical steps during the inflammatory response. Thus, integrity of the organ vasculature is necessary for normal
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system function, and the endothelial barrier must be breached to lead to tissue injury in these diseases. Although much is known about leukocyte-endothelial adhesion and inflammation, less information is available concerning the role played by endothelial cells in regulating permeability and leukocytes and macromolecules. Vascular endothelial cadherin is located at endothelial adherens and junctions and may regulate monolayer permeability to leukocytes and inflammatory factors. The objective of this proposal is to study the role of VE-cadherin in barrier function and cell growth in vascular endothelial cells by disruption via a dominant negative mechanism. A high efficiency if transfection will be achieved using an adenoviral expression system. This approach will allow specific disruption of one component of the adherens junction, and allow subsequent analysis of endothelial specific functions. These techniques will be used to probe the function of adherens junctions in endothelium from various vascular beds and their contribution to inflammation. The proposed studies are anticipated to allow a better understanding of the role of endothelial adherens junctions in normal and disease conditions, and may lead to novel therapeutic approaches and targets for intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “ulcerative colitis” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for ulcerative colitis in the PubMed Central database: •
A national survey on the patterns of treatment of inflammatory bowel disease in Canada. by Hilsden RJ, Verhoef MJ, Best A, Pocobelli G.; 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=166136
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Adoptive transfer of immune enhancement of experimental ulcerative colitis. by Onderdonk AB, Steeves RM, Cisneros RL, Bronson RT.; 1984 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=261421
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Antibodies detectable by counterimmunoelectrophoresis against Bacteroides antigens in serum of patients with inflammatory bowel disease. by Helphingstine CJ, Hentges DJ, Campbell BJ, Butt J, Barrett JT.; 1979 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=273033
3 4
Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.
With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age. 5 The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print.
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Assessing health-related quality of life in patients with inflammatory bowel disease, in Crete, Greece. by Pallis AG, Vlachonikolis IG, Mouzas IA.; 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=65681
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Bacteroides ovatus as the Predominant Commensal Intestinal Microbe Causing a Systemic Antibody Response in Inflammatory Bowel Disease. by Saitoh S, Noda S, Aiba Y, Takagi A, Sakamoto M, Benno Y, Koga Y.; 2002 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=119885
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Citrobacter rodentium Infection in Mice Elicits a Mucosal Th1 Cytokine Response and Lesions Similar to Those in Murine Inflammatory Bowel Disease. by Higgins LM, Frankel G, Douce G, Dougan G, MacDonald TT.; 1999 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=96617
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Clinical Aspects and Pathophysiology of Inflammatory Bowel Disease. by Hendrickson BA, Gokhale R, Cho JH.; 2002 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=118061
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Colonic Bacteria Express an Ulcerative Colitis pANCA-Related Protein Epitope. by Cohavy O, Bruckner D, Gordon LK, Misra R, Wei B, Eggena ME, Targan SR, Braun J.; 2000 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=97313
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Comparison of Bacteroides vulgatus strains in the enhancement of experimental ulcerative colitis. by Onderdonk AB, Bronson R, Cisneros R.; 1987 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=260420
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Correlation of Cecal Microflora of HLA-B27 Transgenic Rats with Inflammatory Bowel Disease. by Onderdonk AB, Richardson JA, Hammer RE, Taurog JD.; 1998 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=108765
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Differential Alteration in Intestinal Epithelial Cell Expression of Toll-Like Receptor 3 (TLR3) and TLR4 in Inflammatory Bowel Disease. by Cario E, Podolsky DK.; 2000 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=97811
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Effects of chronic inflammatory bowel diseases on left ventricular structure and function: a study protocol. by Cioffi U, Ciulla MM, De Simone M, Paliotti R, Pierini A, Magrini F, Botti F, Contessini-Avesani E.; 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128828
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Evidence for a NOD2-independent susceptibility locus for inflammatory bowel disease on chromosome 16p. by Hampe J, Frenzel H, Mirza MM, Croucher PJ, Cuthbert A, Mascheretti S, Huse K, Platzer M, Bridger S, Meyer B, Nurnberg P, Stokkers P, Krawczak M, Mathew CG, Curran M, Schreiber S.; 2002 Jan 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=117559
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Identification of novel susceptibility loci for inflammatory bowel disease on chromosomes 1p, 3q, and 4q: Evidence for epistasis between 1p and IBD1. by Cho JH, Nicolae DL, Gold LH, Fields CT, LaBuda MC, Rohal PM, Pickles MR, Qin L, Fu Y, Mann JS, Kirschner BS, Jabs EW, Weber J, Hanauer SB, Bayless TM, Brant SR.; 1998 Jun 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=22666
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Immune Responses in Ileostomy Fluid and Serum after Oral Cholera Vaccination of Patients Colectomized because of Ulcerative Colitis. by Kilhamn J, Brevinge H, Svennerholm AM, Jertborn M.; 1998 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=108473
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Investigation of association of mycobacteria with inflammatory bowel disease by nucleic acid hybridization. by Yoshimura HH, Graham DY, Estes MK, Merkal RS.; 1987 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=265821
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Molecular Cloning of a Bacteroides caccae TonB-Linked Outer Membrane Protein Identified by an Inflammatory Bowel Disease Marker Antibody. by Wei B, Dalwadi H, Gordon LK, Landers C, Bruckner D, Targan SR, Braun J.; 2001 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=98733
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Neglect of growth and development in the clinical monitoring of children and teenagers with inflammatory bowel disease: review of case records. by Ghosh S, Drummond HE, Ferguson A.; 1998 Jul 11; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28604
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Open access follow up for inflammatory bowel disease: pragmatic randomised trial and cost effectiveness study. by Williams JG, Cheung WY, Russell IT, Cohen DR, Longo M, Lervy B.; 2000 Feb 26; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27297
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Potential role of microorganisms isolated from periodontal lesions in the pathogenesis of inflammatory bowel disease. by Van Dyke TE, Dowell VR Jr, Offenbacher S, Snyder W, Hersh T.; 1986 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=260846
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Prevalence of inflammatory bowel disease in British 26 year olds: national longitudinal birth cohort. by Montgomery SM, Morris DL, Thompson NP, Subhani J, Pounder RE, Wakefield AJ.; 1998 Apr 4; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28509
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Quality-of-Life Research on the Internet Feasibility and Potential Biases in Patients with Ulcerative Colitis. by Soetikno RM, Mrad R, Pao V, Lenert LA.; 1997 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=61260
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Receptor binding sites for substance P, but not substance K or neuromedin K, are expressed in high concentrations by arterioles, venules, and lymph nodules in surgical specimens obtained from patients with ulcerative colitis and Crohn disease. by Mantyh CR, Gates TS, Zimmerman RP, Welton ML, Passaro EP Jr, Vigna SR, Maggio JE, Kruger L, Mantyh PW.; 1988 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=280179
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Results of Multiple Diagnostic Tests for Mycobacterium avium subsp. paratuberculosis in Patients with Inflammatory Bowel Disease and in Controls. by Collins MT, Lisby G, Moser C, Chicks D, Christensen S, Reichelderfer M, Hoiby N, Harms BA, Thomsen OO, Skibsted U, Binder V.; 2000 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=87608
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The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with ulcerative colitis, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “ulcerative colitis” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for ulcerative colitis (hyperlinks lead to article summaries): •
A case of Evans' syndrome in a patient with ulcerative colitis. Author(s): Ucci G, Ferrando P, Valentini D, Zavallone L. Source: Dig Liver Dis. 2003 June; 35(6): 439-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12868682&dopt=Abstract
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A cluster-randomised controlled trial of a patient-centred guidebook for patients with ulcerative colitis: effect on knowledge, anxiety and quality of life. Author(s): Kennedy A, Robinson A, Hann M, Thompson D, Wilkin D; North-West Region Gastrointestinal Research Group. Source: Health & Social Care in the Community. 2003 January; 11(1): 64-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14629234&dopt=Abstract
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A different therapeutic approach in patients with severe ulcerative colitis: hyperbaric oxygen treatment. Author(s): Gurbuz AK, Elbuken E, Yazgan Y, Yildiz S. Source: Southern Medical Journal. 2003 June; 96(6): 632-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12938799&dopt=Abstract
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A group-based patient education programme for high-anxiety patients with Crohn disease or ulcerative colitis. Author(s): Larsson K, Sundberg Hjelm M, Karlbom U, Nordin K, Anderberg UM, Loof L. Source: Scandinavian Journal of Gastroenterology. 2003 July; 38(7): 763-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12889564&dopt=Abstract
6 PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.
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A pilot trial of Saccharomyces boulardii in ulcerative colitis. Author(s): Guslandi M, Giollo P, Testoni PA. Source: European Journal of Gastroenterology & Hepatology. 2003 June; 15(6): 697-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12840682&dopt=Abstract
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A specific genetic alteration on chromosome 6 in ulcerative colitis-associated colorectal cancers. Author(s): Ezaki T, Watanabe M, Inoue N, Kanai T, Ogata H, Iwao Y, Ishii H, Hibi T. Source: Cancer Research. 2003 July 1; 63(13): 3747-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12839969&dopt=Abstract
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A study of the relationships between self-evaluation of physical condition and perception of difficulties of life in ulcerative colitis patients. Author(s): Tanaka M, Miyawaki I, Kazuma K. Source: Gastroenterology Nursing : the Official Journal of the Society of Gastroenterology Nurses and Associates. 2003 May-June; 26(3): 115-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12811322&dopt=Abstract
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Abnormal p53 immunohistochemistry is associated with an increased colorectal cancer-related mortality in patients with ulcerative colitis. Author(s): Lashner BA, Bauer WM, Rybicki LA, Goldblum JR. Source: The American Journal of Gastroenterology. 2003 June; 98(6): 1423-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12818291&dopt=Abstract
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Acute CMV-colitis in a patient with a history of ulcerative colitis. Author(s): Streetz KL, Buhr T, Wedemeyer H, Bleck J, Schedel I, Manns MP, Goke MN. Source: Scandinavian Journal of Gastroenterology. 2003 January; 38(1): 119-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12608474&dopt=Abstract
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Acute pancreatitis after long-term therapy with mesalazine, and hyperamylasaemia associated with azathioprine in a patient with ulcerative colitis. Author(s): Toubanakis C, Batziou E, Sipsas N, Galanopoulos G, Tzivras M, Archimandritis A. Source: European Journal of Gastroenterology & Hepatology. 2003 August; 15(8): 933-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12867808&dopt=Abstract
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Addition of leukocytapheresis to steroid therapy: is it beneficial in recurrence of moderate-to-severe ulcerative colitis? Author(s): Jo Y, Matsumoto T, Mibu R, Iida M. Source: Diseases of the Colon and Rectum. 2003 October; 46(10 Suppl): S3-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14530652&dopt=Abstract
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Adenocarcinoma in the anal transitional zone after ileal pouch for ulcerative colitis: report of a case. Author(s): Bell SW, Parry B, Neill M. Source: Diseases of the Colon and Rectum. 2003 August; 46(8): 1134-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12907913&dopt=Abstract
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Altered expression of epimorphin in ulcerative colitis. Author(s): Shirasaka T, Iizuka M, Yukawa M, Hirai Y, Horie Y, Itou H, Kon-No S, Fukushima T, Watanabe S. Source: Journal of Gastroenterology and Hepatology. 2003 May; 18(5): 570-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12702050&dopt=Abstract
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An open-label trial of the PPAR-gamma ligand rosiglitazone for active ulcerative colitis. Author(s): Lewis JD, Lichtenstein GR, Stein RB, Deren JJ, Judge TA, Fogt F, Furth EE, Demissie EJ, Hurd LB, Su CG, Keilbaugh SA, Lazar MA, Wu GD. Source: The American Journal of Gastroenterology. 2001 December; 96(12): 3323-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11774944&dopt=Abstract
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Apoptosis regulation differs between ulcerative colitis-associated and sporadic colonic tumors. Association with survivin and bcl-2. Author(s): Mikami T, Yoshida T, Akino F, Motoori T, Yajima M, Okayasu I. Source: American Journal of Clinical Pathology. 2003 May; 119(5): 723-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760292&dopt=Abstract
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Appendicectomy and ulcerative colitis. Author(s): ter Borg PC, van Buuren HR. Source: Gut. 2003 May; 52(5): 768; Author Reply 768-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12692069&dopt=Abstract
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Assessment of mucosal inflammation and circulation in response to probiotics in patients operated with ileal pouch anal anastomosis for ulcerative colitis. Author(s): Laake KO, Line PD, Aabakken L, Lotveit T, Bakka A, Eide J, Roseth A, Grzyb K, Bjorneklett A, Vatn MH. Source: Scandinavian Journal of Gastroenterology. 2003 April; 38(4): 409-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12739713&dopt=Abstract
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Association of ulcerative colitis with pulmonary sarcoidosis, subcutaneous lipomatosis and appendiceal adenocarcinoma. Author(s): Vaiphei K, Gupta N, Sinha SK, Nagi B, Singh K. Source: Indian J Gastroenterol. 2003 September-October; 22(5): 193-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14658541&dopt=Abstract
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Atrophy and neoplastic transformation of the ileal pouch mucosa in patients with ulcerative colitis and primary sclerosing cholangitis: a case control study. Author(s): Stahlberg D, Veress B, Tribukait B, Broome U. Source: Diseases of the Colon and Rectum. 2003 June; 46(6): 770-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794579&dopt=Abstract
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Azathioprine versus sulfasalazine in maintenance of remission in severe ulcerative colitis. Author(s): Sood A, Midha V, Sood N, Avasthi G. Source: Indian J Gastroenterol. 2003 May-June; 22(3): 79-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12839376&dopt=Abstract
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Backwash ileitis is strongly associated with colorectal carcinoma in ulcerative colitis. Author(s): Heuschen UA, Hinz U, Allemeyer EH, Stern J, Lucas M, Autschbach F, Herfarth C, Heuschen G. Source: Gastroenterology. 2001 March; 120(4): 841-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11231938&dopt=Abstract
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Bacteria as the cause of ulcerative colitis. Author(s): Campieri M, Gionchetti P. Source: Gut. 2001 January; 48(1): 132-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11115835&dopt=Abstract
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Balsalazide is superior to mesalamine in the time to improvement of signs and symptoms of acute mild-to-moderate ulcerative colitis. Author(s): Pruitt R, Hanson J, Safdi M, Wruble L, Hardi R, Johanson J, Koval G, Riff D, Winston B, Cross A, Doty P, Johnson LK. Source: The American Journal of Gastroenterology. 2002 December; 97(12): 3078-86. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492193&dopt=Abstract
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Balsalazide: a review of its therapeutic use in mild-to-moderate ulcerative colitis. Author(s): Muijsers RB, Goa KL. Source: Drugs. 2002; 62(11): 1689-705. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12109930&dopt=Abstract
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Basedow's disease and chronic ulcerative colitis: a case report and review of the Japanese literature. Author(s): Nishimura M, Yamamoto T, Iijima H, Moriwaki Y, Takahashi S, Hada T. Source: Intern Med. 2001 January; 40(1): 44-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11201369&dopt=Abstract
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Basiliximab (anti-CD25) in combination with steroids may be an effective new treatment for steroid-resistant ulcerative colitis. Author(s): Creed TJ, Norman MR, Probert CS, Harvey RF, Shaw IS, Smithson J, Anderson J, Moorghen M, Gupta J, Shepherd NA, Dayan CM, Hearing SD. Source: Alimentary Pharmacology & Therapeutics. 2003 July 1; 18(1): 65-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12848627&dopt=Abstract
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Bax is downregulated in inflamed colonic mucosa of ulcerative colitis. Author(s): Iimura M, Nakamura T, Shinozaki S, Iizuka B, Inoue Y, Suzuki S, Hayashi N. Source: Gut. 2000 August; 47(2): 228-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10896914&dopt=Abstract
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Biological therapies for ulcerative colitis. Author(s): Sands BE. Source: Acta Gastroenterol Belg. 2001 April-June; 64(2): 205-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11475137&dopt=Abstract
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Biopsy pathology predicts patients with ulcerative colitis subsequently requiring surgery. Author(s): Tanaka M, Saito H, Kusumi T, Shimoyama T, Fukuda S, Morita T, Sugita A, Hara M, Kudo H. Source: Scandinavian Journal of Gastroenterology. 2002 February; 37(2): 200-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11843058&dopt=Abstract
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Birth outcomes of women with ulcerative colitis: a nationwide Danish cohort study. Author(s): Norgard B, Fonager K, Sorensen HT, Olsen J. Source: The American Journal of Gastroenterology. 2000 November; 95(11): 3165-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11095336&dopt=Abstract
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Bloody diarrhea, fever, and pancytopenia in a patient with active ulcerative colitis. Author(s): Jani AL, Hamilos D. Source: Annals of Allergy, Asthma & Immunology : Official Publication of the American College of Allergy, Asthma, & Immunology. 2003 April; 90(4): 383-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12722958&dopt=Abstract
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Blurred vision during exacerbation of ulcerative colitis. Author(s): Alcalde M, Lopez-Bernal I, Galvan A, Pecellin I, Narvaez I, Herrera JM. Source: Postgraduate Medical Journal. 1998 September; 74(875): 551-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10211333&dopt=Abstract
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Bone mineral density and body composition in patients with ulcerative colitis. Author(s): Ulivieri FM, Lisciandrano D, Ranzi T, Taioli E, Cermesoni L, Piodi LP, Nava MC, Vezzoli M, Bianchi PA. Source: The American Journal of Gastroenterology. 2000 June; 95(6): 1491-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10894585&dopt=Abstract
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Bone mineral density and body composition in ulcerative colitis: a six-year follow-up. Author(s): Ulivieri FM, Piodi LP, Taioli E, Lisciandrano D, Ranzi T, Vezzoli M, Cermesoni L, Bianchi P. Source: Osteoporosis International : a Journal Established As Result of Cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the Usa. 2001; 12(5): 343-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11444080&dopt=Abstract
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Brain-gut interactions in ulcerative colitis. Author(s): Peck OC, Wood JD. Source: Gastroenterology. 2000 April; 118(4): 807-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10777351&dopt=Abstract
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Breath alkanes determination in ulcerative colitis and Crohn's disease. Author(s): Pelli MA, Trovarelli G, Capodicasa E, De Medio GE, Bassotti G. Source: Diseases of the Colon and Rectum. 1999 January; 42(1): 71-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10211523&dopt=Abstract
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Bronchiolitis obliterans in a patient with ulcerative colitis receiving mesalamine. Author(s): Haralambou G, Teirstein AS, Gil J, Present DH. Source: The Mount Sinai Journal of Medicine, New York. 2001 November; 68(6): 384-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11687866&dopt=Abstract
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Budd-Chiari syndrome in a patient with ulcerative colitis: association with anticardiolipin antibodies. Author(s): Praderio L, Dagna L, Longhi P, Rubin G, Sabbadini MG. Source: Journal of Clinical Gastroenterology. 2000 March; 30(2): 203-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10730929&dopt=Abstract
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Bullous pemphigoid following use of sulphasalazine for ulcerative colitis: druginduced eruption or true association? Author(s): Vaccaro M, D'Amico D, Borgia F, Guarneri F, Cannavo S. Source: Dermatology (Basel, Switzerland). 2001; 203(2): 194-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11586028&dopt=Abstract
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Butyrate inhibits NF-kappaB activation in lamina propria macrophages of patients with ulcerative colitis. Author(s): Luhrs H, Gerke T, Muller JG, Melcher R, Schauber J, Boxberge F, Scheppach W, Menzel T. Source: Scandinavian Journal of Gastroenterology. 2002 April; 37(4): 458-66. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11989838&dopt=Abstract
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Ca2+ response in neutrophils after exposure to bacterial N-formyl-methionyl-leucylphenylalanine: delayed response in ulcerative colitis. Author(s): Vainer B, Lamberth K, Brimnes J, Nielsen OH, Claesson MH. Source: European Journal of Gastroenterology & Hepatology. 2003 March; 15(3): 267-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610322&dopt=Abstract
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Case 11-2003: ulcerative colitis and primary sclerosing cholangitis in a 14-year-old boy. Author(s): Mukherjee S. Source: The New England Journal of Medicine. 2003 October 9; 349(15): 1482. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14535266&dopt=Abstract
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Case 11-2003: ulcerative colitis and primary sclerosing cholangitis in a 14-year-old boy. Author(s): Drewe E, Zaitoun AM, Walker DA. Source: The New England Journal of Medicine. 2003 October 9; 349(15): 1482. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14534348&dopt=Abstract
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Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 11-2003. A 14-year-old boy with ulcerative colitis, primary sclerosing cholangitis, and partial duodenal obstruction. Author(s): Ross AM 4th, Anupindi SA, Balis UJ. Source: The New England Journal of Medicine. 2003 April 10; 348(15): 1464-76. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12686704&dopt=Abstract
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Caution in the interpretation of safety and efficacy differences in clinical trials comparing aminosalicylates for ulcerative colitis. Author(s): Hanauer SB. Source: The American Journal of Gastroenterology. 2003 January; 98(1): 215-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12526968&dopt=Abstract
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Changes in chemical coding of myenteric neurones in ulcerative colitis. Author(s): Neunlist M, Aubert P, Toquet C, Oreshkova T, Barouk J, Lehur PA, Schemann M, Galmiche JP. Source: Gut. 2003 January; 52(1): 84-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12477766&dopt=Abstract
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Chromoscopy might improve diagnostic accuracy in cancer surveillance for ulcerative colitis. Author(s): Matsumoto T, Nakamura S, Jo Y, Yao T, Iida M. Source: The American Journal of Gastroenterology. 2003 August; 98(8): 1827-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12907339&dopt=Abstract
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Chronic autoreactive urticaria in a patient with ulcerative colitis. Author(s): Tedeschi A, Lorini M, Airaghi L. Source: Journal of Clinical Gastroenterology. 2003 May-June; 36(5): 454-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12702996&dopt=Abstract
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Clinical and genetic heterogeneity in Mexican patients with ulcerative colitis. Author(s): Yamamoto-Furusho JK, Uscanga LF, Vargas-Alarcon G, Ruiz-Morales JA, Higuera L, Cutino T, Rodriguez-Perez JM, Villarreal-Garza C, Granados J. Source: Human Immunology. 2003 January; 64(1): 119-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12507822&dopt=Abstract
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Clinical features and pattern of indeterminate colitis: Crohn's disease with ulcerative colitis-like clinical presentation. Author(s): Matsui T, Yao T, Sakurai T, Yao K, Hirai F, Matake H, Tsuda S, Wada Y, Iwashita A, Kamachi S. Source: Journal of Gastroenterology. 2003; 38(7): 647-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12898357&dopt=Abstract
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Collagenous colitis evolving into ulcerative colitis: a case report and review of the literature. Author(s): Aqel B, Bishop M, Krishna M, Cangemi J. Source: Digestive Diseases and Sciences. 2003 December; 48(12): 2323-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14714620&dopt=Abstract
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Colorectal cancer and high grade dysplasia complicating ulcerative colitis in Italy. A retrospective co-operative IG-IBD study. Author(s): Riegler G, Bossa F, Caserta L, Pera A, Tonelli F, Sturniolo GC, Oliva L, Contessini Avesani E, Poggioli G; IG-IBD Group. Source: Dig Liver Dis. 2003 September; 35(9): 628-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14563184&dopt=Abstract
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Commentary on the 1958 National Institutes of Health conference on “New frontiers in ulcerative colitis”. Author(s): Kirsner JB. Source: Inflammatory Bowel Diseases. 2003 January; 9(1): 61-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12656138&dopt=Abstract
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Complete resolution of refractory immune thrombocytopenic purpura after colectomy for ulcerative colitis. Author(s): Kathula SK, Polenakovik H, el-Tarabily M, Polenakovik S. Source: Int J Clin Pract. 2001 November; 55(9): 647-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11770367&dopt=Abstract
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Correlation between circulating soluble ICAM-1 and prednisolone-induced amelioration of ulcerative colitis. Author(s): Vainer B, Nielsen OH. Source: Scandinavian Journal of Gastroenterology. 2003 March; 38(3): 283-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12737443&dopt=Abstract
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Cost-effectiveness of colorectal cancer surveillance in ulcerative colitis. Author(s): Inadomi JM. Source: Scandinavian Journal of Gastroenterology. Supplement. 2003; (237): 17-21. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12797675&dopt=Abstract
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Cumulative experience with short- and long-term toxicity to 6-mercaptopurine in the treatment of Crohn's disease and ulcerative colitis. Author(s): Warman JI, Korelitz BI, Fleisher MR, Janardhanam R. Source: Journal of Clinical Gastroenterology. 2003 September; 37(3): 220-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12960720&dopt=Abstract
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Cyclin D1 and p21 in ulcerative colitis-related inflammation and epithelial neoplasia: a study of aberrant expression and underlying mechanisms. Author(s): Wong NA, Mayer NJ, Anderson CE, McKenzie HC, Morris RG, Diebold J, Mayr D, Brock IW, Royds JA, Gilmour HM, Harrison DJ. Source: Human Pathology. 2003 June; 34(6): 580-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12827612&dopt=Abstract
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Cyclosporin for refractory ulcerative colitis. Author(s): Loftus CG, Loftus EV Jr, Sandborn WJ. Source: Gut. 2003 February; 52(2): 172-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12524395&dopt=Abstract
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Cytology and image cytometry after colonic lavage: a complementary diagnostic tool in patients with ulcerative colitis. Author(s): Keller R, Brandt B, Terpe HJ, Winde G, Foerster EC, Domschke W. Source: Dig Liver Dis. 2003 January; 35(1): 24-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12725604&dopt=Abstract
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Decreased sulphur aminoacid intake in ulcerative colitis. Author(s): Roediger WE. Source: Lancet. 1998 May 23; 351(9115): 1555. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10326542&dopt=Abstract
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Defining relapse of ulcerative colitis using a symptom-based activity index. Author(s): Jowett SL, Seal CJ, Phillips E, Gregory W, Barton JR, Welfare MR. Source: Scandinavian Journal of Gastroenterology. 2003 February; 38(2): 164-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678333&dopt=Abstract
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Delayed pressure urticaria in a patient with ulcerative colitis. Author(s): Hassiko H, Le Guilchard F, Nembo J, Lespessailles E, Martin L, Benhamou CL. Source: Joint, Bone, Spine : Revue Du Rhumatisme. 2002 October; 69(5): 519-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12477241&dopt=Abstract
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Depletion and decreased function of antigen-presenting dendritic cells caused by lymphocytapheresis in ulcerative colitis. Author(s): Ikeda Y, Akbar SM, Matsui H, Murakami H, Onji M. Source: Diseases of the Colon and Rectum. 2003 April; 46(4): 521-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12682548&dopt=Abstract
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Depletion of non specific esterase activity in the colonic mucosa of patients with ulcerative colitis. Author(s): Kolios G, Valatas V, Psilopoulos D, Petraki K, Kouroumalis E. Source: European Journal of Clinical Investigation. 2002 April; 32(4): 265-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11952812&dopt=Abstract
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Development of ulcerative colitis despite long-term immunosuppression with cyclosporin and azathioprine in an Australian Aborigine. Author(s): Teo M, Rodgers NG, Cummins AG. Source: Journal of Gastroenterology and Hepatology. 2002 October; 17(10): 1130-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12201879&dopt=Abstract
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Dexamethasone pulse steroids in ulcerative colitis--is it time for a change? Author(s): Patel SM, Falchuk K. Source: Inflammatory Bowel Diseases. 2003 May; 9(3): 213. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12797351&dopt=Abstract
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Differential expression of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) in ulcerative colitis and Crohn's disease. Author(s): Arihiro S, Ohtani H, Suzuki M, Murata M, Ejima C, Oki M, Kinouchi Y, Fukushima K, Sasaki I, Nakamura S, Matsumoto T, Torii A, Toda G, Nagura H. Source: Pathology International. 2002 May-June; 52(5-6): 367-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12100519&dopt=Abstract
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Differentiation between ulcerative colitis and Crohn's disease by a quantitative immunohistochemical evaluation of T lymphocytes, neutrophils, histiocytes and mast cells. Author(s): Sasaki Y, Tanaka M, Kudo H. Source: Pathology International. 2002 April; 52(4): 277-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12031083&dopt=Abstract
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Digitate dermatosis associated with ulcerative colitis? Author(s): Sawamura D, Umeki K. Source: Clinical and Experimental Dermatology. 2002 November; 27(8): 716-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12472556&dopt=Abstract
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Distal ulcerative colitis refractory to rectal mesalamine: role of transdermal nicotine versus oral mesalamine. Author(s): Guslandi M, Frego R, Viale E, Testoni PA. Source: Canadian Journal of Gastroenterology = Journal Canadien De Gastroenterologie. 2002 May; 16(5): 293-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12045777&dopt=Abstract
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Distinct gene expression of osteopontin in patients with ulcerative colitis. Author(s): Masuda H, Takahashi Y, Asai S, Takayama T. Source: The Journal of Surgical Research. 2003 May 1; 111(1): 85-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12842452&dopt=Abstract
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Diverse p53 alterations in ulcerative colitis-associated low-grade dysplasia: fulllength gene sequencing in microdissected single crypts. Author(s): Yoshida T, Mikami T, Mitomi H, Okayasu I. Source: The Journal of Pathology. 2003 February; 199(2): 166-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12533829&dopt=Abstract
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DNA fingerprinting abnormalities can distinguish ulcerative colitis patients with dysplasia and cancer from those who are dysplasia/cancer-free. Author(s): Chen R, Rabinovitch PS, Crispin DA, Emond MJ, Koprowicz KM, Bronner MP, Brentnall TA. Source: American Journal of Pathology. 2003 February; 162(2): 665-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12547724&dopt=Abstract
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Do immunosuppressants really work as maintenance therapy after the achievement of remission of severe ulcerative colitis? Author(s): Naganuma M, Hibi T. Source: Journal of Gastroenterology. 2002; 37(4): 315-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11993519&dopt=Abstract
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Does length really matter?. Oral and topical 5-aminosalicylic acid therapy for ulcerative colitis. Author(s): Lashner BA. Source: Dig Liver Dis. 2002 November; 34(11): 766-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12546510&dopt=Abstract
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Does patient knowledge affect the colorectal cancer risk in ulcerative colitis? Author(s): Eaden JA, Abrams K, Mayberry JF. Source: Postgraduate Medical Journal. 2002 October; 78(924): 615-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12415086&dopt=Abstract
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Doppler US of superior mesenteric artery in the assessment of ulcerative colitis. A prospective study. Author(s): Kalantzis N, Rouvella P, Tarazis S, Mourikis D, Kalantzis C, Kourkoutsakis N, Barbatzas Ch, Antoniou AG. Source: Hepatogastroenterology. 2002 January-February; 49(43): 168-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11941944&dopt=Abstract
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Double stapled ileal pouch anal anastomosis (DS-IPAA) for mucosal ulcerative colitis (MUC): is there a correlation between the tissue type in the circular stapler donuts and in follow-up biopsy? Author(s): Saigusa N, Choi HJ, Wexner SD, Woodhouse SL, Singh JJ, Weiss EG, Nogueras JJ, Belin B. Source: Colorectal Disease : the Official Journal of the Association of Coloproctology of Great Britain and Ireland. 2003 March; 5(2): 153-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12780905&dopt=Abstract
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Double-contrast magnetic resonance examination of ulcerative colitis. Author(s): Sardanelli F, de Cicco E, Renzetti P, Parodi RC, Calabrese M. Source: European Radiology. 1999; 9(5): 875-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10369982&dopt=Abstract
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Earlier surveillance colonoscopy programme improves survival in patients with ulcerative colitis associated colorectal cancer: results of a 23-year surveillance programme in the Japanese population. Author(s): Hata K, Watanabe T, Kazama S, Suzuki K, Shinozaki M, Yokoyama T, Matsuda K, Muto T, Nagawa H. Source: British Journal of Cancer. 2003 October 6; 89(7): 1232-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14520452&dopt=Abstract
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Early experience with laparoscopic ileal pouch-anal anastomosis for ulcerative colitis. Author(s): Pace DE, Seshadri PA, Chiasson PM, Poulin EC, Schlachta CM, Mamazza J. Source: Surgical Laparoscopy, Endoscopy & Percutaneous Techniques. 2002 October; 12(5): 337-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12409700&dopt=Abstract
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Early gallbladder carcinoma associated with primary sclerosing cholangitis and ulcerative colitis. Author(s): Yamamoto T, Uki K, Takeuchi K, Nagashima N, Honjo H, Sakurai N, Okuda C, Watanabe G, Mori M, Kuyama Y. Source: Journal of Gastroenterology. 2003; 38(7): 704-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12898366&dopt=Abstract
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Effect of oral tacrolimus (FK 506) on steroid-refractory moderate/severe ulcerative colitis. Author(s): Hogenauer C, Wenzl HH, Hinterleitner TA, Petritsch W. Source: Alimentary Pharmacology & Therapeutics. 2003 August 15; 18(4): 415-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12940927&dopt=Abstract
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Effect of smoking and transdermal nicotine on colonic nicotinic acetylcholine receptors in ulcerative colitis. Author(s): Richardson CE, Morgan JM, Jasani B, Green JT, Rhodes J, Williams GT, Lindstrom J, Wonnacott S, Peel S, Thomas GA. Source: Qjm : Monthly Journal of the Association of Physicians. 2003 January; 96(1): 5765. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509650&dopt=Abstract
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Effects of appendicectomy on the course of ulcerative colitis. Author(s): Cosnes J, Carbonnel F, Beaugerie L, Blain A, Reijasse D, Gendre JP. Source: Gut. 2002 December; 51(6): 803-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12427780&dopt=Abstract
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Efficacy and safety of oral ridogrel in the treatment of ulcerative colitis: two multicentre, randomized, double-blind studies. Author(s): Tytgat GN, Van Nueten L, Van De Velde I, Joslyn A, Hanauer SB. Source: Alimentary Pharmacology & Therapeutics. 2002 January; 16(1): 87-99. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11856082&dopt=Abstract
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Efficacy of anti-tumor necrosis factor therapy in patients with ulcerative colitis. Author(s): Su C, Salzberg BA, Lewis JD, Deren JJ, Kornbluth A, Katzka DA, Stein RB, Adler DR, Lichtenstein GR. Source: The American Journal of Gastroenterology. 2002 October; 97(10): 2577-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12385442&dopt=Abstract
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Efficacy of cyclosporin with corticotropin for refractory ulcerative colitis. Author(s): Okamura S, Aoki H, Ohashi S, Urano F, Shimodaira M, Kanamori S, Ishikawa H, Segawa K. Source: Hepatogastroenterology. 2003 January-February; 50(49): 91-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12629999&dopt=Abstract
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Elevated serum values of procollagen III peptide (PIIIP) in patients with ulcerative colitis who will develop pseudopolyps. Author(s): Babic Z, Jagic V, Petrovic Z, Bilic A, Dinko K, Kubat G, Troskot R, Vukelic M. Source: World Journal of Gastroenterology : Wjg. 2003 March; 9(3): 619-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12632532&dopt=Abstract
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Elimination of mucosectomy during restorative proctocolectomy in patients with ulcerative colitis may provide better results in low-volume centers. Author(s): Kayaalp C, Nessar G, Akoglu M, Atalay F. Source: American Journal of Surgery. 2003 March; 185(3): 268-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12620569&dopt=Abstract
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Epidemiological features of ulcerative colitis in Trakya, Turkey. Author(s): Tezel A, Dokmeci G, Eskiocak M, Umit H, Soylu AR. Source: J Int Med Res. 2003 March-April; 31(2): 141-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760318&dopt=Abstract
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Epidermal growth factor enemas with oral mesalamine for mild-to-moderate leftsided ulcerative colitis or proctitis. Author(s): Sinha A, Nightingale J, West KP, Berlanga-Acosta J, Playford RJ. Source: The New England Journal of Medicine. 2003 July 24; 349(4): 350-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12878742&dopt=Abstract
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Epidermal growth factor for ulcerative colitis. Author(s): Farrell RJ. Source: The New England Journal of Medicine. 2003 July 24; 349(4): 395-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12878748&dopt=Abstract
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Epigenetic control of the E-cadherin gene (CDH1) by CpG methylation in colectomy samples of patients with ulcerative colitis. Author(s): Azarschab P, Porschen R, Gregor M, Blin N, Holzmann K. Source: Genes, Chromosomes & Cancer. 2002 October; 35(2): 121-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12203775&dopt=Abstract
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Evaluation of serological markers to differentiate between ulcerative colitis and Crohn's disease: pANCA, ASCA and agglutinating antibodies to anaerobic coccoid rods. Author(s): Linskens RK, Mallant-Hent RC, Groothuismink ZM, Bakker-Jonges LE, van de Merwe JP, Hooijkaas H, von Blomberg BM, Meuwissen SG. Source: European Journal of Gastroenterology & Hepatology. 2002 September; 14(9): 1013-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12352222&dopt=Abstract
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Evolving medical therapies for ulcerative colitis. Author(s): Cohen RD. Source: Current Gastroenterology Reports. 2002 December; 4(6): 497-505. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12441040&dopt=Abstract
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Exacerbation of ulcerative colitis by cytomegalovirus infection in an immunocompetent Indian patient. Author(s): Malhi NS, Bhasin DK, Gupta NM, Vaiphei K, Singh K. Source: Trop Gastroenterol. 2002 April-June; 23(2): 88-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12632977&dopt=Abstract
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Expression of protease-activated receptor 2 in ulcerative colitis. Author(s): Kim JA, Choi SC, Yun KJ, Kim DK, Han MK, Seo GS, Yeom JJ, Kim TH, Nah YH, Lee YM. Source: Inflammatory Bowel Diseases. 2003 July; 9(4): 224-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12902845&dopt=Abstract
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Extracorporeal monocyte granulocytapheresis was effective for a patient of erythema nodosum concomitant with ulcerative colitis. Author(s): Fukunaga K, Sawada K, Fukuda Y, Matoba Y, Natsuaki M, Ohnishi K, Fukui S, Satomi M, Shimoyama T. Source: Therap Apher Dial. 2003 February; 7(1): 122-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12921128&dopt=Abstract
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Factors associated with ileal mucosal morphology and inflammation in patients with ileal pouch-anal anastomosis for ulcerative colitis. Author(s): Kuisma J, Mentula S, Luukkonen P, Jarvinen H, Kahri A, Farkkila M. Source: Diseases of the Colon and Rectum. 2003 November; 46(11): 1476-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14605565&dopt=Abstract
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Factors influencing the functional outcome of restorative proctocolectomy in ulcerative colitis. Author(s): Karlbom U, Raab Y, Ejerblad S, Graf W, Thorn M, Pahlman L. Source: The British Journal of Surgery. 2000 October; 87(10): 1401-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11044167&dopt=Abstract
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Factors predictive of response to cyclosporin treatment for severe, steroid-resistant ulcerative colitis. Author(s): Rowe FA, Walker JH, Karp LC, Vasiliauskas EA, Plevy SE, Targan SR. Source: The American Journal of Gastroenterology. 2000 August; 95(8): 2000-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10950049&dopt=Abstract
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Familial expression of anti-Saccharomyces cerevisiae Mannan antibodies in Crohn's disease and ulcerative colitis: a GISC study. Author(s): Annese V, Andreoli A, Andriulli A, Dinca R, Gionchetti P, Latiano A, Lombardi G, Piepoli A, Poulain D, Sendid B, Colombel JF. Source: The American Journal of Gastroenterology. 2001 August; 96(8): 2407-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11513182&dopt=Abstract
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Fas/Fas ligand expression and characteristics of primed CD45RO+ T cells in the inflamed mucosa of ulcerative colitis. Author(s): Suzuki A, Sugimura K, Ohtsuka K, Hasegawa K, Suzuki K, Ishizuka K, Mochizuki T, Honma T, Narisawa R, Asakura H. Source: Scandinavian Journal of Gastroenterology. 2000 December; 35(12): 1278-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11199367&dopt=Abstract
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Fatal ulcerative panenteritis following colectomy in a patient with ulcerative colitis. Author(s): Annese V, Caruso N, Bisceglia M, Lombardi G, Clemente R, Modola G, Tardio B, Villani MR, Andriulli A. Source: Digestive Diseases and Sciences. 1999 June; 44(6): 1189-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10389695&dopt=Abstract
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Female reproductive health after ileal pouch anal anastomosis for ulcerative colitis. Author(s): Wax JR, Pinette MG, Cartin A, Blackstone J. Source: Obstetrical & Gynecological Survey. 2003 April; 58(4): 270-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12665707&dopt=Abstract
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Fertility after ileal pouch-anal anastomosis in women with ulcerative colitis. Author(s): Olsen KO, Joelsson M, Laurberg S, Oresland T. Source: The British Journal of Surgery. 1999 April; 86(4): 493-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10215821&dopt=Abstract
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Filter leukapheresis for patients with ulcerative colitis: clinical results and the possible mechanism. Author(s): Amano K, Amano K. Source: Therapeutic Apheresis : Official Journal of the International Society for Apheresis and the Japanese Society for Apheresis. 1998 May; 2(2): 97-100. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10225707&dopt=Abstract
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First two patients with ulcerative colitis who developed classical thrombotic thrombocytopenic purpura successfully treated with medical therapy and plasma exchange. Author(s): Baron BW, Jeon HR, Glunz C, Peterson A, Cohen R, Hanauer S, Rubin D, Hart J, Baron JM. Source: Journal of Clinical Apheresis. 2002; 17(4): 204-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12494414&dopt=Abstract
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Flow cytometric and histologic evaluation in a large cohort of patients with ulcerative colitis: correlation with clinical characteristics and impact on surveillance. Author(s): Holzmann K, Klump B, Borchard F, Gregor M, Porschen R. Source: Diseases of the Colon and Rectum. 2001 October; 44(10): 1446-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11598473&dopt=Abstract
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Fluorescence endoscopy for the detection of low and high grade dysplasia in ulcerative colitis using systemic or local 5-aminolaevulinic acid sensitisation. Author(s): Messmann H, Endlicher E, Freunek G, Rummele P, Scholmerich J, Knuchel R. Source: Gut. 2003 July; 52(7): 1003-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12801958&dopt=Abstract
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Focally enhanced gastritis in children with Crohn's disease and ulcerative colitis. Author(s): Sharif F, McDermott M, Dillon M, Drumm B, Rowland M, Imrie C, Kelleher S, Harty S, Bourke B. Source: The American Journal of Gastroenterology. 2002 June; 97(6): 1415-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12094859&dopt=Abstract
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Fracture risk in patients with celiac Disease, Crohn's disease, and ulcerative colitis: a nationwide follow-up study of 16,416 patients in Denmark. Author(s): Vestergaard P, Mosekilde L. Source: American Journal of Epidemiology. 2002 July 1; 156(1): 1-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12076883&dopt=Abstract
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From uninformed patient to CWOCN: My life with ulcerative colitis and the ileoanal reservoir. Author(s): Follett SB. Source: Journal of Wound, Ostomy, and Continence Nursing : Official Publication of the Wound, Ostomy and Continence Nurses Society / Wocn. 2003 January; 30(1): 4-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12529587&dopt=Abstract
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Fulminant acute and diffuse chronic ulcerative colitis--the argument for surgery. Author(s): Mortensen N. Source: Acta Gastroenterol Belg. 2000 July-September; 63(3): 289. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11189990&dopt=Abstract
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Functional outcome after restorative panproctocolectomy for ulcerative colitis decreases an otherwise enhance quality of life. Author(s): Gee SH, Seow-Choen F. Source: The British Journal of Surgery. 2001 March; 88(3): 472. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11269271&dopt=Abstract
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Functional outcome and patient satisfaction after ileal pouch anal anastomosis for ulcerative colitis in a developing country. Author(s): Rao YG, Saxena R, Sahni P, Pande GK, Chattopadhyay TK. Source: Trop Gastroenterol. 2002 April-June; 23(2): 66-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12632971&dopt=Abstract
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Functional outcomes in patients with mucosal ulcerative colitis after ileal pouch-anal anastomosis by the double stapling technique: is there a relation to tissue type? Author(s): Choi JS, Potenti F, Wexner SD, Nam YS, Hwang YH, Nogueras JJ, Weiss EG, Pikarsky AJ. Source: Diseases of the Colon and Rectum. 2000 October; 43(10): 1398-404. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11052517&dopt=Abstract
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Fusobacterium varium localized in the colonic mucosa of patients with ulcerative colitis stimulates species-specific antibody. Author(s): Ohkusa T, Sato N, Ogihara T, Morita K, Ogawa M, Okayasu I. Source: Journal of Gastroenterology and Hepatology. 2002 August; 17(8): 849-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12164960&dopt=Abstract
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Gasless laparoscopic surgery for ulcerative colitis and familial adenomatous polyposis:initial experience of 7 cases. Author(s): Ishida H, Hashimoto D, Inokuma S, Nakada H, Ohsawa T, Hoshino T. Source: Surgical Endoscopy. 2003 June; 17(6): 899-902. Epub 2003 March 07. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12618933&dopt=Abstract
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Gastric emptying function after ileal J pouch-anal anastomosis for ulcerative colitis. Author(s): Tomita R, Fujisaki S, Tanjoh K. Source: Surgery. 2004 January; 135(1): 81-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14694304&dopt=Abstract
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Gastrointestinal stromal tumor (GIST) and ulcerative colitis. Author(s): Grieco A, Cavallaro A, Potenza AE, Mule A, Tarquini E, Miele L, Gasbarrini G. Source: J Exp Clin Cancer Res. 2002 December; 21(4): 617-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12636111&dopt=Abstract
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Genetic alterations in chronic ulcerative colitis-associated adenoma-like DALMs are similar to non-colitic sporadic adenomas. Author(s): Odze RD, Brown CA, Hartmann CJ, Noffsinger AE, Fogt F. Source: The American Journal of Surgical Pathology. 2000 September; 24(9): 1209-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10976694&dopt=Abstract
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Genetic heterogeneity within ulcerative colitis determined by an interleukin-1 receptor antagonist gene polymorphism and antineutrophil cytoplasmic antibodies. Author(s): Papo M, Quer JC, Gutierrez C, Broch M, Casellas F, Pastor RM, Olona M, Richart C. Source: European Journal of Gastroenterology & Hepatology. 1999 April; 11(4): 413-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10321759&dopt=Abstract
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Genetic instability and the mutator phenotype. Studies in ulcerative colitis. Author(s): Loeb KR, Loeb LA. Source: American Journal of Pathology. 1999 June; 154(6): 1621-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10362784&dopt=Abstract
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Germinated barley foodstuff feeding. A novel neutraceutical therapeutic strategy for ulcerative colitis. Author(s): Kanauchi O, Iwanaga T, Mitsuyama K. Source: Digestion. 2001; 63 Suppl 1: 60-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11173912&dopt=Abstract
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GI distension in severe ulcerative colitis. Author(s): Latella G, Vernia P, Viscido A, Frieri G, Cadau G, Cocco A, Cossu A, Tomei E, Caprilli R. Source: The American Journal of Gastroenterology. 2002 May; 97(5): 1169-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12014723&dopt=Abstract
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Giant hamartoma of the ascending colon in an adult with ulcerative colitis. Author(s): Mesiya S, Chotiprasidhi P, Kida M, Harty RF. Source: The American Journal of Gastroenterology. 2001 October; 96(10): 3014-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11693342&dopt=Abstract
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Glomerular and tubular renal functions after long-term medication of sulphasalazine, olsalazine, and mesalazine in patients with ulcerative colitis. Author(s): Birketvedt GS, Berg KJ, Fausa O, Florholmen J. Source: Inflammatory Bowel Diseases. 2000 November; 6(4): 275-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11149559&dopt=Abstract
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Glucagon-like peptide-2 and common therapeutics in a murine model of ulcerative colitis. Author(s): L'Heureux MC, Brubaker PL. Source: The Journal of Pharmacology and Experimental Therapeutics. 2003 July; 306(1): 347-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12815012&dopt=Abstract
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Glucocorticoid receptor mRNA in patients with ulcerative colitis: a study of responders and nonresponders to glucocorticosteroid therapy. Author(s): Flood L, Lofberg R, Stierna P, Wikstrom AC. Source: Inflammatory Bowel Diseases. 2001 August; 7(3): 202-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11515845&dopt=Abstract
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Glutamine distribution in patients with ulcerative colitis and in patients with familial adenomatous polyposis coli before and after restorative proctocolectomy. Author(s): Heuschen UA, Allemeyer EH, Hinz U, Langer K, Heuschen G, DeckerBaumann C, Herfarth C, Stern J. Source: International Journal of Colorectal Disease. 2002 July; 17(4): 245-52. Epub 2001 December 18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12073073&dopt=Abstract
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Grading system for inflammation in ulcerative colitis. Author(s): Cross SS. Source: Gut. 2001 May; 48(5): 737. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11336029&dopt=Abstract
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Granulocyte adsorptive apheresis for pediatric patients with ulcerative colitis. Author(s): Tomomasa T, Kobayashi A, Kaneko H, Mika S, Maisawa S, Chino Y, Syou H, Yoden A, Fujino J, Tanikawa M, Yamashita T, Kimura S, Kanoh M, Sawada K, Morikawa A. Source: Digestive Diseases and Sciences. 2003 April; 48(4): 750-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12741466&dopt=Abstract
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Granulocyte and monocyte adsorption apheresis in a patient with antiglomerular basement membrane glomerulonephritis and active ulcerative colitis. Author(s): Nakamura T, Suzuki Y, Koide H. Source: The American Journal of the Medical Sciences. 2003 May; 325(5): 296-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12792251&dopt=Abstract
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Granulocyte and monocyte adsorptive apheresis in a case with severe ulcerative colitis unresponsive to conventional medication. Author(s): Suzuki Y, Yoshimura N, Saitoh Y, Saniabadi AR. Source: Journal of Clinical Apheresis. 2003; 18(1): 40-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12717793&dopt=Abstract
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Granulomatous ulcerative colitis: a re-appraisal of the mucosal granuloma in the distinction of Crohn's disease from ulcerative colitis. Author(s): Mahadeva U, Martin JP, Patel NK, Price AB. Source: Histopathology. 2002 July; 41(1): 50-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12121237&dopt=Abstract
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Guided self-management and patient-directed follow-up of ulcerative colitis: a randomised trial. Author(s): Kurbegow AC, Ferry GD. Source: Journal of Pediatric Gastroenterology and Nutrition. 2002 April; 34(4): 428-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11981954&dopt=Abstract
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Guided self-management and patient-directed follow-up of ulcerative colitis: a randomised trial. Author(s): Robinson A, Thompson DG, Wilkin D, Roberts C; Northwest Gastrointestinal Research Group. Source: Lancet. 2001 September 22; 358(9286): 976-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11583752&dopt=Abstract
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Health-related quality of life after ileal pouch anal anastomosis for ulcerative colitis: right answer-wrong question. Author(s): Robb BW, Pritts TA, Warner BW. Source: Gastroenterology. 2002 April; 122(4): 1180-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11910374&dopt=Abstract
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Hemichorea, moya-moya, and ulcerative colitis. Author(s): Shanahan P, Hutchinson M, Bohan A, O' Donoghue D, Sheahan K, Owens A. Source: Movement Disorders : Official Journal of the Movement Disorder Society. 2001 May; 16(3): 570-2. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11391762&dopt=Abstract
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Heparin therapy for ulcerative colitis. Author(s): Folwaczny C. Source: Gastroenterology. 2001 April; 120(5): 1307; Author Reply 1307-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11288746&dopt=Abstract
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Heparin therapy for ulcerative colitis? Effects and mechanisms. Author(s): Michell NP, Lalor P, Langman MJ. Source: European Journal of Gastroenterology & Hepatology. 2001 April; 13(4): 449-56. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11338079&dopt=Abstract
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Hepatocyte growth factor facilitates colonic mucosal repair in experimental ulcerative colitis in rats. Author(s): Tahara Y, Ido A, Yamamoto S, Miyata Y, Uto H, Hori T, Hayashi K, Tsubouchi H. Source: The Journal of Pharmacology and Experimental Therapeutics. 2003 October; 307(1): 146-51. Epub 2003 September 03. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12954797&dopt=Abstract
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High epithelial and stromal genetic instability of chromosome 17 in ulcerative colitisassociated carcinogenesis. Author(s): Matsumoto N, Yoshida T, Okayasu I. Source: Cancer Research. 2003 October 1; 63(19): 6158-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14559796&dopt=Abstract
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High frequency of antigliadin antibodies and absence of antireticulin and antiendomysium antibodies in patients with ulcerative colitis. Author(s): Kull K, Uibo O, Salupere R, Metskula K, Uibo R. Source: Journal of Gastroenterology. 1999 February; 34(1): 61-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10204612&dopt=Abstract
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High level perinuclear antineutrophil cytoplasmic antibody (pANCA) in ulcerative colitis patients before colectomy predicts the development of chronic pouchitis after ileal pouch-anal anastomosis. Author(s): Fleshner PR, Vasiliauskas EA, Kam LY, Fleshner NE, Gaiennie J, AbreuMartin MT, Targan SR. Source: Gut. 2001 November; 49(5): 671-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11600470&dopt=Abstract
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High normal serum levels of C3 and C1 inhibitor, two acute-phase proteins belonging to the complement system, occur more frequently in patients with Crohn's disease than ulcerative colitis. Author(s): Bene L, Fust G, Fekete B, Kovacs A, Horvath L, Prohaszka Z, Miklos K, Palos G, Daha M, Farkas H, Varga L. Source: Digestive Diseases and Sciences. 2003 June; 48(6): 1186-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12822883&dopt=Abstract
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High prevalence of undetected ulcerative colitis: data from the Nottingham fecal occult blood screening trial. Author(s): Howarth GF, Robinson MH, Jenkins D, Hardcastle JD, Logan RF. Source: The American Journal of Gastroenterology. 2002 March; 97(3): 690-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11926210&dopt=Abstract
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High resolution analysis of chromosome 18 alterations in ulcerative colitis-related colorectal cancer. Author(s): Terdiman JP, Aust DE, Chang CG, Willenbucher RF, Baretton GB, Waldman FM. Source: Cancer Genetics and Cytogenetics. 2002 July 15; 136(2): 129-37. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12237237&dopt=Abstract
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Histological and immunological features of appendix in patients with ulcerative colitis. Author(s): Jo Y, Matsumoto T, Yada S, Nakamura S, Yao T, Hotokezaka M, Mibu R, Iida M. Source: Digestive Diseases and Sciences. 2003 January; 48(1): 99-108. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12645797&dopt=Abstract
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Histopathology of ulcerative colitis in initial rectal biopsy in children. Author(s): Washington K, Greenson JK, Montgomery E, Shyr Y, Crissinger KD, Polk DB, Barnard J, Lauwers GY. Source: The American Journal of Surgical Pathology. 2002 November; 26(11): 1441-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12409720&dopt=Abstract
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HLA-DRB1*1502 confers susceptibility to ulcerative colitis, but is negatively associated with its intractability: a Korean study. Author(s): Myung SJ, Yang SK, Jung HY, Chang HS, Park B, Hong WS, Kim JH, Min I. Source: International Journal of Colorectal Disease. 2002 July; 17(4): 233-7. Epub 2001 December 21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12073071&dopt=Abstract
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Hodgkin s disease with nephrotic syndrome as a complication of ulcerative colitis: case report. Author(s): Basic-Jukic N, Radman I, Roncevic T, Jakic-Razumovic J. Source: Croatian Medical Journal. 2002 October; 43(5): 573-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12402399&dopt=Abstract
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Human neutrophil lipocalin is a unique marker of neutrophil inflammation in ulcerative colitis and proctitis. Author(s): Carlson M, Raab Y, Seveus L, Xu S, Hallgren R, Venge P. Source: Gut. 2002 April; 50(4): 501-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11889070&dopt=Abstract
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Hydrogen sulfide and colonic epithelial metabolism: implications for ulcerative colitis. Author(s): Jorgensen J, Mortensen PB. Source: Digestive Diseases and Sciences. 2001 August; 46(8): 1722-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11508674&dopt=Abstract
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Hyperbaric oxygen therapy for severe ulcerative colitis. Author(s): Buchman AL, Fife C, Torres C, Smith L, Aristizibal J. Source: Journal of Clinical Gastroenterology. 2001 October; 33(4): 337-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11588553&dopt=Abstract
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Hypermethylation of the p14(ARF) gene in ulcerative colitis-associated colorectal carcinogenesis. Author(s): Sato F, Harpaz N, Shibata D, Xu Y, Yin J, Mori Y, Zou TT, Wang S, Desai K, Leytin A, Selaru FM, Abraham JM, Meltzer SJ. Source: Cancer Research. 2002 February 15; 62(4): 1148-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11861396&dopt=Abstract
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Hypertrophic osteoarthropathy in untreated ulcerative colitis. Author(s): Crone J, Huber WD, Resch R, Ponhold W, Granditsch G. Source: Journal of Pediatric Gastroenterology and Nutrition. 2002 August; 35(2): 213-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12187300&dopt=Abstract
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IBD5 is a general risk factor for inflammatory bowel disease: replication of association with Crohn disease and identification of a novel association with ulcerative colitis. Author(s): Giallourakis C, Stoll M, Miller K, Hampe J, Lander ES, Daly MJ, Schreiber S, Rioux JD. Source: American Journal of Human Genetics. 2003 July; 73(1): 205-11. Epub 2003 May 29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12776251&dopt=Abstract
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Ileal pouch-anal anastomosis for ulcerative colitis: the University of Puerto Rico experience. Author(s): Vendrell R, Inesta M, Mera R, Iturrino J, Soto A, Mas M, Lojo JJ, Torres EA. Source: P R Health Sci J. 2001 September; 20(3): 221-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11776722&dopt=Abstract
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Images in clinical medicine. Chronic ulcerative colitis with megacolon. Author(s): Kaiser AM, Beart RW. Source: The New England Journal of Medicine. 2003 July 24; 349(4): 358. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12878743&dopt=Abstract
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Immune abnormalities and endotoxemia in patients with ulcerative colitis and in their first degree relatives: attempts at neutralizing endotoxin-mediated effects. Author(s): Amati L, Caradonna L, Leandro G, Magrone T, Minenna M, Faleo G, Pellegrino NM, Jirillo E, Caccavo D. Source: Current Pharmaceutical Design. 2003; 9(24): 1937-45. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12871178&dopt=Abstract
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Impaired expression of peroxisome proliferator-activated receptor gamma in ulcerative colitis. Author(s): Dubuquoy L, Jansson EA, Deeb S, Rakotobe S, Karoui M, Colombel JF, Auwerx J, Pettersson S, Desreumaux P. Source: Gastroenterology. 2003 May; 124(5): 1265-76. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730867&dopt=Abstract
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In search of a better treatment for ulcerative colitis. Author(s): Sharma MP, Makharia G. Source: Indian J Gastroenterol. 2003 May-June; 22(3): 77-8. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12839375&dopt=Abstract
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Incidence and prevalence of ulcerative colitis in Punjab, North India. Author(s): Sood A, Midha V, Sood N, Bhatia AS, Avasthi G. Source: Gut. 2003 November; 52(11): 1587-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14570727&dopt=Abstract
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Increasing fecal butyrate in ulcerative colitis patients by diet: controlled pilot study. Author(s): Hallert C, Bjorck I, Nyman M, Pousette A, Granno C, Svensson H. Source: Inflammatory Bowel Diseases. 2003 March; 9(2): 116-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12769445&dopt=Abstract
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Inducible and constitutive beta-defensins are differentially expressed in Crohn's disease and ulcerative colitis. Author(s): Wehkamp J, Harder J, Weichenthal M, Mueller O, Herrlinger KR, Fellermann K, Schroeder JM, Stange EF. Source: Inflammatory Bowel Diseases. 2003 July; 9(4): 215-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12902844&dopt=Abstract
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Inflammatory bowel disease Part 1: ulcerative colitis--pathophysiology and conventional and alternative treatment options. Author(s): Head KA, Jurenka JS. Source: Alternative Medicine Review : a Journal of Clinical Therapeutic. 2003 August; 8(3): 247-83. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12946238&dopt=Abstract
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Infliximab for refractory ulcerative colitis or indeterminate colitis: an open-label multicentre study. Author(s): Gornet JM, Couve S, Hassani Z, Delchier JC, Marteau P, Cosnes J, Bouhnik Y, Dupas JL, Modigliani R, Taillard F, Lemann M. Source: Alimentary Pharmacology & Therapeutics. 2003 July 15; 18(2): 175-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12869077&dopt=Abstract
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Infliximab in moderately severe glucocorticoid resistant ulcerative colitis: a randomised controlled trial. Author(s): Probert CS, Hearing SD, Schreiber S, Kuhbacher T, Ghosh S, Arnott ID, Forbes A. Source: Gut. 2003 July; 52(7): 998-1002. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12801957&dopt=Abstract
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Infliximab in refractory pouchitis complicated by fistulae following ileo-anal pouch for ulcerative colitis. Author(s): Viscido A, Habib FI, Kohn A, Papi C, Marcheggiano A, Pimpo MT, Vernia P, Cadau G, Caprilli R. Source: Alimentary Pharmacology & Therapeutics. 2003 May 15; 17(10): 1263-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12755839&dopt=Abstract
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Infliximab in ulcerative colitis: is there a placebo (effect) in the house? Author(s): Cohen RD. Source: Gastroenterology. 2003 June; 124(7): 1990-1; Discussion 1991. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12806639&dopt=Abstract
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Interferon beta-1a in ulcerative colitis: a placebo controlled, randomised, dose escalating study. Author(s): Nikolaus S, Rutgeerts P, Fedorak R, Steinhart AH, Wild GE, Theuer D, Mohrle J, Schreiber S. Source: Gut. 2003 September; 52(9): 1286-90. Erratum In: Gut. 2003 November; 52(11): 1657. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912859&dopt=Abstract
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Intractable ulcerative colitis caused by cytomegalovirus infection: a prospective study on prevalence, diagnosis, and treatment. Author(s): Wada Y, Matsui T, Matake H, Sakurai T, Yamamoto J, Kikuchi Y, Yorioka M, Tsuda S, Yao T, Yao S, Haraoka S, Iwashita A. Source: Diseases of the Colon and Rectum. 2003 October; 46(10 Suppl): S59-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14530660&dopt=Abstract
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Is colonoscopy alone sufficient to screen for ulcerative colitis-associated colorectal carcinoma? Author(s): Bruewer M, Krieglstein CF, Utech M, Bode M, Rijcken E, Anthoni C, Laukoetter MG, Schuermann G, Senninger N. Source: World Journal of Surgery. 2003 May; 27(5): 611-5. Epub 2003 April 28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12715233&dopt=Abstract
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J ileal pouch-anal anastomosis for chronic ulcerative colitis: complications and longterm outcome in 1310 patients. Author(s): Meagher AP, Farouk R, Dozois RR, Kelly KA, Pemberton JH. Source: The British Journal of Surgery. 1998 June; 85(6): 800-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9667712&dopt=Abstract
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Keratinocyte growth factor in inflammatory bowel disease. Increased mRNA transcripts in ulcerative colitis compared with Crohn's disease in biopsies and isolated mucosal myofibroblasts. Author(s): Bajaj-Elliott M, Breese E, Poulsom R, Fairclough PD, MacDonald TT. Source: American Journal of Pathology. 1997 November; 151(5): 1469-76. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9358773&dopt=Abstract
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Ketotifen therapy for acute ulcerative colitis in children: a pilot study. Author(s): Jones NL, Roifman CM, Griffiths AM, Sherman P. Source: Digestive Diseases and Sciences. 1998 March; 43(3): 609-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9539658&dopt=Abstract
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Ki-67: a useful marker for the evaluation of dysplasia in ulcerative colitis. Author(s): Andersen SN, Rognum TO, Bakka A, Clausen OP. Source: Molecular Pathology : Mp. 1998 December; 51(6): 327-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10193513&dopt=Abstract
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Kimura's disease associated with ulcerative colitis: detection of IL-5 mRNA expression of peripheral blood mononuclear cells and colon lesion. Author(s): Sugaya M, Suzuki T, Asahina A, Nakamura K, Ohtsuki M, Tamaki K. Source: Acta Dermato-Venereologica. 1998 September; 78(5): 375-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9779259&dopt=Abstract
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Kui jie qing in the treatment of chronic non-specific ulcerative colitis. Author(s): Wang B, Ren S, Feng W, Zhong Z, Qin C. Source: J Tradit Chin Med. 1997 March; 17(1): 10-3. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10437236&dopt=Abstract
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Laparoscopic restorative proctocolectomy for patients with ulcerative colitis. Author(s): Hasegawa H, Watanabe M, Baba H, Nishibori H, Kitajima M. Source: Journal of Laparoendoscopic & Advanced Surgical Techniques. Part A. 2002 December; 12(6): 403-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12590719&dopt=Abstract
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Large-bowel obstruction secondary to localized rectal giant pseudopolyposis complicating ulcerative colitis: first reported case. Author(s): Hurlstone DP. Source: Endoscopy. 2002 December; 34(12): 1025. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12471554&dopt=Abstract
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Leucocytoclastic vasculitis as onset symptom of ulcerative colitis. Author(s): Iannone F, Scioscia C, Musio A, Piscitelli D, Lapadula G. Source: Annals of the Rheumatic Diseases. 2003 August; 62(8): 785-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860742&dopt=Abstract
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Liaison between rheumatoid arthritis and ulcerative colitis. Author(s): Aydin Y, Ozcakar L, Yildiz M, Akinci A. Source: Rheumatology International. 2003 January; 23(1): 47-8. Epub 2002 December 18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12548442&dopt=Abstract
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Linear IgA bullous dermatosis: an association with ulcerative colitis versus renal cell carcinoma. Author(s): Keller AS, Bouldin MB, Drage LA, Hauser SC, Davis MD. Source: Digestive Diseases and Sciences. 2003 April; 48(4): 783-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12741472&dopt=Abstract
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Liver abscess and diarrhea as initial manifestations of ulcerative colitis: case report and review of the literature. Author(s): Song J, Swekla M, Colorado P, Reddy R, Hoffmann S, Fine S. Source: Digestive Diseases and Sciences. 2003 February; 48(2): 417-21. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12643625&dopt=Abstract
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Long-term failure after restorative proctocolectomy for ulcerative colitis. Author(s): Tulchinsky H, Hawley PR, Nicholls J. Source: Annals of Surgery. 2003 August; 238(2): 229-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894016&dopt=Abstract
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Long-term functional results after ileal pouch anal restorative proctocolectomy for ulcerative colitis: a prospective observational study. Author(s): Michelassi F, Lee J, Rubin M, Fichera A, Kasza K, Karrison T, Hurst RD. Source: Annals of Surgery. 2003 September; 238(3): 433-41; Discussion 442-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14501509&dopt=Abstract
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Long-term results of low-dose intravenous ciclosporin for acute severe ulcerative colitis. Author(s): Rayner CK, McCormack G, Emmanuel AV, Kamm MA. Source: Alimentary Pharmacology & Therapeutics. 2003 August 1; 18(3): 303-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12895214&dopt=Abstract
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Lymphatic vessels in the colonic mucosa in ulcerative colitis. Author(s): Kaiserling E, Krober S, Geleff S. Source: Lymphology. 2003 June; 36(2): 52-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12926829&dopt=Abstract
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Management of ovarian cysts in women undergoing restorative proctocolectomy for ulcerative colitis. Author(s): Thakur A, Yang I, Lin A, Buchmiller-Crair T, Fonkalsrud EW. Source: The American Surgeon. 2003 April; 69(4): 339-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716094&dopt=Abstract
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Mediastinal widening in a patient of ulcerative colitis. Author(s): Mohapatra PR, Das SK, Deb A, Saini V. Source: Indian J Chest Dis Allied Sci. 2003 April-June; 45(2): 131-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12715937&dopt=Abstract
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Mesalazine for ulcerative colitis complicated with diabetic nephropathy. Author(s): Oshimoto H, Okamura S, Onozato Y, Ishihara H, Mori M. Source: Journal of Gastroenterology. 2001 December; 36(12): 863-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11777217&dopt=Abstract
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Mesalazine-associated benign intracranial hypertension in a patient with ulcerative colitis. Author(s): Rosa N, Giamundo A, Jura A, Iaccarino G, Romano A. Source: American Journal of Ophthalmology. 2003 July; 136(1): 212-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12834704&dopt=Abstract
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Mesangiocapillary glomerulonephritis associated with ulcerative colitis: a 6-year follow-up of 2 cases. Author(s): Ashman N, Sheaff M, Raftery MJ. Source: Clinical Nephrology. 2003 August; 60(2): 146-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12940620&dopt=Abstract
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Methylene blue-aided chromoendoscopy for the detection of intraepithelial neoplasia and colon cancer in ulcerative colitis. Author(s): Kiesslich R, Fritsch J, Holtmann M, Koehler HH, Stolte M, Kanzler S, Nafe B, Jung M, Galle PR, Neurath MF. Source: Gastroenterology. 2003 April; 124(4): 880-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12671882&dopt=Abstract
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Motion - colonoscopic surveillance is more cost effective than colectomy in patients with ulcerative colitis: arguments against the motion. Author(s): Ekbom A. Source: Canadian Journal of Gastroenterology = Journal Canadien De Gastroenterologie. 2003 February; 17(2): 122-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12605251&dopt=Abstract
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Mucosal expression of matrix metalloproteinases and their tissue inhibitors in ulcerative colitis patients. Author(s): Kusugami K, Nobata K, Tsuzuki T, Ando T, Ina K. Source: Journal of Gastroenterology. 2003; 38(4): 412-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12743787&dopt=Abstract
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Multiple microcarcinoids in a patient with long standing ulcerative colitis. Author(s): Matsumoto T, Jo Y, Mibu R, Hirahashi M, Yao T, Iida M. Source: Journal of Clinical Pathology. 2003 December; 56(12): 963-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14645360&dopt=Abstract
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Myopericarditis associated with ulcerative colitis. Author(s): Anagnostopoulos G, Margantinis G, Tsiakos S, Kostopoulos P, Pantes A, Arvanitidis D. Source: N Z Med J. 2003 November 7; 116(1185): U667. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14615809&dopt=Abstract
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N-acetyltransferase 1 and 2 genotypes do not predict response or toxicity to treatment with mesalamine and sulfasalazine in patients with ulcerative colitis. Author(s): Ricart E, Taylor WR, Loftus EV, O'Kane D, Weinshilboum RM, Tremaine WJ, Harmsen WS, Zinsmeister AR, Sandborn WJ. Source: The American Journal of Gastroenterology. 2002 July; 97(7): 1763-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12135032&dopt=Abstract
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Nephronophthisis and ulcerative colitis in siblings: a new association. Author(s): Ala-Mello S, Kaariainen H, Koskimies O. Source: Pediatric Nephrology (Berlin, Germany). 2001 June; 16(6): 507-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11420917&dopt=Abstract
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Neutrophil and eosinophil granule proteins as markers of response to local prednisolone treatment in distal ulcerative colitis and proctitis. Author(s): Sangfelt P, Carlson M, Thorn M, Loof L, Raab Y. Source: The American Journal of Gastroenterology. 2001 April; 96(4): 1085-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11316151&dopt=Abstract
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Neutrophilic pustulosis and ulcerative colitis. Author(s): Vazquez J, Almagro M, del Pozo J, Fonseca E. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2003 January; 17(1): 77-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12602978&dopt=Abstract
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Nitric oxide mediates a therapeutic effect of nicotine in ulcerative colitis. Author(s): Green JT, Richardson C, Marshall RW, Rhodes J, McKirdy HC, Thomas GA, Williams GT. Source: Alimentary Pharmacology & Therapeutics. 2000 November; 14(11): 1429-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11069313&dopt=Abstract
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Nocardia asteroides lung abscess in acute ulcerative colitis treated with cyclosporine. Author(s): Stack WA, Richardson PD, Logan RP, Mahida YR, Hawkey CJ. Source: The American Journal of Gastroenterology. 2001 July; 96(7): 2255-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11467663&dopt=Abstract
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Nodular duodenitis involving CD8+ cell infiltration in patients with ulcerative colitis. Author(s): Honma J, Mitomi H, Murakami K, Igarashi M, Saigenji K, Toyama K. Source: Hepatogastroenterology. 2001 November-December; 48(42): 1604-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11813583&dopt=Abstract
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Novel therapies in the treatment of ulcerative colitis. Author(s): Kane SV. Source: Expert Opinion on Investigational Drugs. 2001 July; 10(7): 1223-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11772246&dopt=Abstract
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Novel therapies in the treatment of ulcerative colitis. Author(s): Tuvlin JA, Kane SV. Source: Expert Opinion on Investigational Drugs. 2003 March; 12(3): 483-90. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12605569&dopt=Abstract
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Nutritional therapies for ulcerative colitis: literature review, chart review study, and future research. Author(s): Edman JS, Williams WH, Atkins RC. Source: Alternative Therapies in Health and Medicine. 2000 January; 6(1): 55-63. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10631823&dopt=Abstract
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Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis. Author(s): Sutherland L, MacDonald JK. Source: Cochrane Database Syst Rev. 2003; (3): Cd000543. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917894&dopt=Abstract
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Oral 5-aminosalicylic acid for maintenance of remission in ulcerative colitis. Author(s): Sutherland L, Roth D, Beck P, May G, Makiyama K. Source: Cochrane Database Syst Rev. 2002; (4): Cd000544. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12519547&dopt=Abstract
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Oral and topical 5-aminosalicylic acid (mesalazine) in inducing and maintaining remission in mild-moderate relapse of ulcerative colitis: one-year randomised multicentre trial. Author(s): Paoluzi P, D'Albasio G, Pera A, Bianchi Porro G, Paoluzi OA, Pica R, Cottone M, Miglioli M, Prantera C, Sturniolo G, Ardizzone S. Source: Dig Liver Dis. 2002 November; 34(11): 787-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12546514&dopt=Abstract
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Oral beclometasone dipropionate in the treatment of extensive and left-sided active ulcerative colitis: a multicentre randomised study. Author(s): Campieri M, Adamo S, Valpiani D, D'Arienzo A, D'Albasio G, Pitzalis M, Cesari P, Casetti T, Castiglione GN, Rizzello F, Manguso F, Varoli G, Gionchetti P. Source: Alimentary Pharmacology & Therapeutics. 2003 June 15; 17(12): 1471-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12823149&dopt=Abstract
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Oral prednisolone metasulphobenzoate in the treatment of active ulcerative colitis. Author(s): Cameron EA, Binnie JA, Balan K, Skerratt SA, Swift A, Solanki C, Middleton SJ. Source: Scandinavian Journal of Gastroenterology. 2003 May; 38(5): 535-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12795466&dopt=Abstract
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Orbital myositis associated with ulcerative colitis. Author(s): Jain S, Gottlob I. Source: The American Journal of Gastroenterology. 2001 December; 96(12): 3442-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11774970&dopt=Abstract
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Outcome of patients undergoing ileal pouch-anal anastomosis for left-sided chronic ulcerative colitis. Author(s): Hassan I, Horgan AF, Nivatvongs S, Harrington J, Larson DR. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2003 May-June; 7(4): 567-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763418&dopt=Abstract
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Outpatient treatment of moderately severe active ulcerative colitis with pulsed steroid therapy and conventional steroid therapy. Author(s): Oshitani N, Kamata N, Ooiso R, Kawashima D, Inagawa M, Sogawa M, Iimuro M, Jinno Y, Watanabe K, Higuchi K, Matsumoto T, Arakawa T. Source: Digestive Diseases and Sciences. 2003 May; 48(5): 1002-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12772803&dopt=Abstract
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Over-expression of interleukin 10 in mucosal T cells of patients with active ulcerative colitis. Author(s): Melgar S, Yeung MM, Bas A, Forsberg G, Suhr O, Oberg A, Hammarstrom S, Danielsson A, Hammarstrom ML. Source: Clinical and Experimental Immunology. 2003 October; 134(1): 127-37. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12974765&dopt=Abstract
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Oxidative stress and ulcerative colitis-associated carcinogenesis: studies in humans and animal models. Author(s): Seril DN, Liao J, Yang GY, Yang CS. Source: Carcinogenesis. 2003 March; 24(3): 353-62. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663492&dopt=Abstract
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Patterns of disease and surgical treatment among United States veterans more than 50 years of age with ulcerative colitis. Author(s): Longo WE, Virgo KS, Bahadursingh AN, Johnson FE. Source: American Journal of Surgery. 2003 November; 186(5): 514-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14599617&dopt=Abstract
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Plasma and mucosal prostaglandin E2 as a surrogate marker of ulcerative colitis activity. Author(s): Wiercinska-Drapalo A, Flisiak R, Prokopowicz D. Source: Rocz Akad Med Bialymst. 2001; 46: 60-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11780581&dopt=Abstract
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Pouchitis following restorative proctocolectomy for ulcerative colitis: incidence and therapeutic outcome. Author(s): Madiba TE, Bartolo DC. Source: Journal of the Royal College of Surgeons of Edinburgh. 2001 December; 46(6): 334-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11768572&dopt=Abstract
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Pregnancy delivery and pouch function after ileal pouch-anal anastomosis for ulcerative colitis. Author(s): Ramalingam T, Box B, Mortensen NM. Source: Diseases of the Colon and Rectum. 2003 September; 46(9): 1292. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12972978&dopt=Abstract
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Progression of flat low-grade dysplasia to advanced neoplasia in patients with ulcerative colitis. Author(s): Ullman T, Croog V, Harpaz N, Sachar D, Itzkowitz S. Source: Gastroenterology. 2003 November; 125(5): 1311-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14598247&dopt=Abstract
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Pronounced chromosomal instability and multiple gene amplifications characterize ulcerative colitis-associated colorectal carcinomas. Author(s): Habermann JK, Upender MB, Roblick UJ, Kruger S, Freitag S, Blegen H, Bruch HP, Schimmelpenning H, Auer G, Ried T. Source: Cancer Genetics and Cytogenetics. 2003 November; 147(1): 9-17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14580765&dopt=Abstract
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Psychosocial determinants of relapse in ulcerative colitis: a longitudinal study. Author(s): Bitton A, Sewitch MJ, Peppercorn MA, deB Edwardes MD, Shah S, Ransil B, Locke SE. Source: The American Journal of Gastroenterology. 2003 October; 98(10): 2203-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14572569&dopt=Abstract
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Pulmonary and hematological alterations in idiopathic ulcerative colitis. Author(s): Sethy PK, Dutta U, Aggrawal AN, Das R, Gulati M, Sinha SK, Singh K. Source: Indian J Gastroenterol. 2003 September-October; 22(5): 176-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14658533&dopt=Abstract
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Pure red cell aplasia associated with parvovirus B19 infection in a patient with ulcerative colitis. Author(s): Isomoto H, Fukuda Y, Bando Y, Machida I, Machida H, Omagari K, Mizuta Y, Murase K, Fukushima T, Murata I, Kohno S. Source: Digestive Diseases and Sciences. 2003 October; 48(10): 2104-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14627362&dopt=Abstract
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Pyoderma gangrenosum of the “sinus mammarum” in ulcerative colitis. Author(s): Angio LG, Pirrone G, Rivoli G, Fracassi MG, Rosato A, Piazzese E, Pacile V, Sfuncia G, Fiumara F. Source: G Chir. 2003 June-July; 24(6-7): 247-54. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14569923&dopt=Abstract
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Quality of life after proctocolectomy and ileo-anal anastomosis for severe ulcerative colitis. Author(s): Martin A, Dinca M, Leone L, Fries W, Angriman I, Tropea A, Naccarato R. Source: The American Journal of Gastroenterology. 1998 February; 93(2): 166-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9468234&dopt=Abstract
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Quality of life in Korean patients with inflammatory bowel diseases: ulcerative colitis, Crohn's disease and intestinal Behcet's disease. Author(s): Kim WH, Cho YS, Yoo HM, Park IS, Park EC, Lim JG. Source: International Journal of Colorectal Disease. 1999 February; 14(1): 52-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10207731&dopt=Abstract
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Quality-of-life assessment after ileoanal pull-through for ulcerative colitis and familial adenomatous polyposis. Author(s): Shamberger RC, Masek BJ, Leichtner AM, Winter HS, Lillehei CW. Source: Journal of Pediatric Surgery. 1999 January; 34(1): 163-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10022164&dopt=Abstract
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Quality-of-life research on the Internet: feasibility and potential biases in patients with ulcerative colitis. Author(s): Soetikno RM, Mrad R, Pao V, Lenert LA. Source: Journal of the American Medical Informatics Association : Jamia. 1997 November-December; 4(6): 426-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9391930&dopt=Abstract
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Quantification of the placebo response in ulcerative colitis. Author(s): Ilnyckyj A, Shanahan F, Anton PA, Cheang M, Bernstein CN. Source: Gastroenterology. 1997 June; 112(6): 1854-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9178676&dopt=Abstract
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Quantitation of chemokines (MDC, TARC) expression in mucosa from Crohn's disease and ulcerative colitis. Author(s): Jugde F, Alizadeh M, Boissier C, Chantry D, Siproudhis L, Corbinais S, Quelvennec E, Dyard F, Campion JP, Gosselin M, Bretagne JF, Semana G, Heresbach D. Source: European Cytokine Network. 2001 July-September; 12(3): 468-77. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11566628&dopt=Abstract
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Quantitative comparison of growth-associated protein-43 and substance P in ulcerative colitis. Author(s): Vento P, Kiviluoto T, Keranen U, Jarvinen HJ, Kivilaakso E, Soinila S. Source: The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society. 2001 June; 49(6): 749-58. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11373321&dopt=Abstract
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Quiz case 12. Marie-Bamberger syndrome (MBS) (hypertrophic osteoarthropathy (HOA) secondary to ulcerative colitis (UC). Author(s): Herneth AM, Breitenseher MJ, Funovics M, Nehrer S, Huber WD, Imhof H. Source: European Journal of Radiology. 1999 November; 32(2): 124-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10628421&dopt=Abstract
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Quiz case. Ulcerative colitis? Crohn's disease? Author(s): Mako EK, Mester AR, Gyorke T, Tarjan Z, Karlinger K. Source: European Journal of Radiology. 2000 September; 35(3): 209-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11203025&dopt=Abstract
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Randomized, double-blind comparison of 4 mg/kg versus 2 mg/kg intravenous cyclosporine in severe ulcerative colitis. Author(s): Van Assche G, D'Haens G, Noman M, Vermeire S, Hiele M, Asnong K, Arts J, D'Hoore A, Penninckx F, Rutgeerts P. Source: Gastroenterology. 2003 October; 125(4): 1025-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14517785&dopt=Abstract
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Re: Mann--melatonin for ulcerative colitis? Author(s): Jan JE, Freeman RD. Source: The American Journal of Gastroenterology. 2003 June; 98(6): 1446. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12818299&dopt=Abstract
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Relationship between disease activity indices and colonoscopic findings in ulcerative colitis. Author(s): Saddiq M, Hussain S, Farooq MA. Source: J Coll Physicians Surg Pak. 2003 February; 13(2): 120. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12685962&dopt=Abstract
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Relationship between gastrointestinal transit time and daily stool frequency in patients after Ileal J pouch-anal anastomosis for ulcerative colitis. Author(s): Tomita R, Fujisaki S, Tanjoh K. Source: American Journal of Surgery. 2004 January; 187(1): 76-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14706591&dopt=Abstract
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Repifermin (keratinocyte growth factor-2) for the treatment of active ulcerative colitis: a randomized, double-blind, placebo-controlled, dose-escalation trial. Author(s): Sandborn WJ, Sands BE, Wolf DC, Valentine JF, Safdi M, Katz S, Isaacs KL, Wruble LD, Katz J, Present DH, Loftus EV Jr, Graeme-Cook F, Odenheimer DJ, Hanauer SB. Source: Alimentary Pharmacology & Therapeutics. 2003 June 1; 17(11): 1355-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12786629&dopt=Abstract
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Restorative proctocolectomy with ileal pouch-anal anastomosis in very young patients with refractory ulcerative colitis. Author(s): Robb BW, Gang GI, Hershko DD, Stoops MM, Seeskin CS, Warner BW. Source: Journal of Pediatric Surgery. 2003 June; 38(6): 863-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12778382&dopt=Abstract
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Retropharyngeal and splenic aseptic abscesses treated with prednisone and cyclophosphamide in a patient with ulcerative colitis. Author(s): Andre M, Piette JC, Frances C, Wechsler B, Delevaux I, Aumaitre O. Source: Digestive Diseases and Sciences. 2003 June; 48(6): 1193-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12822884&dopt=Abstract
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Review article: Immunosuppressants in distal ulcerative colitis. Author(s): Falasco G, Zinicola R, Forbes A. Source: Alimentary Pharmacology & Therapeutics. 2002 February; 16(2): 181-7. Review. Erratum In: Aliment Pharmacol Ther 2002 May; 16(5): 1035. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11860400&dopt=Abstract
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Review article: medical treatment of severe ulcerative colitis. Author(s): Rizzello F, Gionchetti P, Venturi A, Campieri M. Source: Alimentary Pharmacology & Therapeutics. 2003 June; 17 Suppl 2: 7-10. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12786606&dopt=Abstract
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Risk of congenital abnormalities in children born to women with ulcerative colitis: a population-based, case-control study. Author(s): Norgard B, Puho E, Pedersen L, Czeizel AE, Sorensen HT. Source: The American Journal of Gastroenterology. 2003 September; 98(9): 2006-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14499779&dopt=Abstract
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Simultaneous assays for Clostridium difficile and faecal lactoferrin in ulcerative colitis. Author(s): Vaishnavi C, Kochhar R, Bhasin D, Thennarasu K, Singh K. Source: Trop Gastroenterol. 2003 January-March; 24(1): 13-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12974208&dopt=Abstract
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Sporadic adenomas in chronic ulcerative colitis. Author(s): Fogt F. Source: Zeitschrift Fur Gastroenterologie. 2003 April; 41(4): 343-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12695941&dopt=Abstract
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Steatohepatitis during methylprednisolone therapy for ulcerative colitis exacerbation. Author(s): Candelli M, Nista EC, Pignataro G, Zannoni G, de Pascalis B, Gasbarrini G, Gasbarrini A. Source: Journal of Internal Medicine. 2003 March; 253(3): 391-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12603510&dopt=Abstract
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Stool interleukin 1beta and interleukin 1 receptor antagonist concentrations in children with active ulcerative colitis and during recovery. Author(s): Wedrychowicz A, Stopyrowa J, Fyderek K, Miezynski W. Source: European Journal of Pediatrics. 2003 July; 162(7-8): 541-2. Epub 2003 April 26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12719967&dopt=Abstract
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Stress and ulcerative colitis: convincing the doubting Thomases. Author(s): Levenstein S. Source: The American Journal of Gastroenterology. 2003 October; 98(10): 2112-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14572553&dopt=Abstract
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Successful treatment of steroid resistant ulcerative colitis associated with severe autoimmune hemolytic anemia with oral microemulsion cyclosporin--a brief case report. Author(s): Molnar T, Szepes Z, Nagy F, Lonovics J. Source: The American Journal of Gastroenterology. 2003 May; 98(5): 1207-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12809856&dopt=Abstract
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Suppression of pro-inflammatory cytokine release by selective inhibition of inducible nitric oxide synthase in mucosal explants from patients with ulcerative colitis. Author(s): Kankuri E, Hamalainen M, Hukkanen M, Salmenpera P, Kivilaakso E, Vapaatalo H, Moilanen E. Source: Scandinavian Journal of Gastroenterology. 2003 February; 38(2): 186-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678336&dopt=Abstract
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Surgery for ulcerative colitis: is quality of life an issue? Author(s): Torres EA. Source: P R Health Sci J. 2001 September; 20(3): 209-10. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11776719&dopt=Abstract
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Surgical management of ulcerative colitis in the presence of primary sclerosing cholangitis. Author(s): Poritz LS, Koltun WA. Source: Diseases of the Colon and Rectum. 2003 February; 46(2): 173-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12576890&dopt=Abstract
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Survival and cause-specific mortality in ulcerative colitis: follow-up of a populationbased cohort in Copenhagen County. Author(s): Winther KV, Jess T, Langholz E, Munkholm P, Binder V. Source: Gastroenterology. 2003 December; 125(6): 1576-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14724807&dopt=Abstract
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Ten year follow up of ulcerative colitis patients with and without low grade dysplasia. Author(s): Lim CH, Dixon MF, Vail A, Forman D, Lynch DA, Axon AT. Source: Gut. 2003 August; 52(8): 1127-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12865270&dopt=Abstract
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TGF-beta1 production in inflammatory bowel disease: differing production patterns in Crohn's disease and ulcerative colitis. Author(s): Del Zotto B, Mumolo G, Pronio AM, Montesani C, Tersigni R, Boirivant M. Source: Clinical and Experimental Immunology. 2003 October; 134(1): 120-6. Erratum In: Clin Exp Immunol. 2003 November; 134(2): 365. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12974764&dopt=Abstract
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The color of dysplasia in ulcerative colitis. Author(s): Bernstein CN. Source: Gastroenterology. 2003 April; 124(4): 1135-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12671905&dopt=Abstract
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The correlation between quality of life and functional outcome in ulcerative colitis patients after proctocolectomy ileal pouch anal anastomosis. Author(s): Carmon E, Keidar A, Ravid A, Goldman G, Rabau M. Source: Colorectal Disease : the Official Journal of the Association of Coloproctology of Great Britain and Ireland. 2003 May; 5(3): 228-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12780883&dopt=Abstract
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The expression of matrix metalloproteinase matrilysin indicates the degree of inflammation in ulcerative colitis. Author(s): Matsuno K, Adachi Y, Yamamoto H, Goto A, Arimura Y, Endo T, Itoh F, Imai K. Source: Journal of Gastroenterology. 2003; 38(4): 348-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12743774&dopt=Abstract
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The impact of surgery for ulcerative colitis on fertility and sexual function in women. Author(s): Wolf JL. Source: Gastroenterology. 2002 January; 122(1): 226-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11781297&dopt=Abstract
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The influence of demographic and disease-related factors on health-related quality of life in patients with ulcerative colitis. Author(s): Hjortswang H, Jarnerot G, Curman B, Sandberg-Gertzen H, Tysk C, Blomberg B, Almer S, Strom M. Source: European Journal of Gastroenterology & Hepatology. 2003 September; 15(9): 1011-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12923375&dopt=Abstract
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The promoter methylation status of the DNA repair gene O6-methylguanine-DNA methyltransferase in ulcerative colitis. Author(s): Matsumura S, Oue N, Ito R, Nakayama H, Kitadai Y, Yokozaki H, Chayama K, Yasui W. Source: Virchows Archiv : an International Journal of Pathology. 2003 October; 443(4): 518-23. Epub 2003 August 15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12920593&dopt=Abstract
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The use of a mini-laparotomy in total abdominal colectomy for mucosal ulcerative colitis. Author(s): Nakagoe T, Sawai T, Tsuji T, Jibiki MA, Nanashima A, Yamaguchi H, Yasutake T, Ayabe H. Source: Hepatogastroenterology. 2003 May-June; 50(51): 704-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828065&dopt=Abstract
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Treatment of ulcerative colitis using fecal bacteriotherapy. Author(s): Borody TJ, Warren EF, Leis S, Surace R, Ashman O. Source: Journal of Clinical Gastroenterology. 2003 July; 37(1): 42-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12811208&dopt=Abstract
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Ulcerative colitis associated with aplastic anemia. Author(s): Kishikawa H, Nishida J, Nakano M, Hirano E, Morishita T, Ishii H. Source: Digestive Diseases and Sciences. 2003 July; 48(7): 1376-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12870799&dopt=Abstract
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Ulcerative colitis associated with Takayasu arteritis. Author(s): Bansal R, Aggarwal P, Handa R, Biswas A, Bandhu S, Wali JP. Source: International Journal of Cardiology. 2003 March; 88(1): 91-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12659990&dopt=Abstract
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Ulcerative colitis in a patient with Wiskott-Aldrich syndrome. Author(s): Folwaczny C, Ruelfs C, Walther J, Konig A, Emmerich B. Source: Endoscopy. 2002 October; 34(10): 840-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12244510&dopt=Abstract
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Ulcerative colitis in children: medical management. Author(s): Gremse DA, Crissinger KD. Source: Paediatric Drugs. 2002; 4(12): 807-15. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12431133&dopt=Abstract
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Ulcerative colitis in Kuwait: a review of 90 cases. Author(s): Al-Shamali MA, Kalaoui M, Patty I, Hasan F, Khajah A, Al-Nakib B. Source: Digestion. 2003; 67(4): 218-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966229&dopt=Abstract
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Ulcerative colitis, primary sclerosing cholangitis and coeliac disease: two cases and review of the literature. Author(s): Wurm P, Dixon AD, Rathbone BJ. Source: European Journal of Gastroenterology & Hepatology. 2003 July; 15(7): 815-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12811313&dopt=Abstract
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Ulcerative colitis, seronegative spondyloarthropathies and allergic diseases: the search for a link. Author(s): D'Arienzo A, Manguso F, Scarpa R, Astarita C, D'Armiento FP, Bennato R, Gargano D, Sanges M, Mazzacca G. Source: Scandinavian Journal of Gastroenterology. 2002 October; 37(10): 1156-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12408520&dopt=Abstract
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Ulcerative colitis: female fecundity before diagnosis, during disease, and after surgery compared with a population sample. Author(s): Ording Olsen K, Juul S, Berndtsson I, Oresland T, Laurberg S. Source: Gastroenterology. 2002 January; 122(1): 15-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11781275&dopt=Abstract
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Ursodeoxycholic acid as a chemopreventive agent in patients with ulcerative colitis and primary sclerosing cholangitis. Author(s): Pardi DS, Loftus EV Jr, Kremers WK, Keach J, Lindor KD. Source: Gastroenterology. 2003 April; 124(4): 889-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12671884&dopt=Abstract
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Usefulness of analysis of p53 alteration and observation of surface microstructure for diagnosis of ulcerative colitis-associated colorectal neoplasia. Author(s): Fujii S, Fujimori T, Chiba T. Source: J Exp Clin Cancer Res. 2003 March; 22(1): 107-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12725330&dopt=Abstract
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Validation of the inflammatory bowel disease questionnaire in Swedish patients with ulcerative colitis. Author(s): Hjortswang H, Jarnerot G, Curman B, Sandberg-Gertzen H, Tysk C, Blomberg B, Almer S, Strom M. Source: Scandinavian Journal of Gastroenterology. 2001 January; 36(1): 77-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11218243&dopt=Abstract
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Validation of the spanish version of the inflammatory bowel disease questionnaire on ulcerative colitis and Crohn's disease. Author(s): Lopez-Vivancos J, Casellas F, Badia X, Vilaseca J, Malagelada JR. Source: Digestion. 1999; 60(3): 274-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10343142&dopt=Abstract
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Validity of simple mucosal biopsy criteria combined with endoscopy predicting patients with ulcerative colitis ultimately requiring surgery: a multicenter study. Author(s): Tanaka M, Kusumi T, Oshitani N, Nishigami T, Iwao Y, Hatada Y, Sugita A, Yao T, Takano M, Iizuka B, Mukai M, Maeda K, Fukuda S, Morita T, Hara M, Saito H, Kudo H. Source: Scandinavian Journal of Gastroenterology. 2003 June; 38(6): 594-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12825866&dopt=Abstract
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Variability of the symptoms of chronic abacterial prostatitis/chronic pelvic pain syndrome during intermittent therapy with rectal prednisolone foam for ulcerative colitis. Author(s): Talbot M, Bates S. Source: International Journal of Std & Aids. 2001 November; 12(11): 752-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11589817&dopt=Abstract
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VEGF, basic-FGF, and TGF-beta in Crohn's disease and ulcerative colitis: a novel mechanism of chronic intestinal inflammation. Author(s): Kanazawa S, Tsunoda T, Onuma E, Majima T, Kagiyama M, Kikuchi K. Source: The American Journal of Gastroenterology. 2001 March; 96(3): 822-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11280558&dopt=Abstract
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Veno-occlusive disease, nodular regenerative hyperplasia and hepatocellular carcinoma after azathioprine treatment in a patient with ulcerative colitis. Author(s): Russmann S, Zimmermann A, Krahenbuhl S, Kern B, Reichen J. Source: European Journal of Gastroenterology & Hepatology. 2001 March; 13(3): 287-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11293451&dopt=Abstract
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Villous, hypermucinous mucosa in long standing ulcerative colitis shows high frequency of K-ras mutations. Author(s): Andersen SN, Lovig T, Clausen OP, Bakka A, Fausa O, Rognum TO. Source: Gut. 1999 November; 45(5): 686-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10517904&dopt=Abstract
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Vulvar lichen planus associated with ulcerative colitis. A case report. Author(s): Giomi B, Pestelli E, Massi D, Caproni M, Fabbri P. Source: J Reprod Med. 2003 March; 48(3): 209-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12698783&dopt=Abstract
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What dose of 5-aminosalicylic acid (mesalazine) in ulcerative colitis? Author(s): Riley SA. Source: Gut. 1998 June; 42(6): 761-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9691909&dopt=Abstract
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What functional outcomes and complications should be taught to the patient with ulcerative colitis or familial adenomatous polyposis who undergoes ileal pouch anal anastomosis? Author(s): Colwell JC, Gray M. Source: Journal of Wound, Ostomy, and Continence Nursing : Official Publication of the Wound, Ostomy and Continence Nurses Society / Wocn. 2001 July; 28(4): 184-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11452254&dopt=Abstract
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What happened to drug trials in ulcerative colitis? Problems, PPARs, placebos, and (possible) progress. Author(s): Kornbluth A. Source: The American Journal of Gastroenterology. 2001 December; 96(12): 3232-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11774930&dopt=Abstract
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What have we learned from the biological therapies in ulcerative colitis? Author(s): Pena AS. Source: The American Journal of Gastroenterology. 2001 June; 96(6): 1681-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11419814&dopt=Abstract
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What is the optimal strategy for colon cancer surveillance in patients with ulcerative colitis? Author(s): Bauer WM, Lashner BA. Source: Cleve Clin J Med. 1999 May; 66(5): 273, 277. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10330779&dopt=Abstract
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Wheat grass juice in the treatment of active distal ulcerative colitis: a randomized double-blind placebo-controlled trial. Author(s): Ben-Arye E, Goldin E, Wengrower D, Stamper A, Kohn R, Berry E. Source: Scandinavian Journal of Gastroenterology. 2002 April; 37(4): 444-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11989836&dopt=Abstract
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When can unfractionated heparin really be useful in the treatment of ulcerative colitis? Author(s): Papa A, Danese S, Gasbarrini G, Gasbarrini A. Source: Gastroenterology. 2001 April; 120(5): 1306-7; Author Reply 1307-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11288745&dopt=Abstract
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When should prophylactic colectomy be considered in patients with ulcerative colitis? Author(s): Lashner BA. Source: Cleve Clin J Med. 2003 March; 70(3): 221-2. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678211&dopt=Abstract
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Which immunosuppressors do you use to treat Crohn's disease and ulcerative colitis? In which order of priority and how worried are you about toxicity? Author(s): Scholmerich J. Source: Inflammatory Bowel Diseases. 1998 August; 4(3): 248-52; Discussion 253-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9741031&dopt=Abstract
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Which immunosuppressors do you use to treat Crohn's disease and ulcerative colitis? In which order of priority and how worried are you about toxicity? Author(s): Modigliani R. Source: Inflammatory Bowel Diseases. 1998 August; 4(3): 244-7; Discussion 253-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9741030&dopt=Abstract
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CHAPTER 2. NUTRITION AND ULCERATIVE COLITIS Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and ulcerative colitis.
Finding Nutrition Studies on Ulcerative Colitis The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail:
[email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.7 The IBIDS includes references and citations to both human and animal research studies. As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “ulcerative colitis” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.
7 Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.
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The following is a typical result when searching for recently indexed consumer information on ulcerative colitis: •
Nutritional support in chronic inflammatory bowel disease. Source: Kirschner, B.S. Nutrition-and-the-M.D (USA). (February 1986). volume 12(2) page 1-2.
Additional consumer oriented references include: •
Short-chain fatty acids in ulcerative colitis. Author(s): Department of Medicine, University of Toronto, Canada. Source: Kim, Y I Nutr-Revolume 1998 January; 56(1 Pt 1): 17-24 0029-6643
The following information is typical of that found when using the “Full IBIDS Database” to search for “ulcerative colitis” (or a synonym): •
23 cases of chronic nonspecific ulcerative colitis treated by acupuncture and moxibustion. Author(s): Department of Acupuncture and Moxibustion, Beijing Hospital of Traditional Chinese Medicine. Source: Zhang, X J-Tradit-Chin-Med. 1998 September; 18(3): 188-91 0254-6272
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Absence of effect on faecal microflora of long-term supplementation of dietary fibres in juvenile ulcerative colitis. Author(s): Department of Paediatrics, Karolinska Institutet, Huddinge University Hospital, Stockholm, Sweden. Source: Ejderhamn, J Nord, C E Strandvik, B Int-J-Clin-Pharmacol-Res. 1991; 11(5): 24752 0251-1649
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Alterations of the immune system in ulcerative colitis and Crohn's disease. Author(s): Department of Medicine, Washington University School of Medicine, Barnes Hospital, St. Louis, Missouri. Source: MacDermott, R P Stenson, W F Adv-Immunol. 1988; 42285-328 0065-2776
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An analysis of 10218 ulcerative colitis cases in China. Author(s): Department of Gastroenterology, Chinese PLA General Hospital of Jinan Command,25 Shifanlu,Jinan 250031,Shandong Province,China.
[email protected] Source: Jiang, Xue Liang Cui, Hui Fei World-J-Gastroenterol. 2002 February; 8(1): 158-61 1007-9327
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Calming ulcerative colitis. Source: Anonymous Health-News. 1998 June 25; 4(8): 6 1081-5880
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Catgut point-embedding therapy in treatment of 76 cases of ulcerative colitis. Author(s): Xuchang Municipal Hospital of Traditional Chinese Medicine, Henan Province 461000. Source: Xiao, G Zhou, G J-Tradit-Chin-Med. 2001 June; 21(2): 116-7 0254-6272
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Cerebral venous thrombosis in ulcerative colitis. Author(s): Department of Neurology, Neurosciences Center, All India Institute of Medical Sciences, New Delhi, 110029, India. Source: Srivastava, A K Khanna, N Sardana, V Gaekwad, S Prasad, K Behari, M NeurolIndia. 2002 June; 50(2): 215-7 0028-3886
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Chemoprevention of colorectal cancer in inflammatory bowel disease? A potential role for folate. Author(s): Gastroenterology Department, University Hospital, Heraklion, Greece.
[email protected] Source: Mouzas, I A Papavassiliou, E Koutroubakis, I Ital-J-Gastroenterol-Hepatol. 1998 August; 30(4): 421-5 1125-8055
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Cigarette smoking should not be prescribed for the treatment of ulcerative colitis. Author(s): Inflammatory Bowel Disease Clinic, Mayo Clinic, Rochester, Minnesota 55905, USA. Source: Tremaine, W J Inflamm-Bowel-Dis. 1998 November; 4(4): 324-5; discussion 327 1078-0998
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Clinical analysis and results of treatment of ulcerative colitis in children. Source: Iwanczak, F Kochanska, E Cader, J Stawarski, A Mater-Med-Pol. 1988 JanMarch; 20(1): 46-9 0025-5246
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Clinical study on 118 cases of ulcerative colitis treated by integration of traditional Chinese and Western medicine. Author(s): Kanshi Township Hospital, Yongding County, Fujian Province. Source: Chen, Q Zhang, H J-Tradit-Chin-Med. 1999 September; 19(3): 163-5 0254-6272
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Concanavalin A induced suppressor activity exerted by peripheral blood mononuclear cells--with special reference to chronic inflammatory bowel disease. Author(s): Medical Department C, Herlev Hospital, University of Copenhagen, Denmark. Source: Davidsen, B D Dan-Med-Bull. 1988 June; 35(3): 201-22 0907-8916
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Congenital Guillain-Barre syndrome associated with maternal inflammatory bowel disease is responsive to intravenous immunoglobulin. Author(s): Department of Neurology, Columbia University College of Physicians and Surgeons, Neurological Institute, New York, NY 10032, USA.
[email protected] Source: Bamford, N S Trojaborg, W Sherbany, A A De Vivo, D C Eur-J-Paediatr-Neurol. 2002; 6(2): 115-9 1090-3798
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Diet and inflammatory bowel disease: a case-control study. Author(s): Department of Epidemiology, Karolinska Institutet, Stockholm, Sweden. Source: Persson, P G Ahlbom, A Hellers, G Epidemiology. 1992 January; 3(1): 47-52 1044-3983
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Effect of fat and retinol loading on serum triglyceride and retinol levels in patients with ulcerative colitis. Author(s): National Institute of Food Hygiene and Nutrition, Budapest, Hungary. Source: Regoly Merei, A Ferencz, A Frenkl, R Gergely, A Zajkas, G Antal, M Nahrung. 1991; 35(1): 21-6 0027-769X
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Effect of short-term topical corticosteroid treatment on mucosal enzyme systems in patients with distal inflammatory bowel disease. Author(s): Department of General Internal Medicine, University of Bonn, Germany. Source: Scheurlen, C Allgayer, H Hardt, M Kruis, W Hepatogastroenterology. 1998 SepOctober; 45(23): 1539-45 0172-6390
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Effective maintenance leukocytapheresis for patients with steroid dependent or resistant ulcerative colitis. Author(s): Department of Medicine, Division of Gastroenterology, Social Insurance Chuo General Hospital, Hyakunincho, Tokyo, Japan.
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Source: Kondo, K Shinoda, T Yoshimoto, H Takazoe, M Hamada, T Ther-Apher. 2001 December; 5(6): 462-5 1091-6660 •
Efficacy and efficiency of oral microemulsion cyclosporin versus intravenous and soft gelatin capsule cyclosporin in the treatment of severe steroid-refractory ulcerative colitis: an open-label retrospective trial. Author(s): Department of Gastroenterology and Nutrition, Ospedale Molinette, Torino, Italy. Source: Actis, G C Aimo, G Priolo, G Moscato, D Rizzetto, M Pagni, R Inflamm-BowelDis. 1998 November; 4(4): 276-9 1078-0998
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Epidemiology of inflammatory bowel disease. Author(s): Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden. Source: Ekbom, A Nestle-Nutr-Workshop-Ser-Clin-Perform-Programme. 1999; 2: 7-18; discussion 18-21 1422-7584
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Etiology and pathophysiology of inflammatory bowel disease--environmental factors. Author(s): Klinik und Poliklinik fur Innere Medizin I, Klinikum der Universitat, Regensburg, Germany.
[email protected] Source: Andus, T Gross, V Hepatogastroenterology. 2000 Jan-February; 47(31): 29-43 0172-6390
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Evaluation of oral administration of folic and folinic acid to prevent folate deficiency in patients with inflammatory bowel disease treated with salicylazosulfapyridine. Author(s): First Medical Clinic, University of Bologna, Italy. Source: Pironi, L Cornia, G L Ursitti, M A Dallasta, M A Miniero, R Fasano, F Miglioli, M Barbara, L Int-J-Clin-Pharmacol-Res. 1988; 8(2): 143-8 0251-1649
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Glycoaminoglycan (GAG) deficiency in protective barrier as an underlying, primary cause of ulcerative colitis, Crohn's disease interstitial cystitis and possibly Reiter's syndrome. Source: Russell, A L Med-Hypotheses. 1999 April; 52(4): 297-301 0306-9877
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Histiocytic ulcerative colitis in three non-boxer dogs. Author(s): Department of Small Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing 48824, USA. Source: Stokes, J E Kruger, J M Mullaney, T Holan, K Schall, W J-Am-Anim-Hosp-Assoc. 2001 Sep-October; 37(5): 461-5 0587-2871
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Hodgkin s disease with nephrotic syndrome as a complication of ulcerative colitis: case report. Author(s): Division of Hematology, Department of Medicine, Zagreb University Hospital Center, Kispaticeva 12, Croatia.
[email protected] Source: Basic Jukic, N Radman, I Roncevic, T Jakic Razumovic, J Croat-Med-J. 2002 October; 43(5): 573-5 0353-9504
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Immunology of inflammatory bowel disease. Author(s): Department of Medicine, Washington University School of Medicine, St. Louis, Mo. Source: Stenson, W F MacDermott, R P Year-Immunol. 1989; 4286-95 0256-2308
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Inflammatory bowel disease in Japan: studies of epidemiology and etiopathogenesis. Author(s): First Department of Internal Medicine, Hirosaki University School of Medicine, Japan. Source: Yoshida, Y Murata, Y Med-Clin-North-Am. 1990 January; 74(1): 67-90 0025-7125
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Infliximab in the treatment of severe, steroid-refractory ulcerative colitis: a pilot study. Author(s): Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital, Boston 02114, USA. Source: Sands, B E Tremaine, W J Sandborn, W J Rutgeerts, P J Hanauer, S B Mayer, L Targan, S R Podolsky, D K Inflamm-Bowel-Dis. 2001 May; 7(2): 83-8 1078-0998
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Interleukin-10 (IL-10) genotypes in inflammatory bowel disease. Author(s): School of Biological Sciences, University of Manchester, UK. Source: Tagore, A Gonsalkorale, W M Pravica, V Hajeer, A H McMahon, R Whorwell, P J Sinnott, P J Hutchinson, I V Tissue-Antigens. 1999 October; 54(4): 386-90 0001-2815
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Intestinal microflora as a therapeutic target in inflammatory bowel disease. Author(s): Second Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume 830-0011, Japan. Source: Mitsuyama, K Toyonaga, A Sata, M J-Gastroenterol. 2002 November; 37 Suppl 14: 73-7 0944-1174
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I've heard that the nicotine skin patch is a new treatment for ulcerative colitis. Is this true? Source: Anonymous Mayo-Clin-Health-Lett. 1998 February; 16(2): 8 0741-6245
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Long-term effects of a single course of nicotine treatment in acute ulcerative colitis: remission maintenance in a 12-month follow-up study. Author(s): Gastroenterology Unit, S. Raffaele Hospital, Milan, Italy.
[email protected] Source: Guslandi, M Int-J-Colorectal-Dis. 1999 November; 14(4-5): 261-2 0179-1958
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Management of fulminating ulcerative colitis. Author(s): Second Department of Surgery, University Central Hospital, Helsinki, Finland. Source: Mikkola, K A Jarvinen, H J Ann-Chir-Gynaecol. 1992; 81(1): 37-41 0355-9521
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Managing Crohn's disease and ulcerative colitis. Author(s): St Thomas Hospital, London. Source: Evans, S Ciclitira, P J Practitioner. 1999 April; 243(1597): 307-14 0032-6518
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Metabolism of vitamin A in inflammatory bowel disease. Author(s): Department of Gastroenterology and Metabolism, Medical Center of Postgraduate Education, Warsaw, Poland. Source: Janczewska, I Bartnik, W Butruk, E Tomecki, R Kazik, E Ostrowski, J Hepatogastroenterology. 1991 October; 38(5): 391-5 0172-6390
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Mucosal dysplasia of the colon in patients with chronic ulcerative colitis. Source: Lashner, B.A. Pennington-Cent-Nutr-Ser. Baton Rouge : Louisiana State University Press. 1993. volume 3 page 209-219.
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Prediction of treatment refractoriness in ulcerative colitis and Crohn's disease--do we have reliable markers? Author(s): Department of Internal Medicine I, University of Regensburg, Germany. Source: Gelbmann, C M Inflamm-Bowel-Dis. 2000 May; 6(2): 123-31 1078-0998
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Probiotics and inflammatory bowel disease: is there a scientific rationale? Author(s): Department of Medicine, University College Cork, National University of Ireland. Source: Shanahan, F Inflamm-Bowel-Dis. 2000 May; 6(2): 107-15 1078-0998
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Reduced bone mineral density and unbalanced bone metabolism in patients with inflammatory bowel disease. Author(s): Department of Internal Medicine, University of Essen, Germany. Source: Schulte, C Dignass, A U Mann, K Goebell, H Inflamm-Bowel-Dis. 1998 November; 4(4): 268-75 1078-0998
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Simultaneous onset of pyoderma gangrenosum and bitemporal abscesses of the upper eyelids during a flare of ulcerative colitis. Author(s): Department of Medicine I, University of Ulm, Germany. Source: von Tirpitz, C Buchwald, H J Lang, G K Adler, G Reinshagen, M InflammBowel-Dis. 1998 May; 4(2): 98-100 1078-0998
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TCM differential treatment of 57 cases of chronic gastritis complicated by ulcerative colitis. Author(s): Second Affiliated Hospital, Guangxi TCM College, Nanning. Source: Meng, M J-Tradit-Chin-Med. 1999 March; 19(1): 10-5 0254-6272
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The relationship between habits of food consumption and reported reactions to food in people with inflammatory bowel disease--testing the limits. Author(s): School of Nursing, University of British Columbia, Vancouver, Canada.
[email protected] Source: Joachim, G Nutr-Health. 1999; 13(2): 69-83 0260-1060
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Topical treatment of ulcerative colitis. Author(s): Division of Gastroenterology, University of Calgary, Alberta, Canada. Source: Sutherland, L R Med-Clin-North-Am. 1990 January; 74(1): 119-31 0025-7125
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Transdermal nicotine decreases mucosal IL-8 expression but has no effect on mucin gene expression in ulcerative colitis. Author(s): Laboratoire de recherche sur les MICI (CRI 4U004B), Centre Hospitalier Universitaire (CHU), Lille, France. Source: Louvet, B Buisine, M P Desreumaux, P Tremaine, W J Aubert, J P Porchet, N Capron, M Cortot, A Colombel, J F Sandborn, W J Inflamm-Bowel-Dis. 1999 August; 5(3): 174-81 1078-0998
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Transepithelial transport processes at the intestinal mucosa in inflammatory bowel disease. Author(s): Department of General Surgery, Westfalian Wilhelms University, Munster, Germany.
[email protected] Source: Schurmann, G Bruwer, M Klotz, A Schmid, K W Senninger, N Zimmer, K P IntJ-Colorectal-Dis. 1999 February; 14(1): 41-6 0179-1958
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Treating inflammatory bowel disease. Author(s): Chesterfield and North Derbyshire Royal Hospital NHS Trust. Source: Shepherd, M Nurs-Times. 2000 August 3; 96(31 Suppl): 18 0954-7762
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Treatment of ulcerative colitis by feeding with germinated barley foodstuff: first report of a multicenter open control trial. Author(s): Nutrient Food and Feed Division, Kirin Brewery, 10-1-2 Shinkawa, Chuo-ku, Tokyo 104-8288, Japan. Source: Kanauchi, O Suga, T Tochihara, M Hibi, T Naganuma, M Homma, T Asakura, H Nakano, H Takahama, K Fujiyama, Y Andoh, A Shimoyama, T Hida, N Haruma, K Koga, H Mitsuyama, K Sata, M Fukuda, M Kojima, A Bamba, T J-Gastroenterol. 2002 November; 37 Suppl 14: 67-72 0944-1174
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Ulcerative colitis in Thailand: a clinical study and long term follow-up. Author(s): Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand. Source: Pongprasobchai, S Manatsathit, S Leelakusolvong, S Sattawatthamrong, Y Boonyapisit, S J-Med-Assoc-Thai. 2001 September; 84(9): 1281-8 0125-2208
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Update on medical management of inflammatory bowel disease: ulcerative colitis. Author(s): Section of Gastroenterology and Nutrition, University of Chicago, Pritzker School of Medicine, Chicago, IL, USA. Source: Hanauer, S B Rev-Gastroenterol-Disord. 2001; 1(4): 169-76 1533-001X
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What do patients want to know about their inflammatory bowel disease? Author(s): Istituto di Medicina Interna, Divisione di Gastroenterologia, Universita di Padova, Italy. Source: Martin, A Leone, L Castagliuolo, I Di Mario, F Naccarato, R Ital-J-Gastroenterol. 1992 Nov-December; 24(9): 477-80 0392-0623
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What is the association of primary sclerosing cholangitis with sex and inflammatory bowel disease in Turkish patients? Author(s): Department of Gastroenterology, School of Medicine, Hacettepe University, Ankara, Turkey. Source: Bayraktar, Y Arslan, S Saglam, F Uzunalimoglu, B Kayhan, B Hepatogastroenterology. 1998 Nov-December; 45(24): 2064-72 0172-6390
Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: •
healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0
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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov
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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov
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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/
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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/
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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/
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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/
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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/
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Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html
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Google: http://directory.google.com/Top/Health/Nutrition/
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Healthnotes: http://www.healthnotes.com/
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Open Directory Project: http://dmoz.org/Health/Nutrition/
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Yahoo.com: http://dir.yahoo.com/Health/Nutrition/
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WebMDHealth: http://my.webmd.com/nutrition
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
The following is a specific Web list relating to ulcerative colitis; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
Vitamins Folic Acid Source: Healthnotes, Inc.; www.healthnotes.com Folic Acid Alternative names: Vitamin B9 (Folic Acid) Source: Integrative Medicine Communications; www.drkoop.com Vitamin A Source: Prima Communications, Inc.www.personalhealthzone.com Vitamin A Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10066,00.html Vitamin B9 (Folic Acid) Alternative names: Folate Source: Integrative Medicine Communications; www.drkoop.com Vitamin K Source: Prima Communications, Inc.www.personalhealthzone.com
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Minerals Biotin Source: Healthnotes, Inc.; www.healthnotes.com
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Folate Alternative names: Vitamin B9 (Folic Acid) Source: Integrative Medicine Communications; www.drkoop.com Iron Source: Healthnotes, Inc.; www.healthnotes.com Sulfur Source: Integrative Medicine Communications; www.drkoop.com Zinc Source: Integrative Medicine Communications; www.drkoop.com Zinc Source: Prima Communications, Inc.www.personalhealthzone.com Zinc Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10071,00.html •
Food and Diet Omega-3 Fatty Acids Source: Integrative Medicine Communications; www.drkoop.com Saturated Fats Source: Healthnotes, Inc.; www.healthnotes.com Trans-Fats Source: Healthnotes, Inc.; www.healthnotes.com
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CHAPTER 3. ALTERNATIVE MEDICINE AND ULCERATIVE COLITIS Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to ulcerative colitis. At the conclusion of this chapter, we will provide additional sources.
National Center for Complementary and Alternative Medicine The National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (http://nccam.nih.gov/) has created a link to the National Library of Medicine’s databases to facilitate research for articles that specifically relate to ulcerative colitis and complementary medicine. To search the database, go to the following Web site: http://www.nlm.nih.gov/nccam/camonpubmed.html. Select “CAM on PubMed.” Enter “ulcerative colitis” (or synonyms) into the search box. Click “Go.” The following references provide information on particular aspects of complementary and alternative medicine that are related to ulcerative colitis: •
(51)CrEDTA colonic permeability and therapy response in patients with ulcerative colitis. Author(s): Arslan G, Atasever T, Cindoruk M, Yildirim IS. Source: Nuclear Medicine Communications. 2001 September; 22(9): 997-1001. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11505209&dopt=Abstract
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23 cases of chronic nonspecific ulcerative colitis treated by acupuncture and moxibustion. Author(s): Zhang X. Source: J Tradit Chin Med. 1998 September; 18(3): 188-91. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10453610&dopt=Abstract
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A 66-year-old woman with ulcerative colitis. Author(s): Peppercorn MA. Source: Jama : the Journal of the American Medical Association. 1998 March 25; 279(12): 949-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9544770&dopt=Abstract
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A different therapeutic approach in patients with severe ulcerative colitis: hyperbaric oxygen treatment. Author(s): Gurbuz AK, Elbuken E, Yazgan Y, Yildiz S. Source: Southern Medical Journal. 2003 June; 96(6): 632-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12938799&dopt=Abstract
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A double-blind, randomized, placebo-controlled trial of essential fatty acid supplementation in the maintenance of remission of ulcerative colitis. Author(s): Middleton SJ, Naylor S, Woolner J, Hunter JO. Source: Alimentary Pharmacology & Therapeutics. 2002 June; 16(6): 1131-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12030955&dopt=Abstract
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A new prebiotic from germinated barley for nutraceutical treatment of ulcerative colitis. Author(s): Bamba T, Kanauchi O, Andoh A, Fujiyama Y. Source: Journal of Gastroenterology and Hepatology. 2002 August; 17(8): 818-24. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12164955&dopt=Abstract
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A pilot trial of Saccharomyces boulardii in ulcerative colitis. Author(s): Guslandi M, Giollo P, Testoni PA. Source: European Journal of Gastroenterology & Hepatology. 2003 June; 15(6): 697-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12840682&dopt=Abstract
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A randomized controlled study of evening primrose oil and fish oil in ulcerative colitis. Author(s): Greenfield SM, Green AT, Teare JP, Jenkins AP, Punchard NA, Ainley CC, Thompson RP. Source: Alimentary Pharmacology & Therapeutics. 1993 April; 7(2): 159-66. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8485269&dopt=Abstract
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A rare isoenzyme of alkaline phosphatase in 4 patients with ulcerative colitis. Author(s): Streifler C, Schnitzer N, Harell A. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 1972 April; 38(1): 244-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4624227&dopt=Abstract
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A review of recent clinical trials of the nutritional supplement Chlorella pyrenoidosa in the treatment of fibromyalgia, hypertension, and ulcerative colitis. Author(s): Merchant RE, Andre CA. Source: Alternative Therapies in Health and Medicine. 2001 May-June; 7(3): 79-91. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11347287&dopt=Abstract
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Absorption of 51Cr-EDTA in ulcerative colitis following rectal instillation. Author(s): Rask-Madsen J, Schwartz M. Source: Scandinavian Journal of Gastroenterology. 1970; 5(5): 361-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4989516&dopt=Abstract
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Allergic and psychogenic factors in ulcerative colitis in children. Author(s): Schapiro S. Source: Gp. 1967 January; 35(1): 110-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6037479&dopt=Abstract
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An analysis of 10218 ulcerative colitis cases in China. Author(s): Jiang XL, Cui HF. Source: World Journal of Gastroenterology : Wjg. 2002 February; 8(1): 158-61. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11833094&dopt=Abstract
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An evaluation of the effectiveness of psychotherapy in the treatment of ulcerative colitis. Author(s): O'CONNER JF, DANIELS G, FLOOD C, KARUSH A, MOSES L, STERN LO. Source: Annals of Internal Medicine. 1964 April; 60: 587-602. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14138879&dopt=Abstract
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An open trial of Cedemin, a Gingko biloba extract with PAF-antagonistic effects for ulcerative colitis. Author(s): Sandberg-Gertzen H. Source: The American Journal of Gastroenterology. 1993 April; 88(4): 615-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8470656&dopt=Abstract
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Assessment of mucosal inflammation and circulation in response to probiotics in patients operated with ileal pouch anal anastomosis for ulcerative colitis. Author(s): Laake KO, Line PD, Aabakken L, Lotveit T, Bakka A, Eide J, Roseth A, Grzyb K, Bjorneklett A, Vatn MH. Source: Scandinavian Journal of Gastroenterology. 2003 April; 38(4): 409-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12739713&dopt=Abstract
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Bacteria as the cause of ulcerative colitis. Author(s): Campieri M, Gionchetti P.
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Source: Gut. 2001 January; 48(1): 132-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11115835&dopt=Abstract •
Betel nut and smoking. Are they both protective in ulcerative colitis? A pilot study. Author(s): Lee CN, Jayanthi V, McDonald B, Probert CS, Mayberry JF. Source: Arquivos De Gastroenterologia. 1996 January-March; 33(1): 3-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8762679&dopt=Abstract
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Biological therapies for ulcerative colitis. Author(s): Sands BE. Source: Acta Gastroenterol Belg. 2001 April-June; 64(2): 205-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11475137&dopt=Abstract
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Bowman-Birk inhibitor concentrate reduces colon inflammation in mice with dextran sulfate sodium-induced ulcerative colitis. Author(s): Ware JH, Wan XS, Newberne P, Kennedy AR. Source: Digestive Diseases and Sciences. 1999 May; 44(5): 986-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10235608&dopt=Abstract
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Castor oil or senna preparation before colonoscopy for inactive chronic ulcerative colitis. Author(s): Gould SR, Williams CB. Source: Gastrointestinal Endoscopy. 1982 February; 28(1): 6-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7056466&dopt=Abstract
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Catgut point-embedding therapy in treatment of 76 cases of ulcerative colitis. Author(s): Xiao G, Zhou G. Source: J Tradit Chin Med. 2001 June; 21(2): 116-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11498899&dopt=Abstract
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Children with ulcerative colitis: their own perception of the disease. Author(s): McDermott JF Jr. Source: Psychosomatics. 1966 May-June; 7(3): 163-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5931739&dopt=Abstract
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Clinical study on 118 cases of ulcerative colitis treated by integration of traditional Chinese and Western medicine. Author(s): Chen Q, Zhang H. Source: J Tradit Chin Med. 1999 September; 19(3): 163-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10921142&dopt=Abstract
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Colonic motility in ulcerative colitis after opiate administration. Author(s): Garrett JM, Sauer WG, Moertel CG. Source: Gastroenterology. 1967 July; 53(1): 93-100. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4381766&dopt=Abstract
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Comparison of omega-3 fatty acids and sulfasalazine in ulcerative colitis. Author(s): Dichi I, Frenhane P, Dichi JB, Correa CR, Angeleli AY, Bicudo MH, Rodrigues MA, Victoria CR, Burini RC. Source: Nutrition (Burbank, Los Angeles County, Calif.). 2000 February; 16(2): 87-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10696629&dopt=Abstract
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Dietary monounsaturated n-3 and n-6 long-chain polyunsaturated fatty acids affect cellular antioxidant defense system in rats with experimental ulcerative colitis induced by trinitrobenzene sulfonic acid. Author(s): Nieto N, Fernandez MI, Torres MI, Rios A, Suarez MD, Gil A. Source: Digestive Diseases and Sciences. 1998 December; 43(12): 2676-87. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9881500&dopt=Abstract
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Dietary polyunsaturated fatty acids improve histological and biochemical alterations in rats with experimental ulcerative colitis. Author(s): Nieto N, Torres MI, Rios A, Gil A. Source: The Journal of Nutrition. 2002 January; 132(1): 11-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11773501&dopt=Abstract
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Dietary supplementation of catechins and alpha-tocopherol accelerates the healing of trinitrobenzene sulfonic acid-induced ulcerative colitis in rats. Author(s): Sato K, Kanazawa A, Ota N, Nakamura T, Fujimoto K. Source: J Nutr Sci Vitaminol (Tokyo). 1998 December; 44(6): 769-78. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10197308&dopt=Abstract
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Dietary supplementation with fish oil in ulcerative colitis. Author(s): Stenson WF, Cort D, Rodgers J, Burakoff R, DeSchryver-Kecskemeti K, Gramlich TL, Beeken W. Source: Annals of Internal Medicine. 1992 April 15; 116(8): 609-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1312317&dopt=Abstract
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Double-blind comparison of an oral Escherichia coli preparation and mesalazine in maintaining remission of ulcerative colitis. Author(s): Kruis W, Schutz E, Fric P, Fixa B, Judmaier G, Stolte M. Source: Alimentary Pharmacology & Therapeutics. 1997 October; 11(5): 853-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9354192&dopt=Abstract
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Downregulation of electroacupuncture at ST36 on TNF-alpha in rats with ulcerative colitis. Author(s): Tian L, Huang YX, Tian M, Gao W, Chang Q. Source: World Journal of Gastroenterology : Wjg. 2003 May; 9(5): 1028-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12717850&dopt=Abstract
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Effect of folate supplementation on the incidence of dysplasia and cancer in chronic ulcerative colitis. Author(s): Gomez G. Source: Gastroenterology. 1991 June; 100(6): 1789-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1859539&dopt=Abstract
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Effect of folate supplementation on the incidence of dysplasia and cancer in chronic ulcerative colitis. A case-control study. Author(s): Lashner BA, Heidenreich PA, Su GL, Kane SV, Hanauer SB. Source: Gastroenterology. 1989 August; 97(2): 255-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2568304&dopt=Abstract
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Effects of Boswellia serrata gum resin in patients with ulcerative colitis. Author(s): Gupta I, Parihar A, Malhotra P, Singh GB, Ludtke R, Safayhi H, Ammon HP. Source: European Journal of Medical Research. 1997 January; 2(1): 37-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9049593&dopt=Abstract
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Effects of smoking on the urine excretion of oral 51Cr EDTA in ulcerative colitis. Author(s): Benoni C, Prytz H. Source: Gut. 1998 May; 42(5): 656-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9659159&dopt=Abstract
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Efficacy of use of colonoscopy in dextran sulfate sodium induced ulcerative colitis in rats: the evaluation of the effects of antioxidant by colonoscopy. Author(s): Ahn BO, Ko KH, Oh TY, Cho H, Kim WB, Lee KJ, Cho SW, Hahm KB. Source: International Journal of Colorectal Disease. 2001 June; 16(3): 174-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11459291&dopt=Abstract
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Evaluation of antigenicity of germinated barley foodstuff for the treatment of ulcerative colitis in a chronic murine colitis model. Author(s): Kanauchi O, Serizawa I, Matsumura T, Fukuda Y, Satomi M. Source: International Journal of Molecular Medicine. 2001 February; 7(2): 143-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11172616&dopt=Abstract
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Family research on the problem of ulcerative colitis. Author(s): Jackson DD, Yalom I.
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Source: Archives of General Psychiatry. 1966 October; 15(4): 410-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5954717&dopt=Abstract •
Fatal outcome in untreated adolescent ulcerative colitis: an unusual case of child neglect. Author(s): Jackson DL, Korbin J, Youngner S, Carter KJ, Robertson AL Jr. Source: Critical Care Medicine. 1983 October; 11(10): 832-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6617225&dopt=Abstract
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Fish oil fatty acid supplementation in active ulcerative colitis: a double-blind, placebo-controlled, crossover study. Author(s): Aslan A, Triadafilopoulos G. Source: The American Journal of Gastroenterology. 1992 April; 87(4): 432-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1553930&dopt=Abstract
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Fish oil supplementation and ulcerative colitis. Author(s): Gorson DM. Source: Annals of Internal Medicine. 1992 September 15; 117(6): 535; Author Reply 536. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1503361&dopt=Abstract
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Folate supplementation in ulcerative colitis. Author(s): Ransohoff DF. Source: Gastroenterology. 1990 February; 98(2): 544. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2295414&dopt=Abstract
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Folic acid supplementation and cell kinetics of rectal mucosa in patients with ulcerative colitis. Author(s): Biasco G, Zannoni U, Paganelli GM, Santucci R, Gionchetti P, Rivolta G, Miniero R, Pironi L, Calabrese C, Di Febo G, Miglioli M. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 1997 June; 6(6): 469-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9184782&dopt=Abstract
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Gastric emptying function after ileal J pouch-anal anastomosis for ulcerative colitis. Author(s): Tomita R, Fujisaki S, Tanjoh K. Source: Surgery. 2004 January; 135(1): 81-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14694304&dopt=Abstract
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Hodgkin s disease with nephrotic syndrome as a complication of ulcerative colitis: case report. Author(s): Basic-Jukic N, Radman I, Roncevic T, Jakic-Razumovic J.
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Source: Croatian Medical Journal. 2002 October; 43(5): 573-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12402399&dopt=Abstract •
Hyperbaric oxygen therapy for severe ulcerative colitis. Author(s): Buchman AL, Fife C, Torres C, Smith L, Aristizibal J. Source: Journal of Clinical Gastroenterology. 2001 October; 33(4): 337-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11588553&dopt=Abstract
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Hypnosis and the treatment of ulcerative colitis and Crohn's disease. Author(s): Schafer DW. Source: Am J Clin Hypn. 1997 October; 40(2): 111-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9385722&dopt=Abstract
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Idiopathic ulcerative colitis in the African: a report of 4 cases. Author(s): Billinghurst JR, Welchman JM. Source: British Medical Journal. 1966 January 22; 5481: 211-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5902054&dopt=Abstract
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Impact on the composition of the faecal flora by a new probiotic preparation: preliminary data on maintenance treatment of patients with ulcerative colitis. Author(s): Venturi A, Gionchetti P, Rizzello F, Johansson R, Zucconi E, Brigidi P, Matteuzzi D, Campieri M. Source: Alimentary Pharmacology & Therapeutics. 1999 August; 13(8): 1103-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10468688&dopt=Abstract
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In vivo butyrate metabolism and colonic permeability in extensive ulcerative colitis. Author(s): Den Hond E, Hiele M, Evenepoel P, Peeters M, Ghoos Y, Rutgeerts P. Source: Gastroenterology. 1998 September; 115(3): 584-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9721155&dopt=Abstract
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Increasing fecal butyrate in ulcerative colitis patients by diet: controlled pilot study. Author(s): Hallert C, Bjorck I, Nyman M, Pousette A, Granno C, Svensson H. Source: Inflammatory Bowel Diseases. 2003 March; 9(2): 116-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12769445&dopt=Abstract
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Inflammatory bowel disease Part 1: ulcerative colitis--pathophysiology and conventional and alternative treatment options. Author(s): Head KA, Jurenka JS. Source: Alternative Medicine Review : a Journal of Clinical Therapeutic. 2003 August; 8(3): 247-83. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12946238&dopt=Abstract
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Influence of intravenous n-3 lipid supplementation on fatty acid profiles and lipid mediator generation in a patient with severe ulcerative colitis. Author(s): Grimminger F, Fuhrer D, Papavassilis C, Schlotzer E, Mayer K, Heuer KU, Kiss L, Walmrath D, Piberhofer S, Lubbecke F, et al. Source: European Journal of Clinical Investigation. 1993 November; 23(11): 706-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8307090&dopt=Abstract
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Inhibition of soybean lipoxygenase by sulfasalazine and 5-aminosalicylic acid: a possible mode of action in ulcerative colitis. Author(s): Sircar JC, Schwender CF, Carethers ME. Source: Biochemical Pharmacology. 1983 January 1; 32(1): 170-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6131674&dopt=Abstract
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Intestinal bacteria and ulcerative colitis. Author(s): Cummings JH, Macfarlane GT, Macfarlane S. Source: Curr Issues Intest Microbiol. 2003 March; 4(1): 9-20. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12691258&dopt=Abstract
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Intestinal permeability to 51Cr-ethylenediaminetetraacetate in patients with ulcerative colitis. Author(s): Zuckerman MJ, Watts MT. Source: The American Journal of Gastroenterology. 1993 November; 88(11): 1978-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8237961&dopt=Abstract
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Ispaghula husk may relieve gastrointestinal symptoms in ulcerative colitis in remission. Author(s): Hallert C, Kaldma M, Petersson BG. Source: Scandinavian Journal of Gastroenterology. 1991 July; 26(7): 747-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1654592&dopt=Abstract
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Kui jie qing in the treatment of chronic non-specific ulcerative colitis. Author(s): Wang B, Ren S, Feng W, Zhong Z, Qin C. Source: J Tradit Chin Med. 1997 March; 17(1): 10-3. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10437236&dopt=Abstract
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Long-term double-blind study on the influence of dietary fibres on faecal bile acid excretion in juvenile ulcerative colitis. Author(s): Ejderhamn J, Hedenborg G, Strandvik B. Source: Scandinavian Journal of Clinical and Laboratory Investigation. 1992 November; 52(7): 697-706. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1360699&dopt=Abstract
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Maintenance of remission in ulcerative colitis with sulphasalazine or a high-fibre diet: a clinical trial. Author(s): Davies PS, Rhodes J. Source: British Medical Journal. 1978 June 10; 1(6126): 1524-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=26448&dopt=Abstract
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Microsatellite instability in non-neoplastic mucosa of patients with ulcerative colitis: effect of folate supplementation. Author(s): Cravo ML, Albuquerque CM, Salazar de Sousa L, Gloria LM, Chaves P, Dias Pereira A, Nobre Leitao C, Quina MG, Costa Mira F. Source: The American Journal of Gastroenterology. 1998 November; 93(11): 2060-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9820373&dopt=Abstract
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Mormons, smoking, and ulcerative colitis. Author(s): Penny WJ, Penny E, Mayberry JF, Rhodes J. Source: Lancet. 1983 December 3; 2(8362): 1315. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6139666&dopt=Abstract
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Morphological study on colonic pathology in ulcerative colitis treated by moxibustion. Author(s): Wu HG, Zhou LB, Shi DR, Liu SM, Liu HR, Zhang BM, Chen HP, Zhang LS. Source: World Journal of Gastroenterology : Wjg. 2000 December; 6(6): 861-865. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11819709&dopt=Abstract
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Mucosal inflammatory cytokine production by intestinal biopsies in patients with ulcerative colitis and Crohn's disease. Author(s): Reimund JM, Wittersheim C, Dumont S, Muller CD, Baumann R, Poindron P, Duclos B. Source: Journal of Clinical Immunology. 1996 May; 16(3): 144-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8734357&dopt=Abstract
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n-3 fatty acids only delay early relapse of ulcerative colitis in remission. Author(s): Loeschke K, Ueberschaer B, Pietsch A, Gruber E, Ewe K, Wiebecke B, Heldwein W, Lorenz R. Source: Digestive Diseases and Sciences. 1996 October; 41(10): 2087-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8888725&dopt=Abstract
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Non-pathogenic Escherichia coli versus mesalazine for the treatment of ulcerative colitis: a randomised trial. Author(s): Rembacken BJ, Snelling AM, Hawkey PM, Chalmers DM, Axon AT. Source: Lancet. 1999 August 21; 354(9179): 635-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10466665&dopt=Abstract
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Non-specific ulcerative colitis in Bedouin Arabs. Author(s): Salem SN, Shubair KS. Source: Lancet. 1967 March 4; 1(7488): 473-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4164069&dopt=Abstract
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Notes on a case of ulcerative colitis. Author(s): Klein HS. Source: The International Journal of Psycho-Analysis. 1965 July; 46(3): 342-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5834997&dopt=Abstract
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Novel therapies in the treatment of ulcerative colitis. Author(s): Tuvlin JA, Kane SV. Source: Expert Opinion on Investigational Drugs. 2003 March; 12(3): 483-90. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12605569&dopt=Abstract
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Nutritional therapies for ulcerative colitis: literature review, chart review study, and future research. Author(s): Edman JS, Williams WH, Atkins RC. Source: Alternative Therapies in Health and Medicine. 2000 January; 6(1): 55-63. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10631823&dopt=Abstract
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Obstructed defecation after undiverted ileoanal pouch reconstruction for ulcerative colitis: pharmacologic approach. Report of a case. Author(s): Abbasakoor F, Evans A, Stephenson BM. Source: Diseases of the Colon and Rectum. 2000 November; 43(11): 1599-600. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11089600&dopt=Abstract
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Probiotic therapy with E. coli for ulcerative colitis: take the good with the bad. Author(s): Faubion WA, Sandborn WJ. Source: Gastroenterology. 2000 March; 118(3): 630-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10702217&dopt=Abstract
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Prognostic implications of psychiatric diagnosis in ulcerative colitis. Author(s): O'Connor JF, Daniels G, Karush A, Flood C, Stern LO. Source: Psychosomatic Medicine. 1966 July-August; 28(4): 375-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5966668&dopt=Abstract
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Psychiatric observations on attacks of gout in a patient with ulcerative colitis. Report of a case. Author(s): Castelnuovo-Tedesco P.
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Source: Psychosomatic Medicine. 1966 November-December; 28(6): 781-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5972491&dopt=Abstract •
Psychiatric study of a consecutive series of 34 patients with ulcerative colitis. Author(s): Feldman F, Cantor D, Soll S, Bachrach W. Source: British Medical Journal. 1967 July 1; 3(556): 14-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6028848&dopt=Abstract
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Psychologic aspect of ulcerative colitis in children. Author(s): Josselyn IM, Littner N, Spurlock J. Source: J Am Med Womens Assoc. 1966 April; 21(4): 303-6. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4223411&dopt=Abstract
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Psychosomatic factors in ulcerative colitis in children. Author(s): CROHN BB. Source: N Y State J Med. 1963 May 15; 63: 1456-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14023926&dopt=Abstract
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Psychosomatic medicine. XII. Psychosomatic aspects of ulcerative colitis. Author(s): Shields R. Source: The Practitioner. 1972 December; 209(254): 851-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4654758&dopt=Abstract
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Pyoderma gangrenosum induced by acupuncture in a patient with ulcerative colitis. Author(s): Castro-Duran J, Martin-Armada M, Jimenez-Alonso J. Source: Archives of Internal Medicine. 2000 August 14-28; 160(15): 2394. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10927741&dopt=Abstract
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Randomized clinical trial of Plantago ovata seeds (dietary fiber) as compared with mesalamine in maintaining remission in ulcerative colitis. Spanish Group for the Study of Crohn's Disease and Ulcerative Colitis (GETECCU). Author(s): Fernandez-Banares F, Hinojosa J, Sanchez-Lombrana JL, Navarro E, Martinez-Salmeron JF, Garcia-Puges A, Gonzalez-Huix F, Riera J, Gonzalez-Lara V, Dominguez-Abascal F, Gine JJ, Moles J, Gomollon F, Gassull MA. Source: The American Journal of Gastroenterology. 1999 February; 94(2): 427-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10022641&dopt=Abstract
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Randomized controlled trial of the effect of bifidobacteria-fermented milk on ulcerative colitis. Author(s): Ishikawa H, Akedo I, Umesaki Y, Tanaka R, Imaoka A, Otani T.
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Source: Journal of the American College of Nutrition. 2003 February; 22(1): 56-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12569115&dopt=Abstract •
Rectal electrolyte transport and mucosal permeability in ulcerative colitis and Crohn's disease. Author(s): Rask-Madsen J, Hammersgaard EA, Knudsen E. Source: The Journal of Laboratory and Clinical Medicine. 1973 March; 81(3): 342-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4631401&dopt=Abstract
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Relaxation training as a treatment for chronic pain caused by ulcerative colitis. Author(s): Shaw L, Ehrlich A. Source: Pain. 1987 June; 29(3): 287-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3302842&dopt=Abstract
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Response to article by Buchman et al. Use of hyperbaric oxygenation in the treatment of ulcerative colitis. Author(s): Connor DJ, Bennett M. Source: Journal of Clinical Gastroenterology. 2002 July; 35(1): 98; Author Reply 98. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12080236&dopt=Abstract
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Serum bile acids in relation to disease activity and intake of dietary fibers in juvenile ulcerative colitis. Author(s): Ejderhamn J, Strandvik B. Source: Digestion. 1991; 50(3-4): 162-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1667392&dopt=Abstract
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Should folic acid supplementation be used to reduce the risk of cancer in ulcerative colitis? Author(s): Williams CN. Source: Canadian Journal of Gastroenterology = Journal Canadien De Gastroenterologie. 1999 November; 13(9): 715-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10633822&dopt=Abstract
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Studies in ulcerative colitis. Author(s): ASKEVOLD F. Source: Journal of Psychosomatic Research. 1964 September; 173: 89-100. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14212254&dopt=Abstract
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Study of the mechanisms of acupuncture and moxibustion treatment for ulcerative colitis rats in view of the gene expression of cytokines. Author(s): Wu HG, Zhou LB, Pan YY, Huang C, Chen HP, Shi Z, Hua XG.
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Source: World Journal of Gastroenterology : Wjg. 1999 December; 5(6): 515-517. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11819501&dopt=Abstract •
Surgical treatment of ulcerative colitis. Author(s): ROSS ST. Source: Surgery. 1964 June; 55: 782-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14171580&dopt=Abstract
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Symposium. pathogenesis and management of ulcerative colitis. Author(s): ENGLISH OS, KIRSNER JB, LYONS AS, VALD'ES-DAPENA AM, TUMEN HJ. Source: J Albert Einstein Med Cent (Phila). 1964 July; 12: 151-80. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14183358&dopt=Abstract
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TCM differential treatment of 57 cases of chronic gastritis complicated by ulcerative colitis. Author(s): Meng M. Source: J Tradit Chin Med. 1999 March; 19(1): 10-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10453577&dopt=Abstract
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The condition of the biliary tract and cholesecretion in cases of ulcerative colitis. Author(s): Abasov IT, Isaev EG, Iof IM. Source: Hepatogastroenterology. 1985 June; 32(3): 138-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4018708&dopt=Abstract
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The effect of folic acid supplementation on the risk for cancer or dysplasia in ulcerative colitis. Author(s): Lashner BA, Provencher KS, Seidner DL, Knesebeck A, Brzezinski A. Source: Gastroenterology. 1997 January; 112(1): 29-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8978339&dopt=Abstract
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The protective and healing effects of a natural antioxidant formulation based on ubiquinol and Aloe vera against dextran sulfate-induced ulcerative colitis in rats. Author(s): Korkina L, Suprun M, Petrova A, Mikhal'chik E, Luci A, De Luca C. Source: Biofactors (Oxford, England). 2003; 18(1-4): 255-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14695941&dopt=Abstract
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The response to psychotherapy in chronic ulcerative colitis. II. Factors arising from the therapeutic situation. Author(s): Karush A, Daniels GE, O'Connor JF, Stern LO.
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Source: Psychosomatic Medicine. 1969 May-June; 31(3): 201-26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5790112&dopt=Abstract •
The role of marine fish oils in the treatment of ulcerative colitis. Author(s): Ross E. Source: Nutrition Reviews. 1993 February; 51(2): 47-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8455803&dopt=Abstract
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Therapeutic efficacy of hyperbaric oxygenation in ulcerative colitis refractory to medical treatment. Author(s): Demirturk L, Ozel M, Yazgan Y, Buchman AL. Source: Journal of Clinical Gastroenterology. 2002 September; 35(3): 286-7; Author Reply 287-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12192213&dopt=Abstract
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Therapeutic potential of fish oil in the treatment of ulcerative colitis. Author(s): McCall TB, O'Leary D, Bloomfield J, O'Morain CA. Source: Alimentary Pharmacology & Therapeutics. 1989 October; 3(5): 415-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2562385&dopt=Abstract
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Therapy of ulcerative colitis in children; a combined pediatric-psychiatric-surgical approach. Author(s): PASNAU RO. Source: Psychosomatics. 1964 May-June; 92: 137-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14151553&dopt=Abstract
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Treatment of ulcerative colitis using fecal bacteriotherapy. Author(s): Borody TJ, Warren EF, Leis S, Surace R, Ashman O. Source: Journal of Clinical Gastroenterology. 2003 July; 37(1): 42-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12811208&dopt=Abstract
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Treatment of ulcerative colitis with acupuncture. Author(s): Chen Z. Source: J Tradit Chin Med. 1995 September; 15(3): 231-3. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8569266&dopt=Abstract
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Treatment of ulcerative colitis with fish oil n--3-omega-fatty acid: an open trial. Author(s): Salomon P, Kornbluth AA, Janowitz HD. Source: Journal of Clinical Gastroenterology. 1990 April; 12(2): 157-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2109004&dopt=Abstract
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Treatment of ulcerative colitis with fish oil supplementation: a prospective 12 month randomised controlled trial. Author(s): Hawthorne AB, Daneshmend TK, Hawkey CJ, Belluzzi A, Everitt SJ, Holmes GK, Malkinson C, Shaheen MZ, Willars JE. Source: Gut. 1992 July; 33(7): 922-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1353742&dopt=Abstract
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Treatment of ulcerative colitis with germinated barley foodstuff feeding: a pilot study. Author(s): Mitsuyama K, Saiki T, Kanauchi O, Iwanaga T, Tomiyasu N, Nishiyama T, Tateishi H, Shirachi A, Ide M, Suzuki A, Noguchi K, Ikeda H, Toyonaga A, Sata M. Source: Alimentary Pharmacology & Therapeutics. 1998 December; 12(12): 1225-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9882030&dopt=Abstract
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Ulcerative colitis and regional entritis in jews. Author(s): ACHESON ED. Source: Harofe Haivri Heb Med J. 1963; 15: 308-10. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14163088&dopt=Abstract
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Ulcerative colitis in the Kinneret sub district, Israel 1965-1994: incidence and prevalence in different subgroups. Author(s): Shapira M, Tamir A. Source: Journal of Clinical Gastroenterology. 1998 September; 27(2): 134-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9754774&dopt=Abstract
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Ulcerative colitis. Author(s): WEISS J. Source: Del Med J. 1963 October; 35: 261-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14077322&dopt=Abstract
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Ulcerative colitis: a report of progress, based upon the recent literature. april 1963. Author(s): ALMY TP, LEWIS CM. Source: Gastroenterology. 1963 October; 45: 515-28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14070426&dopt=Abstract
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Ulcerative colitis: emotional problems and their management. Author(s): O'Connor JF. Source: Med Times. 1966 January; 94(1): 106-12. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5900553&dopt=Abstract
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Ulcerative colitis--criteria of a “psychosomatic” disease. Author(s): POWLES WE.
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Source: Can Psychiatr Assoc J. 1964 February; 90: 51-6. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14118713&dopt=Abstract •
Ulmus macrocarpa hance for the treatment of ulcerative colitis--a report of 36 cases. Author(s): Ye G, Cao Q, Chen X, Li S, Jia B. Source: J Tradit Chin Med. 1990 June; 10(2): 97-8. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2392003&dopt=Abstract
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Update on medical management of inflammatory bowel disease: ulcerative colitis. Author(s): Hanauer SB. Source: Reviews in Gastroenterological Disorders. 2001; 1(4): 169-76. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12120183&dopt=Abstract
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Use of bromelain for mild ulcerative colitis. Author(s): Kane S, Goldberg MJ. Source: Annals of Internal Medicine. 2000 April 18; 132(8): 680. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10766699&dopt=Abstract
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Wheat grass juice in the treatment of active distal ulcerative colitis: a randomized double-blind placebo-controlled trial. Author(s): Ben-Arye E, Goldin E, Wengrower D, Stamper A, Kohn R, Berry E. Source: Scandinavian Journal of Gastroenterology. 2002 April; 37(4): 444-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11989836&dopt=Abstract
Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •
Alternative Medicine Foundation, Inc.: http://www.herbmed.org/
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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats
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Chinese Medicine: http://www.newcenturynutrition.com/
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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html
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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
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Google: http://directory.google.com/Top/Health/Alternative/
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Healthnotes: http://www.healthnotes.com/
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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
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Open Directory Project: http://dmoz.org/Health/Alternative/
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HealthGate: http://www.tnp.com/
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WebMDHealth: http://my.webmd.com/drugs_and_herbs
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
The following is a specific Web list relating to ulcerative colitis; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
General Overview Abdominal Wall Inflammation Source: Integrative Medicine Communications; www.drkoop.com Amyloidosis Source: Integrative Medicine Communications; www.drkoop.com Colon Cancer Source: Healthnotes, Inc.; www.healthnotes.com Colorectal Cancer Source: Integrative Medicine Communications; www.drkoop.com Crohn's Disease Source: Healthnotes, Inc.; www.healthnotes.com Erythema Source: Integrative Medicine Communications; www.drkoop.com High Blood Pressure Source: Integrative Medicine Communications; www.drkoop.com High Homocysteine Source: Healthnotes, Inc.; www.healthnotes.com Hypertension Source: Integrative Medicine Communications; www.drkoop.com Inflammatory Bowel Disease Source: Healthnotes, Inc.; www.healthnotes.com Inflammatory Bowel Disease Source: Integrative Medicine Communications; www.drkoop.com Irritable Bowel Syndrome Source: Healthnotes, Inc.; www.healthnotes.com Malabsorption Source: Healthnotes, Inc.; www.healthnotes.com
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Peritonitis Source: Integrative Medicine Communications; www.drkoop.com Proctitis Source: Integrative Medicine Communications; www.drkoop.com Rectal Inflammation Source: Integrative Medicine Communications; www.drkoop.com Rubella Source: Integrative Medicine Communications; www.drkoop.com Ulcerative Colitis Source: Healthnotes, Inc.; www.healthnotes.com Ulcerative Colitis Source: Integrative Medicine Communications; www.drkoop.com •
Alternative Therapy Colon Therapy Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,682,00.html Homeopathy Source: Integrative Medicine Communications; www.drkoop.com
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Herbs and Supplements Acidophilus and Other Probiotics Source: Prima Communications, Inc.www.personalhealthzone.com Aloe Alternative names: Aloe vera L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Aloe Alternative names: Aloe vera, Aloe barbadensis Source: Healthnotes, Inc.; www.healthnotes.com Aloe Vera Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10001,00.html Boswellia Alternative names: Frankincense; Boswellia serrata Roxb. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org
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Boswellia Alternative names: Boswellia serrata Source: Healthnotes, Inc.; www.healthnotes.com Boswellia Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,759,00.html Calendula Alternative names: Calendula officinalis Source: Healthnotes, Inc.; www.healthnotes.com Caprylic Acid Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10111,00.html Cascara Sagrada Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10013,00.html Chamomile Alternative names: Matricaria recutita Source: Healthnotes, Inc.; www.healthnotes.com Comfrey Alternative names: Symphytum officinale Source: Healthnotes, Inc.; www.healthnotes.com Comfrey Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Corticosteroids Source: Healthnotes, Inc.; www.healthnotes.com Dehydroepiandrosterone (DHEA) Source: Integrative Medicine Communications; www.drkoop.com Dhea Source: Integrative Medicine Communications; www.drkoop.com Digestive Enzymes Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10051,00.html Dioscorea Villosa Source: Integrative Medicine Communications; www.drkoop.com
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Eicosapentaenoic Acid (EPA) Source: Integrative Medicine Communications; www.drkoop.com Evening Primrose Alternative names: Oenothera biennis, Sun Drop Source: Integrative Medicine Communications; www.drkoop.com Ginger Alternative names: Zingiber officinale Source: Integrative Medicine Communications; www.drkoop.com Glutamine Source: Prima Communications, Inc.www.personalhealthzone.com Glutamine Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10030,00.html Green-Lipped Mussel Source: Healthnotes, Inc.; www.healthnotes.com Guggul Alternative names: Commiphora mukul Source: Healthnotes, Inc.; www.healthnotes.com Gugulipid Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10033,00.html Herbal Digestive Formula Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10104,00.html Ispaghula Source: Integrative Medicine Communications; www.drkoop.com L. Acidophilus Alternative names: Lactobacillus Acidophilus Source: Integrative Medicine Communications; www.drkoop.com Lactobacillus Acidophilus Alternative names: L. Acidophilus Source: Integrative Medicine Communications; www.drkoop.com Licorice Alternative names: Glycyrrhiza glabra, Glycyrrhiza uralensis Source: Healthnotes, Inc.; www.healthnotes.com
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Licorice Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,801,00.html Marshmallow Alternative names: Althea officinalis Source: Healthnotes, Inc.; www.healthnotes.com Mesalamine Source: Healthnotes, Inc.; www.healthnotes.com Myrrh Alternative names: Commiphora molmol Source: Healthnotes, Inc.; www.healthnotes.com Oenothera Biennis Source: Integrative Medicine Communications; www.drkoop.com Oral Corticosteroids Source: Healthnotes, Inc.; www.healthnotes.com Plantago Isphagula Source: Integrative Medicine Communications; www.drkoop.com Plantago Psyllium Alternative names: Psyllium, Ispaghula; Plantago psyllium/ovata Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Prickly Ash Alternative names: Zanthoxylum clava-herculis, Zanthoxylum americanum Source: Healthnotes, Inc.; www.healthnotes.com Probiotics Source: Healthnotes, Inc.; www.healthnotes.com Psyllium Alternative names: Plantago ovata, Plantago ispaghula Source: Healthnotes, Inc.; www.healthnotes.com Psyllium Alternative names: Ispaghula,Plantago isphagula Source: Integrative Medicine Communications; www.drkoop.com Senna Alternative names: Cassia senna, Cassia angustifolia Source: Healthnotes, Inc.; www.healthnotes.com Slippery Elm Source: Prima Communications, Inc.www.personalhealthzone.com
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Slippery Elm Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10056,00.html St. John’s Wort Alternative names: Hypericum perforatum Source: Healthnotes, Inc.; www.healthnotes.com Sulfasalazine Source: Healthnotes, Inc.; www.healthnotes.com Sun Drop Source: Integrative Medicine Communications; www.drkoop.com Wild Yam Alternative names: Dioscorea villosa Source: Integrative Medicine Communications; www.drkoop.com Yarrow Alternative names: Achillea millefolium Source: Healthnotes, Inc.; www.healthnotes.com Zingiber Officinale Source: Integrative Medicine Communications; www.drkoop.com
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.
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CHAPTER 4. DISSERTATIONS ON ULCERATIVE COLITIS Overview In this chapter, we will give you a bibliography on recent dissertations relating to ulcerative colitis. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “ulcerative colitis” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on ulcerative colitis, we have not necessarily excluded nonmedical dissertations in this bibliography.
Dissertations on Ulcerative Colitis ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to ulcerative colitis. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •
Followup Study of Inflammatory Bowel Disease: Effect of Stress and Biological Markers by Duffy, Linda Claire, PhD from State University of New York at Buffalo, 1987, 303 pages http://wwwlib.umi.com/dissertations/fullcit/8718533
•
Formulation Development and In-Vitro Evaluation of a Polysaccharide-Based ColonSpecific Drug Delivery System (CSDDS) for the Treatment of Inflammatory Bowel Disease by Singh, Brahma N.; PhD from St. John's University (New York), School of Pharmacy, 2003, 191 pages http://wwwlib.umi.com/dissertations/fullcit/3080556
•
Inflammatory Bowel Disease As a Cultural Artifact: an Ethnography of the Politics of Suffering by Foulds, John Simon, PhD from The University of British Columbia (Canada), 1984 http://wwwlib.umi.com/dissertations/fullcit/f1933605
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Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.
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CHAPTER 5. CLINICAL TRIALS AND ULCERATIVE COLITIS Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning ulcerative colitis.
Recent Trials on Ulcerative Colitis The following is a list of recent trials dedicated to ulcerative colitis.8 Further information on a trial is available at the Web site indicated. •
A Randomized Trial of Rosiglitazone for Ulcerative Colitis Condition(s): Ulcerative Colitis; Inflammatory Bowel Disease Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); GlaxoSmithKline Purpose - Excerpt: This is a multicenter, randomized, double-blind, placebo-controlled study evaluating rosiglitazone: 4 mg tablets or placebo tablets administered orally twice daily for 12 weeks. The purpose of the study is to evaluate the efficacy and safety of rosiglitazone in the treatment of mild to moderately active ulcerative colitis. Disease activity will be measured using a standard disease activity index. Calculation of the index requires patients to undergo flexible sigmoidoscopy at the start of the study and at week 12. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00065065
•
Clotrimazole Enemas for Pouchitis in Children and Adults Condition(s): Ulcerative Colitis; Pouchitis; Ileitis; Inflammatory Bowel Disease
8
These are listed at www.ClinicalTrials.gov.
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Study Status: This study is currently recruiting patients. Sponsor(s): FDA Office of Orphan Products Development Purpose - Excerpt: Colectomy with creation of an ileal pouch (IPAA) is now the treatment of choice for patients with ulcerative colitis that is resistant to existing medical therapies. The development of inflammation in these ileal reservoirs, a clinical entity referred to as pouchitis, is the most common long-term complication of this procedure and can affect 50-60% of adults and children. We have previously demonstrated that clotrimazole (delivered as a rectal suppository) is generally safe, effective, and displays poor systemic absorption when used in pediatric and adults with active pouchitis. We saw clinical benefit in patients with pouch disease that had previously failed to respond to standard antibiotic, steroid, or immunosuppressive therapies. The clinical trial outlined here will define the effectiveness and safety of topical clotrimazole therapy (delivered as a rectal enema) in pediatric (aged greater than two years) and adult patients with pouchitis. Subjects in this study will be randomly assigned to receive either placebo (no active drug, 4 subjects) or one of two clotrimazole therapy groups: 2500 mg/day (8 subjects) or 4000mg/day (8 subjects). No washout period is required, and subjects will be allowed to continue their existing antiinflammatory medications during their participation in the study. Clotrimazole will be delivered nightly in the form of an enema. Subjects will undergo flexible sigmoidoscopy (pouchoscopy) prior to and again after completing one month of study therapy, and pouch disease activity will be graded at after each procedure using the Pouchitis Disease Activity Index (PDAI). Clinical improvement will be defined as a drop in PDAI score. If the drop in PDAI scores between placebo and either active clotrimazole treatment group is not significant, and no subject experiences what are determined to be study-related adverse effects, a second cohort of subjects will be recruited and studied after receiving one month of either placebo (4 subjects), 6000 mg/day clotrimazole (8 subjects), or 7500mg/day clotrimazole (8 subjects). Subjects will be assessed for adverse effects at the midpoint of the study. Clotrimazole blood levels will be measured during the first and last day of study participation. In addition, adults will complete a health related quality of life assessment at baseline and after completing study drug therapy. All subjects will be eligible for one month of open-label study drug therapy after completing one month of study drug therapy. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00061282 •
FACTS I: A Study to Test the Safety and Effectiveness of a New Medication on the Treatment of Active Ulcerative Colitis Condition(s): Ulcerative Colitis Study Status: This study is currently recruiting patients. Sponsor(s): Otsuka Maryland Research Institute Purpose - Excerpt: The purpose of this study is to evaluate the safety and efficacy of the drug OPC-6535 compared to a placebo in patients with active Ulcerative Colitis. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below
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Web Site: http://clinicaltrials.gov/ct/show/NCT00064441 •
FACTS II: A Study to Test the Safety and Effectiveness of a New Medication on the Treatment of Active Ulcerative Colitis Condition(s): Ulcerative Colitis Study Status: This study is currently recruiting patients. Sponsor(s): Otsuka Maryland Research Institute Purpose - Excerpt: The purpose of this study is to evaluate the safety and efficacy of the drug OPC-6535 compared to a placebo in patients with active Ulcerative Colitis. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00064454
•
Immune Regulation in Ulcerative Colitis or Crohn's Disease Condition(s): Crohn's Disease; Inflammatory Bowel Disease; Ulcerative Colitis Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Allergy and Infectious Diseases (NIAID) Purpose - Excerpt: This study will investigate in patients with Crohn's disease and ulcerative colitis how the body's immune system controls inflammation in the gastrointestinal tract (stomach and intestines)-specifically, how lymphocytes (a type of white blood cell) function in inflammatory responses. This protocol does not involve any experimental treatments. Patients between the ages of 8 and 75 years of age with Crohn's disease or ulcerative colitis or symptoms of inflammatory bowel disease may be eligible for this study. Screening tests may include the following: medical history and physical examination, routine blood tests, examination of stool specimens, X-rays such as barium enema or upper GI series, proctosigmoidoscopy, colonoscopy, gastroduodenoscopy, and small bowel biopsy. Participants will receive medical treatment according to the best generally accepted measures for treating Crohn's disease or ulcerative colitis. This may include anti-inflammatory drugs, immunosuppressive drugs, and antibiotics to treat infections. A surgical consultation may be recommended for patients whose disease does not respond to medical treatment. If surgery to remove intestinal tissue is recommended, a qualified gastrointestinal surgeon will perform the procedure. In addition, participants may undergo the following procedures: - Blood drawing - No more than 450 milliliters (30 tablespoons, or 15 ounces) of blood will be taken from adults over a 6-week period. A maximum of 7 ml (1/2 tablespoon) of blood per kilogram (2.2. pounds) of body weight will be obtained from children within the same time period, with no more than 3 ml/kg taken at any one time. - Leukapheresis This procedure is done to collect large quantities of white blood cells. Whole blood is collected through a needle in an arm vein, similar to donating blood. The blood is circulated through a machine that separates it into its components, and the white cells are removed. The rest of the blood is returned to the body, either through the same needle or through another needle in the other arm. - Intestinal biopsies - Intestinal tissue will be obtained during colonoscopy with intestinal biopsy in patients who require this procedure as part of their standard medical care. Patients are given a sedative to reduce anxiety, but are conscious during the procedure. A flexible tube is inserted into the
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rectum and large intestine, allowing the physician to see the intestinal mucosa. At various places, small pieces of tissue are plucked out. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001184 •
Interferon-beta Treatment of Ulcerative Colitis Condition(s): Ulcerative Colitis Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Allergy and Infectious Diseases (NIAID) Purpose - Excerpt: This study will evaluate the safety and effectiveness of the drug interferon-beta in treating ulcerative colitis and examine the drug's effect on the immune system. People with ulcerative colitis have increased amounts of inflammatory chemicals (cytokines) made by immune cells in the lining of the colon. Studies have shown that interferon-beta may block the activity of these cytokines. Interferon-beta is currently FDA-approved to treat multiple sclerosis, a disease involving inflammation of the brain and spinal cord. Patients 18 years of age and older who have had ulcerative colitis for at least 4 months may be eligible for this study. Candidates will be screened with a review of their medical records, a medical history and physical examination, electrocardiogram (EKG), blood, urine, and stool tests, and a pregnancy test for women of childbearing potential. A colonoscopy will also be done to determine disease activity and extent. This test uses a lighted tube to examine the amount of inflammation in the colon and take tissue samples (biopsies) for testing. Before the test, the patient is given a medicine to allay anxiety and the discomfort of inserting the endoscope into the rectum. This flexible tube allows the doctor to see the intestinal mucosa and project an image of the inner lining of the intestine onto a TV monitor. At various places in the intestine, small pieces of tissue are plucked out by a special device at the tip of the endoscope. The procedure generally lasts 30 minutes to 1 hour. Participants will come to the NIH Clinical Center once a week for 4 weeks to receive an injection of interferon-beta, fill out questionnaires, and have a symptoms check, physical examination, and blood tests. Patients whose colitis has not worsened at the end of the 4 weeks and who have not had significant drug side effects will continue to receive weekly injections for an additional 8 weeks. Some patients may receive some of the last eight injections outside of NIH, but all patients will visit the Clinical Center visits every 3 to 4 weeks for a physical exam, symptoms check and blood tests. After the 12 injections are completed, patients will have another colonoscopy to evaluate the response to treatment and will return to the Clinical Center every 6 weeks for a total of four visits, for a physical examination, symptoms check and blood tests. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00048347
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ISIS 2302-CS22, A 6-Week, Active-Controlled Clinical Study to Evaluate the Effectiveness of Alicaforsen (ISIS 2302) in Patients with Mild to Moderate Active Ulcerative Colitis Condition(s): Ulcerative Colitis
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Study Status: This study is currently recruiting patients. Sponsor(s): Isis Pharmaceuticals Purpose - Excerpt: This is a multi-center trial to test the safety, efficacy and tolerability of alicaforsen (ISIS 2302), a new type of drug called an antisense drug, in patients with mild to moderate active Ulcerative Colitis (UC). Alicaforsen is designed to reduce the production of a specific protein, called ICAM-1, a substance that plays a significant role in the increase of inflammation and is likely to be involved in inflammatory bowel diseases such as ulcerative colitis. The ISIS 2302-CS22 study will examine the effects of one of two dosages of alicaforsen delivered by enema over a six-week period as compared to an active control, mesalamine enema (The probability of receiving the alicaforsen formulation is 2:1). The primary objective of this study is to evaluate the percentage reduction in DAI at Week 6. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00063414 •
ISIS 2302-CS27, A 6-Week, Placebo-Controlled Clinical Study to Evaluate the Effectiveness of Alicaforsen (ISIS 2302) in Patients with Mild to Moderate Active Ulcerative Colitis. Condition(s): Ulcerative Colitis Study Status: This study is currently recruiting patients. Sponsor(s): Isis Pharmaceuticals Purpose - Excerpt: This is a multi-center trial in the US and Europe to test the safety, efficacy and tolerability of alicaforsen (ISIS 2302), a new type of drug called an antisense drug, in patients with mild to moderate active Ulcerative Colitis (UC). Alicaforsen is designed to reduce the production of a specific protein, called ICAM-1, a substance that plays a significant role in the increase of inflammation and is likely to be involved in inflammatory bowel diseases such as ulcerative colitis. The ISIS 2302-CS27 study will compare four dosing regimens and determine the minimum effective dose of alicaforsen enema in UC patients over six weeks as compared to a placebo enema. (The probability of receiving active formulation is 4:1). The primary objective of this study is to evaluate the percentage reduction in DAI at Week 6. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00063830
•
Left-Sided Ulcerative Colitis Study Condition(s): Ulcerative Colitis Study Status: This study is currently recruiting patients. Sponsor(s): Wyeth-Ayerst Research Purpose - Excerpt: To explore the safety of orally delivered rhIL-11 in patients with mild to moderate left-sided ulcerative colitis. To explore the effects of orally administered rhIL-11 on pharmacogenomics in blood samples and in colonic biopsy tissue samples.
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Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00038922 •
Quality of Life in Pediatric Inflammatory Bowel Disease Condition(s): Crohn's Disease; Ulcerative Colitis Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: Measurement of the quality of life (QoL) of children and adolescents with inflammatory bowel diseases (IBD) has had little attention, despite the importance of understanding key factors affecting QoL, especially for measuring the effects of clinical trials to improve IBD outcomes. The main purpose of this pilot study is to examine the impact of clinical severity and treatment social factors on the quality of life (QoL) of a diverse population of children and adolescents with inflammatory bowel disease (IBD). Secondary purposes include determining the effects of sociodemographic factors on QoL and exploring the concordance of views of parents and children of QoL. The study aims are to 1) determine the associations of of clinical characteristics (condition type, activity/severity, and treatment) with specific components of general health-related quality of life and IBD-specific QoL; 2) describe the effects of sociodemographic characteristics (SES, age, and gender) on these measures; and 3) compare the views of different observers (parent and child with IBD) of the child's QoL. The study will apply both general and condition-specific QoL measures among a random sample of 250 children and adolescents with IBD, ages 5-18 years, in six clinical sites. We will obtain measures of QoL from both the child and a parent in each case. The study will obtain additional data regarding the subjects' clinical condition (condition type, severity/activity, treatment [including surgery], age of onset) and socioeconomic status (household structure and income). Main analyses will compare general and specific measures of QoL and examine the influence of clinical and sociodemographic variables on QoL, through multivariate regression techniques. We will also examine the differences in child and parent assessments of QoL. The information from this study will provide a stronger base for future studies of treatment and natural history of IBD. It will help to clarify the life domains that are affected by IBD and will inform interventions to improve QoL for children with IBD. Study Type: Observational Contact(s): James M Perrin, MD
[email protected]; Aziz Chughtai, MPH Web Site: http://clinicaltrials.gov/ct/show/NCT00061737
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Research Study in Patients With Severe Ulcerative Colitis Condition(s): Ulcerative Colitis Study Status: This study is currently recruiting patients. Sponsor(s): Protein Design Labs Purpose - Excerpt: The purpose of the study is to evaluate an intravenous (by injection) investigational medication to treat severe ulcerative colitis refractory to steroid therapy. The research is being conducted at up to 8 clinical research sites in the US and is open to both men and women ages 18 to 70 years old. Participants in the study will have a
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number of visits to a research site. All study-related care and medication is provided to qualified participants at no cost: this includes all visits, examinations and laboratory work. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00032305 •
Safety and efficacy of two diffrent doses of Asacol in the treatment of moderately active ulcerative colitis Condition(s): Ulcerative Colitis Study Status: This study is currently recruiting patients. Sponsor(s): Procter & Gamble Pharmaceuticals Purpose - Excerpt: This study is a prospective clinical study to evalute the safety and efficacy of two different doses of Asacol for the treatment of moderatively active ulcerative colitis. In addition, a new tablet formulation will be evaluated at one of the two doses. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00073021
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Study of Infliximab for the treatment of patients with active Ulcerative Colitis. Condition(s): Ulcerative Colitis Study Status: This study is currently recruiting patients. Sponsor(s): Centocor Purpose - Excerpt: A research study to evaluate the safety and effectiveness of an investigational drug is currently being conducted in adults with moderate to severe ulcerative colitis. The aim of the international study is to evaluate the efficacy and safety of Infliximab in patients with active ulcerative colitis. The study is being conducted in the US, Canada, Denmark, Spain, UK, Belgium and Germany. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00036439
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Humanized anti-IL-2 receptor monoclonal antibody in moderate-to-severe ulcerative colitis Condition(s): Ulcerative Colitis; Gastrointestinal Disease; Inflammatory Bowel Disease Study Status: This study is no longer recruiting patients. Sponsor(s): Protein Design Labs
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Purpose - Excerpt: The purpose of The PROSPECT Study is to evaluate an investigational medication for the treatment of moderate to severe ulcerative colitis. This study is being conducted at up to 38 clinical research centers in the US, Canada, and Belgium, and is open to male and female patients 12 years and older. Participants in the study will have a number of visits to a research center over a five-month period. All study related care and medication is provided to qualified participants at no cost: this includes all visits, examinations, and laboratory work. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00073047 •
A pharmacokinetic study to determine the oral bioavailability of methotrexate in patients with inflammatory bowel disease Condition(s): Inflammatory Bowel Disease Study Status: This study is completed. Sponsor(s): National Center for Research Resources (NCRR); Crohn's and Colitis Foundation Purpose - Excerpt: Patients with inflammatory bowel disease (IBD) who require methotrexate (MTX)for treatment currently receive this drug by injection. MTX is also available as a pill that can be given by mouth but it is not known how well the drug enters the body in patients with Crohn's disease or ulcerative colitis. This study is being done to compare how much MTX enters the body when the drug is taken by mouth compared to when it is given by injection. If the drug is well absorbed, it may allow patients to receive the drug by mouth. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00035074
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Phase II Placebo-Controlled Study of 4-Aminosalicylic Acid for Ulcerative Colitis Condition(s): Ulcerative Colitis Study Status: This study is completed. Sponsor(s): National Center for Research Resources (NCRR); University of Vermont Purpose - Excerpt: Objectives: I. Assess the safety and efficacy of 4-aminosalicylic acid in patients with mildly to moderately severe ulcerative colitis. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004810
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Safety and Efficacy of OP2000 (deligoparin) in the Treatment of Active Ulcerative Colitis Condition(s): Ulcerative Colitis
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Study Status: This study is completed. Sponsor(s): Incara Pharmaceuticals Purpose - Excerpt: This study will evaluate the effectiveness and safety of the experimental compound OP2000 (deligoparin) in patients with active ulcerative colitis. Patients eligible for this study will have received (and will continue to receive) stable doses of aminosalicylates (oral, enema and/or suppository), if tolerated. OP2000 is an ultra low molecular weight heparin with anticoagulant (blood thinning) and antiinflammatory actions that may be of benefit for the treatment of ulcerative colitis. Phase(s): Phase II; Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00033943
Keeping Current on Clinical Trials The U.S. National Institutes of Health, through the National Library of Medicine, has developed ClinicalTrials.gov to provide current information about clinical research across the broadest number of diseases and conditions. The site was launched in February 2000 and currently contains approximately 5,700 clinical studies in over 59,000 locations worldwide, with most studies being conducted in the United States. ClinicalTrials.gov receives about 2 million hits per month and hosts approximately 5,400 visitors daily. To access this database, simply go to the Web site at http://www.clinicaltrials.gov/ and search by “ulcerative colitis” (or synonyms). While ClinicalTrials.gov is the most comprehensive listing of NIH-supported clinical trials available, not all trials are in the database. The database is updated regularly, so clinical trials are continually being added. The following is a list of specialty databases affiliated with the National Institutes of Health that offer additional information on trials: •
For clinical studies at the Warren Grant Magnuson Clinical Center located in Bethesda, Maryland, visit their Web site: http://clinicalstudies.info.nih.gov/
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For clinical studies conducted at the Bayview Campus in Baltimore, Maryland, visit their Web site: http://www.jhbmc.jhu.edu/studies/index.html
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For cancer trials, visit the National Cancer Institute: http://cancertrials.nci.nih.gov/
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For eye-related trials, visit and search the Web page of the National Eye Institute: http://www.nei.nih.gov/neitrials/index.htm
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For heart, lung and blood trials, visit the Web page of the National Heart, Lung and Blood Institute: http://www.nhlbi.nih.gov/studies/index.htm
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For trials on aging, visit and search the Web site of the National Institute on Aging: http://www.grc.nia.nih.gov/studies/index.htm
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For rare diseases, visit and search the Web site sponsored by the Office of Rare Diseases: http://ord.aspensys.com/asp/resources/rsch_trials.asp
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For alcoholism, visit the National Institute on Alcohol Abuse and Alcoholism: http://www.niaaa.nih.gov/intramural/Web_dicbr_hp/particip.htm
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•
For trials on infectious, immune, and allergic diseases, visit the site of the National Institute of Allergy and Infectious Diseases: http://www.niaid.nih.gov/clintrials/
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For trials on arthritis, musculoskeletal and skin diseases, visit newly revised site of the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health: http://www.niams.nih.gov/hi/studies/index.htm
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For hearing-related trials, visit the National Institute on Deafness and Other Communication Disorders: http://www.nidcd.nih.gov/health/clinical/index.htm
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For trials on diseases of the digestive system and kidneys, and diabetes, visit the National Institute of Diabetes and Digestive and Kidney Diseases: http://www.niddk.nih.gov/patient/patient.htm
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For drug abuse trials, visit and search the Web site sponsored by the National Institute on Drug Abuse: http://www.nida.nih.gov/CTN/Index.htm
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For trials on mental disorders, visit and search the Web site of the National Institute of Mental Health: http://www.nimh.nih.gov/studies/index.cfm
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For trials on neurological disorders and stroke, visit and search the Web site sponsored by the National Institute of Neurological Disorders and Stroke of the NIH: http://www.ninds.nih.gov/funding/funding_opportunities.htm#Clinical_Trials
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CHAPTER 6. PATENTS ON ULCERATIVE COLITIS Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.9 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “ulcerative colitis” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on ulcerative colitis, we have not necessarily excluded non-medical patents in this bibliography.
Patents on Ulcerative Colitis By performing a patent search focusing on ulcerative colitis, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We will tell you how to obtain this information later in the chapter. 9Adapted from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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The following is an example of the type of information that you can expect to obtain from a patent search on ulcerative colitis: •
Amide therapeutics and methods for treating inflammatory bowel disease Inventor(s): Flitter; William D. (Mountain View, CA), Garland; William A. (Los Gatos, CA), Greenwood Van-Meerveld; Beverly (Oklahoma City, OK), Irwin; Ian (Palo Alto, CA) Assignee(s): Centaur Pharmaceuticals, Inc. (Sunnyvale, CA) Patent Number: 6,486,349 Date filed: November 17, 2000 Abstract: Disclosed are methods for treating or preventing inflammatory bowel disease (IBD) using amide and related compounds. Pharmaceutical compositions containing amide compounds which are useful for the treatment or prophylaxis of IBD are also disclosed. Excerpt(s): This invention relates to the treatment of inflammatory bowel disease (IBD). More specifically, this invention is directed to methods for treating or preventing IBD using amide compounds. This invention is also directed to pharmaceutical compositions containing amide compounds which are useful for the treatment or prophylaxis of IBD. The term inflammatory bowel disease ("IBD") describes a group of chronic inflammatory disorders of unknown causes involving the gastrointestinal tract ("GI tract"). The prevalence of IBD in the US is estimated to be about 200 per 100,000 population or approximately 500,000 people. Patients with IBD can be divided into two major groups, those with ulcerative colitis ("UC") and those with Crohn's disease ("CD"). In patients with UC, there is an inflammatory reaction primarily involving the colonic mucosa. The inflammation is typically uniform and continuous with no intervening areas of normal mucosa. Surface mucosal cells as well as crypt epithelium and submucosa are involved in an inflammatory reaction with neutrophil infiltration. Ultimately, this situation typically progresses to epithelial damage with loss of epithelial cells resulting in multiple ulcerations, fibrosis, dysplasia and longitudinal retraction of the colon. Web site: http://www.delphion.com/details?pn=US06486349__
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Diagnosis, prevention and treatment of ulcerative colitis, and clinical subtypes thereof, using microbial UC panca antigens Inventor(s): Braun; Jonathan (Tarzana, CA), Cohavy; Offer (Los Angeles, CA) Assignee(s): The Regents of the University of California (Oakland, CA) Patent Number: 6,537,768 Date filed: October 12, 1999 Abstract: The present invention relates to microbial UC pANCA antigens. The invention provides methods of diagnosing ulcerative colitis (UC) and methods of inducing tolerance in a pANCA-positive patient with UC using a histone H1-like antigen. The invention further provides methods of diagnosing UC and methods of inducing tolerance in a pANCA-positive patient with UC using a porin antigen. Methods of diagnosing UC and methods of inducing tolerance in a pANCA-positive patient with UC using a Bacteroides antigen also are provided.
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Excerpt(s): The invention relates generally to the fields of immunology and inflammatory bowel disease and more specifically to the diagnosis and treatment of a clinical subtype of ulcerative colitis. Inflammatory bowel disease (IBD) is the collective term used to describe two gastrointestinal disorders of unknown etiology: Crohn's disease (CD) and ulcerative colitis (UC). The course and prognosis of ulcerative colitis, which occurs world-wide and is reported to afflict as many as two million people, varies widely. Onset of ulcerative colitis is predominantly in young adulthood with diarrhea, abdominal pain, and fever the three most common presenting symptoms. The diarrhea may range from mild to severe and often is accompanied by bleeding. Anemia and weight loss are additional common signs of UC. Ten percent to fifteen percent of all patients with inflammatory bowel diseases such as UC will require surgery over a ten year period. In addition, patients with UC are at increased risk for the development of intestinal cancer. Reports of an increasing occurrence of psychological problems, including anxiety and depression, are perhaps not surprising symptoms of what is often a debilitating disease that strikes people in the prime of life. Unfortunately, the available therapies for ulcerative colitis are few, and both diagnosis and treatment have been hampered by a lack of knowledge regarding the etiology of the disease. What is clear, however, is that the pathogenesis of ulcerative colitis involves immune-mediated damage to the intestinal mucosa. Autoantibodies, specifically antibodies against cytoplasmic components of neutrophils (pANCA), have been reported in 68-80% of patients with ulcerative colitis, further supporting a role for immune dysregulation in this disease. However, the antigens recognized by these pANCA autoantibodies, which would be useful in diagnosing and treating UC patients have, to date, escaped identification. Web site: http://www.delphion.com/details?pn=US06537768__ •
Intestinal function using leptin Inventor(s): O'Connor; Darlise (Newark, DE), Schwartz; Marshall (Bryn Mawr, PA) Assignee(s): The Nemours Foundation (Wilmington, DE) Patent Number: 6,630,444 Date filed: October 23, 2000 Abstract: A method for treating a patient that has inadequate intestinal function is described. Administering leptin to a subject increases the intestinal function beyond that for a normal intestine and beyond that of a normal adaptive response. Further, administering leptin to a subject results in an increase in amino acid absorption, sugar absorption, mucosal mass, transport mechanisms for amino acids, or transport mechanisms for sugars. The method may be used for treating subjects have conditions such as short bowel syndrome, inflammation of the bowel, necrotizing enterocolitis, intestinal atresia, midgut volvulus, severe acute gastroenteritis, chronic gastroenteritis, cholera, chronic infections of the bowel, immunologic disorders affecting the small intestine, and inflammatory bowel disease such as, chronic ulcerative colitis and Crohn's Disease. Excerpt(s): The present invention relates broadly to enhancing the functions of the small intestine and the treatment of inflammatory bowel diseases in a patient by the administration of leptin. Short bowel syndrome ("SBS") is a devastating clinical disorder resulting from massive small bowel resection. SBS affects many infants and children and threatens normal growth and development. The remnant intestine naturally adapts to resection, however, this adaptation process is often inadequate to meet the patients fluid
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and nutritional goals. There is no effective treatment and current management includes total parenteral nutrition ("TPN"), which itself is a source of significant morbidity and mortality. Accordingly, there is a need for an alternative method of management for short bowel syndrome. Other disorders of the small intestine can render the bowel nonfunctional for a prolonged period of time such as severe infection and inflammatory bowel disease. It is an object of the present invention to provide an alternative method for management for short bowel syndrome and other disorders of the intestine. Web site: http://www.delphion.com/details?pn=US06630444__ •
Isoxazole derivatives to be used as phosphodiesterase VII inhibitors Inventor(s): Eggenweiler; Hans-Michael (Weiterstadt, DE), Gassen; Michael (Griesheim, DE), Jonas; Rochus (Darmstadt, DE), Welge; Thomas (Alsbach, DE), Wolf; Michael (Darmstadt, DE) Assignee(s): Merck Patentgesellschaft (Darmstadt, DE) Patent Number: 6,531,498 Date filed: May 3, 2002 Abstract: The invention relates to compounds of formula I and to their physiologically acceptable salts and solvates which act as phosphodiesterse VII inhibitors and are thus useful for the treatment of allergic disorders, asthma, chronic bronchitis, atopic dermatitis, psoriasis and other skin disorders, inflammatory disorders, autoimmune diseases, rheumatoid arthritis, multiple sclerosis, Crohn's disease, diabetes mellitus or ulcerative colitis, osteoporosis, transplant rejection reactions, cachexia, tumor growth, tumor metastases, sepsis, memory disturbances, atherosclerosis and AIDS. Excerpt(s): and their physiologically acceptable salts and/or solvates as phosphodiesterase VII inhibitors. The invention further relates to the use of the compounds of the formula I for producing a pharmaceutical for controlling allergic disorders, asthma, chronic bronchitis, atopic dermatitis, psoriasis and other skin disorders, inflammatory disorders, autoimmune diseases such as, for example, rheumatoid arthritis, multiple sclerosis, Crohn's disease, diabetes mellitus or ulcerative colitis, osteoporosis, transplant rejection reactions, cachexia, tumour growth or tumour metastases, sepsis, memory disturbances, atherosclerosis and AIDS. Compounds of the formula I are described by Bionet. Web site: http://www.delphion.com/details?pn=US06531498__
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LTA4 hydrolase inhibitor pharmaceutical compositions and methods of use Inventor(s): Chandrakumar; Nizal Samuel (Vernon Hills, IL), Chen; Barbara Baosheng (Glenview, IL), Clare; Michael (Skokie, IL), Desai; Bipinchandra Nanubhai (Vernon Hills, IL), Djuric; Stevan Wakefield (Malvern, PA), Docter; Stephen Hermann (Mt. Prospect, IL), Gasiecki; Alan Frank (Vernon Hills, IL), Haack; Richard Arthur (Chicago, IL), Liang; Chi-Dean (Glenview, IL), Miyashiro; Julie Marion (Chicago, IL), Penning; Thomas Dale (Elmhurst, IL), Russell; Mark Andrew (Gurnee, IL), Yu; Stella Siu-tzyy (Morton Grove, IL) Assignee(s): G.D. Searle & Co. (Chicago, IL) Patent Number: 6,506,876 Date filed: October 11, 1994 Abstract: The present invention provides compounds of the formula Ar.sup.1 --Q-Ar.sup.2 --Y--R--Z and pharmaceutically acceptable salts thereof wherein Ar.sup.1 and Ar.sup.2 are optionally substituted aryl moieties, Z is an optionally substituted nitrogencontaining moiety which may be an acyclic, cyclic or bicyclic amine or an optionally substituted monocyclic or bicyclic nitrogen-containing heteroaromatic moiety; Q is a linking group capable of linking two aryl groups; R is an alkylene moiety; Y is a linking moiety capable of linking an aryl group to an alkylene moiety and wherein Z is bonded to R through a nitrogen atom. The compounds and pharmaceutical compositions of the present invention are useful in the treatment of inflammatory diseases which are mediated by LTB.sub.4 production, such as psoriasis, ulcerative colitis, IBD and asthma. Excerpt(s): This invention relates generally to anti-inflammatory compounds and pharmaceutical compositions, and more particularly to anti-inflammatory compounds and compositions which are capable of inhibiting leukotriene A.sub.4 hydrolase. B. Samuelsson, et al., J. Biol Chem., 264, 19469-19472 (1989) have shown that LTB.sub.4 biosynthesis from arachidonic acid involves the action of 2 enzymes, 5-lipoxygenase [5LO] and LTA.sub.4 hydrolase. 5-LO transforms arachidonic acid to 5-HPETE and subsequent formation of LTA.sub.4, which is an unstable allylic epoxide intermediate which is enzymatically hydrolyzed by LTA.sub.4 hydrolase to form the dihydroxy acid LTB.sub.4. wherein X is --CH-- or --N--, and r is 1 or 2, further provided that wherein R.sup.1, R.sup.2 or both R.sup.1 and R.sup.2 are --(CH.sub.2).sub.a COR.sup.15, then a is not O. Web site: http://www.delphion.com/details?pn=US06506876__
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Method for inhibiting inflammatory disease Inventor(s): Hiebert; Charles (Sunnyvale, CA), Laderoute; Keith R. (Palo Alto, CA), Tuse; Daniel (Menlo Park, CA), Waleh; Nahid (Palo Alto, CA) Assignee(s): Large Scale Biology Corp. (Vacaville, CA), SRI International (Menlo Park, CA) Patent Number: 6,433,012 Date filed: September 6, 2000 Abstract: The present invention relates to methods for effectively inhibiting inflammatory diseases, such as Crohn's disease and ulcerative colitis. In other aspects, this invention relates to methods of reducing or inhibiting granulomas.
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Excerpt(s): The present invention relates to methods for effectively inhibiting unwanted angiogenesis. More particularly, this invention relates to methods of treating diseases associated with unwanted angiogenesis and to delivering anti-angiogenic activity to mammals having such diseases. Angiogenesis is the development of new blood vessels from existing microvessels. The process of generating new blood vessels plays an important role in embryonic development, in the inflammatory response, in the development of metastases (tumor induced angiogenesis or TIA), in diabetic retinopathy, in the formation of the arthritic panus and in psoriasis. Under normal physiological conditions, humans or animals only undergo angiogenesis in very specific, restricted situations. For example, angiogenesis is normally observed in wound healing, in fetal and embryonal development and in the formation of the corpus luteum, endometrium and placenta. The control of angiogenesis is a highly regulated system involving angiogenic stimulators and inhibitors. The control of angiogenesis has been found to be altered in certain disease states and, in many cases, the pathological damage associated with the disease is related to the uncontrolled angiogenesis. In tumor angiogenesis, for example, capillary sprouts are formed, their formation being induced by a group of tumor cells. However, compared with blood vessels produced in normal angiogenic microenvironments, tumor microvessels are morphologically and functionally unique. Their vascular networks typically show disorganized or aberrant architecture, luminal sizes vary and blood flow can fluctuate chaotically. There are two principal types of tumor angiogenesis in terms of the events that follow implantation of metastatic seedlings on surfaces and in organs. The first or primary angiogenesis is the initial vascularization of the mass of multiplying tumor cells and is regarded as an essential prerequisite for the survival and further growth of a metastatic deposit. The second is a continuing or secondary angiogenesis and is the phenomenon, which occurs in waves at the periphery of a growing tumor mass. This second angiogenesis is essential for the accretion of new microcirculatory territories into the service of the expanding and infiltrating tumor. Web site: http://www.delphion.com/details?pn=US06433012__ •
Method for the treatment of inflammatory bowel diseases Inventor(s): Ulmius; Jan (Lund, SE) Assignee(s): Aktiebolaget Draco (Sodertalje, SE) Patent Number: 6,423,340 Date filed: September 23, 1998 Abstract: Described herein are methods comprising the oral administration of budesonide for the treatment of ulcerative colitis and Crohn's colitis in its active phase. The methods can also be applied as relapse preventing therapy for Crohn's colitis in its chronic phase and Crohn's disease in the small intestine. Excerpt(s): The present invention relates to oral pharmaceutical compositions for use in the treatment of inflammatory bowel diseases and the use of certain glucocorticosteroids in the preparation of pharmaceutical compositions for the treatment by the oral route of certain inflammatory bowel diseases. Inflammatory bowel disease is the term generally applied to two diseases, namely ulcerative colitis and Crohn's disease. Ulcerative colitis is a chronic inflammatory disease of unknown aetiology afflicting only the large bowel and, except when very severe, limited to the bowel mucosa. The course of the disease may be continuous or relapsing, mild or severe. It is curable by total colectomy which
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may be needed for acute severe disease or chronic unremitting disease. Most patient with ulcerative colitis are managed medically rather than surgically. Web site: http://www.delphion.com/details?pn=US06423340__ •
Method for treating inflammation using soluble receptors to interleukin-20 Inventor(s): Blumberg; Hal (Seattle, WA), Chandrasekher; Yasmin A. (Mercer Island, WA), Foster; Donald C. (Lake Forest Park, WA), Kelly; James D. (Mercer Island, WA), Thompson; Penny (Snohomish, WA), Xu; Wenfeng (Mukilteo, WA) Assignee(s): ZymoGenetics, Inc. (Seattle, WA) Patent Number: 6,610,286 Date filed: December 22, 2000 Abstract: A method for treating IL-20 induced inflammation. An antagonist to IL-20 is administered to treat inflammation and associated diseases. The antagonist can be an antibody that binds to IL-20 or its receptor or a soluble receptor that binds to IL-20. Examples of such diseases are adult respiratory disease, psoriasis, eczema, contact dermatitis, atopic dermatitis, septic shock, multiple organ failure, inflammatory lung injury, bacterial pneumonia, inflammatory bowel disease, rheumatoid arthritis, asthma, ulcerative colitis and Crohn's disease. Excerpt(s): The teachings of all of the references cited herein are incorporated in their entirety herein by reference. Inflammation normally is a localized, protective response to trauma or microbial invasion that destroys, dilutes, or walls-off the injurious agent and the injured tissue. It is characterized in the acute form by the classic signs of pain, heat, redness, swelling, and loss of function. Microscopically, it involves a complex series of events, including dilation of arterioles, capillaries, and venules, with increased permeability and blood flow, exudation of fluids, including plasma proteins, and leukocyte migration into the area of inflammation. Diseases characterized by inflammation are significant causes of morbidity and mortality in humans. Commonly, inflammation occurs as a defensive response to invasion of the host by foreign, particularly microbial, material. Responses to mechanical trauma, toxins, and neoplasia also may results in inflammatory reactions. The accumulation and subsequent activation of leukocytes are central events in the pathogenesis of most forms of inflammation. Deficiencies of inflammation compromise the host. Excessive inflammation caused by abnormal recognition of host tissue as foreign or prolongation of the inflammatory process may lead to inflammatory diseases as diverse as diabetes, arteriosclerosis, cataracts, reperfusion injury, and cancer, to post-infectious syndromes such as in infectious meningitis, rheumatic fever, and to rheumatic diseases such as systemic lupus erythematosus and rheumatoid arthritis. The centrality of the inflammatory response in these varied disease processes makes its regulation a major element in the prevention control or cure of human disease. Web site: http://www.delphion.com/details?pn=US06610286__
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Method of treating gastrointestinal disorders, particularly colitis Inventor(s): Harkins; Robert W. (North Brunswick, NJ), Mazurek; Harry (Bala Cynwyd, PA) Assignee(s): ARCO Chemical Technology L.P. (Greenville, DE) Patent Number: 6,387,952 Date filed: September 19, 2000 Abstract: Administration of alkoxylated acyl glycerine (AAG) containing lower carboxylic acid acyl moieties to mammalian subjects results in increase of lower carboxylate concentration, particularly in the colon, and may be used to treat such disorders as simple colitis, ulcerative colitis, divertive colitis, colorectal cancer, and other diseases of the gastrointestinal tract where lower carboxylates are implicated. The AAG encourage patient compliance due to substantially no odor, even when butyric acid acyl groups are employed. Excerpt(s): The present invention is directed to treating gastrointestinal disorders, including inflammatory bowel disease, particularly colitis, and to methods of increasing the short chain fatty acid content of the colon. It is now well recognized that short chain fatty acids (SCFA), particularly those having from 1 to 4 carbon atoms are implicated in the treatment of numerous diseases and/or conditions of the gastrointestinal tract, particularly the colon. It is universally accepted that SCFA are a major energy source for the colon and other related tissues. Studies have shown that increasing SCFA levels brings about therapeutically significant improvements in areas such as prevention of Colorectal Cancer, W. Sheppach, et al. "Role of Short-Chain Fatty Acids in the Prevention of Colorectal Cancer", EUR J. CANCER, Vol. 31A, No. 7/8, pp. 1077-80, 1995; treatment of colitis, W. Sheppach, "Effects of Short Chain Fatty Acids on Gut Morphology and Function", GUT 1994, Supplement 1, pp. 35-38; ulcerative colitis, Jorgersen, J. R., et al., "Influence of Feces from Patients with Ulcerative Colitis on Butyrate Oxidation in Rat Colonocytes", DIGESTIVE DISEASES AND SCIENCES, Vol. 44, 10 pp. 2099-2109 (1999), Kim, op. cit., Sheppach, Falk Symp. (1994), 73 (Short Chain Fatty Acids), op. cit. (pp. 206-213); and diversion colitis Soergel, op. cit. In addition, SCFA's are implicated in immune system response, Perez, R., et al. "Selective Targeting of Kupffer Cells with Liposomal Butyrate Augments Portal Venous TransfusionInduced Immunosuppression", TRANSPLANTATION, Vol. 65, 10, p. 1294-98, 1998; Perez, R., et al. "Sodium Butyrate Upregulates Kupffer Cell PGE.sub.2 Production and Modulates Immune Function", J. SURGICAL RES., 78 pp. 1-6 (1998); apoptosis in hepatic tumors, Watkins, S. M., et al.; "Butyric Acid and Tributyrin Induce Apoptosis in Human Hepatic Tumor Cells", J. Dairy Res., 66, pp. 559-67 (1999); and in inhibiting fluid loss in chloera-infected mammals, Rabboni, G. H., et al., "Short-Chain Fatty Acids Inhibit Fluid and Electrolyte Loss Inducted by Cholera Toxin in Proximal Colon of Rabbit In Vitro", DIGESTIVE DISEASES AND SCI., Vol. 44, 8, pp. 1547-53 (1999). Web site: http://www.delphion.com/details?pn=US06387952__
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Method of treating inflammatory bowel disease using a topical formulation of IL-11 Inventor(s): Bedrosian; Camille L. (Belmont Hills, MA), Keith, Jr.; James C. (Andover, MA), Schendel; Paul F. (Wayland, MA), Schwerschlag; Ullrich S. (Beverly Farms, MA), Warne; Nicholas W. (Andover, MA) Assignee(s): Wyeth (Madison, NJ) Patent Number: 6,540,993 Date filed: September 15, 2000 Abstract: Provided by the present invention are topical formulations of Interleukin-11 and methods for treating a variety of disorders, including inflammatory bowel diseases (e.g., Crohn's disease, ulcerative colitis, indeterminate colitis, and infectious colitis), mucositis (e.g., oral mucositis, gastrointestinal mucositis, nasal mucositis, and proctitis), necrotizing enterocolitis, inflammatory skin disorders (e.g., psoriasis, atopic dermatitis, and contact hypersensitivity), aphthous ulcers, pharyngitis, esophagitis, peptic ulcers, gingivitis, periodontitis, and ocular diseases (e.g., conjunctivitis, retinitis, and uveitis). Excerpt(s): The present invention relates generally to novel compositions and methods for topical delivery of interleukin-11 (IL-11). In preferred embodiments, patients are treated employing topical delivery of recombinant human IL-11 for inflammatory bowel diseases (e.g., Crohn's disease, ulcerative colitis, indeterminate colitis, and infectious colitis), mucositis (e.g., oral mucositis, gastrointestinal mucositis, nasal mucositis, and proctitis), necrotizing enterocolitis, inflammatory skin disorders (e.g., psoriasis, atopic dermatitis, and contact hypersensitivity), aphthous ulcers, pharyngitis, esophagitis, peptic ulcers, gingivitis, periodontitis, and ocular diseases (e.g., conjunctivitis, retinitis, and uveitis). Inflammatory responses include a broad range of host reaction to a variety of insults, such as injury, infection, or rejection. It is the overproduction of mediators that is believed to be associated with a broad range of disorders, including AIDS, arthritis (rheumatoid arthritis, osteoarthritis, spondyloarthropathies), antibiotic-induced diarrheal diseases, multiple sclerosis, osteoporosis, gingivitis, peptic ulcer disease, esophagitis, diabetes, retinitis, uveitis, reperfusion injury after myocardial infarction, cerebral vascular accident, aphthous ulcers (oral), atherosclerosis, tumor metastases, asthma, preeclampsia, pancreatitis, psoriasis, infertility and allergic disorders such as rhinitis, conjunctivitis, and urticaria. Some of these disorders and their symptoms are briefly summarized below. According to the methods of the present invention, IL-11 is administered topically to modulate the host's over reaction at the site of insult, thereby treating the following disorders. Web site: http://www.delphion.com/details?pn=US06540993__
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Method of treating inflammatory conditions with progesterone analogs Inventor(s): Schreiber; Alan D. (Philadelphia, PA) Assignee(s): University of Pennsylvania (Philadelphia, PA) Patent Number: 6,610,674 Date filed: September 8, 2000 Abstract: The present invention provides methods for treating inflammatory conditions, including but not limited to, inflammatory bowel disease (ulcerative colitis, Crohn's disease, and proctitis), other noninfectious, inflammatory conditions of the GI tract (microscopic colitis, allergic eosinophilic gastroenteritis, food allergies, pill induced
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esophagitis, celiac disease, recurrent polyps, and hemorrhoids), and psoriasis, using progesterone or progesterone analogs such as medroxyprogesterone acetate. Excerpt(s): This invention provides methods for treating inflammatory conditions, including but not limited to, inflammatory bowel disease (ulcerative colitis, Crohn's disease, and proctitis), other noninfectious, inflammatory conditions of the GI tract (microscopic colitis, allergic eosinophilic gastroenteritis, food allergies, pill induced esophagitis, celiac disease, recurrent polyps, and hemorrhoids), and psoriasis using progesterone and progesterone analogs. Proctitis, inflammation of the rectum, is invariably present in UC and is sometimes present in CD. It may also occur independently from these diseases. Proctitis is another manifestation of IBD with pathology similar to UC. A patient presenting with proctitis may later develop fullblown UC or CD. Physicians and medical researchers have not been successful in identifying a cause for these diseases, although several theories have been postulated. The diseases may be caused by a pathogen or other antigen that initiates the inflammatory response in the bowel, accompanied by a defect in the ability to downregulate the immune response. Once initiated, many of the pathophysiological events in IBD are related to amplification of the inflammatory process. In response to antigens, cytokines and other inflammatory mediators are released. Some cytokines promote T cell activity. The inflammatory cascade continues with IL-2, helper T cells, B-cell proliferation, and antibody synthesis. Stimulated neutrophils and macrophages accumulate and further damage the tissue by releasing reactive oxygen species and other biologically active products. Additional acute inflammatory cells respond to the tissue damage, whether or not the primary initiating stimulus has ceased. Web site: http://www.delphion.com/details?pn=US06610674__ •
Method of treating ulcerative colitis or crohn's disease by administering an antibody to.alpha.E.beta.7 integrin Inventor(s): Brenner; Michael B. (Sherborn, MA), Parker; Christina M. (Arlington, MA) Assignee(s): The Brigham and Women's Hospital, Inc. (Boston, MA) Patent Number: 6,455,042 Date filed: April 16, 1999 Abstract: The present invention relates to a method for treating an autoimmune disease, such ulcerative coliteis or crohns disease characterized by lymphocyte accumulation at epithelial sites. The method involves administering to a subject an effective amount of an antibody that selectively binds to an.alpha.sup.E.beta.sub.7 integrin or an.alpha.sup.E subunit thereof. Excerpt(s): This invention relates to a novel integrin alpha chain; functionally-equivalent peptide fragments and analogs thereof; oligonucleotides encoding the peptide fragments and analogs; vectors containing and cell lines expressing the novel peptides; and methods for using the peptide fragments, analogs and oligonucleotides. The integrin mediated adhesive interactions of cells with other cells and between cells and the extracellular matrix are believed to play critical roles in a wide variety of processes including, for example, modulation of the immune system, regulation of developmental processes and tumor progression and metastasis. These molecules also transduce information from the extracellular to the intracellular environment through poorly understood signalling mechanisms. The integrins represent one of the best characterized superfamilies of adhesion receptors. Integrins are glycoprotein heterodimers which
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contain a non-covalently associated.alpha. and.beta. subunit. Integrin subunits are transmembrane proteins which contain an extracellular domain for interacting with an extracellular matrix or cellular component, a transmembrane domain spanning the cell membrane and a cytoplasmic domain for interacting with one or more cytoskeletal components. There are fourteen known.alpha. subunits and eight known.beta. subunits which can pair to form at least twenty different integrin molecules. Several distinct integrin.alpha. chains are capable of pairing with one type of.beta. chain to form a.beta. chain subfamily. Thus, for example, the.beta.sub.1 subfamily includes seven members (also known as the VLA proteins:.alpha.sup.1.beta.sub.1 -.alpha.sup.7.beta.sub.1); the.beta.sub.2 subfamily includes three members (the leukocyte cell adhesion molecules or LeuCAMs:.alpha.sup.L.beta.sub.2 or LFA-1,.alpha.sup.M.beta.sub.2 or Mac-1 and.alpha.sup.x.beta.sub.2 or p150,95) and the.beta.sub.3 subfamily includes two members (a.sup.v.beta.sub.3,.alpha.sup.IIb.beta.sub.3). In some instances, an.alpha. chain may pair with more than one.beta. chain, e.g.,.alpha.sup.4 can pair with.beta.sub.1 or.beta.sub.7. Web site: http://www.delphion.com/details?pn=US06455042__ •
Methods and compositions for treating inflammatory bowel disease Inventor(s): Borody; Thomas Julius (144 Great North Rd., Five Dock, AU 2046) Assignee(s): none reported Patent Number: 6,551,632 Date filed: July 6, 2001 Abstract: The present invention provides a method and composition of medications used to treat inflammatory bowel disease. The invention further provides combinations of anti-atypical mycobacterial agents effective against the atypical mycobacterial strains. It also provides a method of potentiating the anti-atypical mycobacterial agents in treatment of inflammatory bowel disease by immunizing patients with extracts of nonpathogenic mycobacteria. Excerpt(s): The invention relates to compositions and methods for the treatment of inflammatory bowel disease, such as Crohn's disease. Inflammatory bowel disease (IBD) is a disorder of unknown aetiology characterised typically by diarrhoea, cramping, abdominal pains, weight loss and rectal bleeding. It encompasses such disorders as Crohn's disease, ulcerative colitis, indeterminate colitis, microscopic colitis and collagenous colitis. Its cause is unknown. However, in the past there has been some evidence that Mycobacterium paratuberculosis (Mp) and perhaps its various substrains, may play an infective role by entering the cells which make up the bowel wall. The source of this bacterium is unclear but may reside in other animals such as sheep, cattle, rabbits, as well as other humans. It may be transmitted to people perhaps via milk, contaminated water supplies, poorly cooked meat, etc. Although there has been long-standing controversy about the involvement of Mp in causation of Crohn's disease, recent applications of PCR usage are beginning to confirm that most Crohn's cases are indeed infected with this organism which is likely to be the causal infective agent. In the past, therapy directed at the eradication of Mp by using combined anti-TB drugs eg INH, pyrazinamide, streptomycin, ethambutol, rifampicin and PAS have been generally of little help to patients. In other words, although transient improvements in a proportion of patients did occur, no patient was cured. In fact, even if Mp had been the cause of this disease there was no effective therapy available for Mp since it was an "atypical mycobacterium" and for atypical mycobacteria there was no known therapy.
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Furthermore, since Mycobacterium paratuberculosis has a long division time multiple antimicrobial drugs are required to the treat the infection which has to be carried out for a long period of time--akin to the treatment used in the therapy of Mycobacterium tuberculosis. Furthermore, Mycobacterium tuberculosis therapy with the current drugs results in resistant strains forming. Such resistant strains do not become eradicated with known antimicrobial agents. Hence, there is no known effective cure for resistant TB. Accordingly, there is a need for an effective treatment of inflammatory bowel disease, and in particular Crohn's disease. It is an object of this invention to provide such a treatment. Web site: http://www.delphion.com/details?pn=US06551632__ •
Methods for treating disorders in which docosahexaenoic acid (DHA) levels are affected Inventor(s): Alvarez; Juan G. (Boston, MA), Freedman; Steven (Brighton, MA) Assignee(s): Beth Israel Deaconess Medical Center, Inc. (Boston, MA) Patent Number: 6,552,081 Date filed: November 3, 2000 Abstract: A method of treating disorders in which DHA levels are affected is described. The method includes administering to a subject suffering from the disorder a therapeutically affective amount of DHA. This method is particularly useful in treating subjects suffering from a disorder characterized by a defect in the CF gene, e.g., cystic fibrosis, or a chronic inflammatory disorder, e.g., ulcerative colitis, Crohn's disease, chronic pancreatitis, asthma, rheumatoid arthritis or chronic gastritis. A method of ameliorating affects of cystic fibrosis in a newborn and a method of increasing surfactant levels in a fetus are also described. Excerpt(s): Cystic Fibrosis (CF) is the most prevalent autosomal recessive disorder in the Caucasian population (Gorelick (1991) Gastroenterology 103:681-693). Approximately 1 in 2000 live births are afflicted with CF and 5% of Caucasians in the United States are carriers of the abnormal CF gene. CF individuals rarely survive past their mid-thirties, and most mortalities are a result of recurrent pulmonary infection and, ultimately, pulmonary failure. Two other major clinical manifestations of CF are pancreatic dysfunction and male infertility. By 1989, the CF gene had been cloned and was found to code for a chloride channel. Activation of the channel in the normal pancreas activates the chloride/bicarbonate exchanger, resulting in a net secretion of bicarbonate into the lumenal space and alkalinization of the pancreatic juice. Mutations in the chloride channel like those found in CF result in a reduced chloride conductance and a reduced ability of ductal cells to secrete bicarbonate into the lumenal space. This results in the formation of inspissated plugs within the ducts leading to obstruction of the pancreatic ducts. In recent years, the focus in CF research has shifted towards the coupling of defective chloride channel function and membrane recycling. Recent research has demonstrated that membrane internalization at the apical plasma membrane of the pancreatic acinar cell is dependent on pH of the acinar lumen (Freedman et al., Eur. J. Cell Biol. (1998) 75:153-63), Freedman et al., (1994) Am. J. Physiol. 267:G40-G51, and Freedman et al., (1994) Eur. J. Cell Biol. 65:354-365). Since pH of the acinar lumen is reflective of ductal bicarbonate secretion from the proximal duct cells, a phenomenon regulated via the chloride channel, a coupling may exist between duct and acinar cell function, (Freedman et at., (1994) Am. J. Physiol. 267:G40-G51, and Freedman et al, (1994) Eur. J. Cell Biol. 65:354-365). Research has also confirmed the hypothesis that lack
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of alkalinization of the acinar lumen leads to inhibition of apical membrane internalization and defective apical endocytosis in pancreatic acinar cells from CF mice. This block in the recycling of membranes following exocytosis leads to eventual deficiency in membranes for reformation of secretory granules. Thus, pancreatic insufficiency appears to be a result of defects in membrane recycling with obstruction of the ducts occurring as a secondary event. Web site: http://www.delphion.com/details?pn=US06552081__ •
Monocyclic-7H-pyrrolo[2,3-d]pyrimidine compounds, compositions, and methods of use Inventor(s): Blumenkopf; Todd A. (Old Lyme, CT), Brown; Matthew F. (Pawcatuck, CT), Changelian; Paul S. (E. Greenwich, CT), Flanagan; Mark E. (Gales Ferry, CT) Assignee(s): Pfizer Inc. (New York, NY) Patent Number: 6,635,762 Date filed: June 17, 1999 Abstract: Novel pyrrolo[2,3-d]pyrimidine compounds useful as inhibitors of the enzyme protein tyrosine kinases such as Janus Kinase 3 as well as immunosuppressive agents for organ transplants, lupus, multiple sclerosis, rheumatoid arthritis, psoriasis, Type I diabetes and complications from diabetes, cancer, asthma, atopic dermatitis, autoimmune thyroid disorders, ulcerative colitis, Crohn's disease, Alzheimer's disease, Leukemia and other autoimmune diseases are described. Excerpt(s): The present invention relates to pyrrolo[2,3-d]pyrimidine compounds which are inhibitors of protein tyrosine kinases, such as the enzyme Janus Kinase 3 (hereinafter also referred to as JAK3) and as such are useful therapy as immunosuppressive agents for organ transplants, lupus, multiple sclerosis, rheumatoid arthritis, psoriasis, Type I diabetes and complications from diabetes, cancer, asthma, atopic dermatitis, autoimmune thyroid disorders, ulcerative colitis, Crohn's disease, Alzheimer's disease, Leukemia and other indications where immunosuppression would be desirable. This invention also relates to a method of using such compounds in the treatment of the above indications in mammals, especially humans, and the pharmaceutical compositions useful therefor. with the proviso that the groups of formulas IV, V, VI or XIII do not contain two or more oxygens, sulfurs or combinations thereof in adjacent positions. Web site: http://www.delphion.com/details?pn=US06635762__
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Nutritional product for a person having ulcerative colitis Inventor(s): Demichele; Stephen Joseph (Dublin, OH), Fuller; Martha Kay (Westerville, OH), Garleb; Keith Allen (Powell, OH), McEwen; John William (Gahanna, OH) Assignee(s): Abbott Laboratories (Abbott Park, IL) Patent Number: 6,468,987 Date filed: September 14, 1999 Abstract: An enteral nutritional product for a person having ulcerative colitis contains in combination (a) an oil blend which contains eicosapentaenoic acid (20:5n3) and/or docosahexaenoic acid (22:6n3), and (b) a source of indigestible carbohydrate which is
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metabolized to short chain fatty acids by microorganisms present in the human colon. Preferably the nutritional product also contains one or more nutrients which act as antioxidants. Excerpt(s): The present invention relates to a nutritional product for a person having ulcerative colitis. The term "Inflammatory Bowel Disease" is a designation commonly used for two related, but distinct, chronic inflammatory conditions affecting the gastrointestinal tract, namely Crohn's disease and ulcerative colitis. Crohn's disease may involve any segment of the gastrointestinal tract, although characteristically the region of greatest involvement is the distal one quarter of the small intestine and the proximal colon. In ulcerative colitis the inflammation is, by definition, limited to the mucosa of the large bowel. However, the present invention is concerned only with nutritional support for a person having ulcerative colitis. The primary cause of ulcerative colitis is not currently known. At the present time, there is no medical cure for ulcerative colitis and this chronic condition may lead to total proctocolectomy. Current medical treatment is directed toward decreasing the number, frequency and severity of acute exacerbations of inflammatory bowel disease and preventing secondary complications, but at best, the results are disappointing. Long term use of corticosteroids to downregulate the inflammatory response is a common approach to the control of intestinal inflammation. Steroids are considered to exert their antiinflammatory effects through inhibition of the release of free arachidonic acid from membrane phospholipids; Historically the long term use of immunosuppressive agents (steroids) is associated with chronic side effects such as those presented in Table 1. Web site: http://www.delphion.com/details?pn=US06468987__ •
Pharmaceutical preparations for the targeted treatment of crohn's disease and ulcerative colitis Inventor(s): Posanski; Ulrich (Freiburg, DE) Assignee(s): Novartis AG (CH) Patent Number: 6,503,883 Date filed: November 28, 2000 Abstract: The invention relates to a pharmaceutical preparation, which contains an immunosuppressive active agent in dissolved form in a starch capsule, or hard or soft gelatin capsule which has been coated with one or several polymer films. The invention further relates to a process for the production of the pharmaceutical preparation. Excerpt(s): The invention relates to a pharmaceutical preparation for the enteral treatment of Crohn's disease and ulcerative colitis, which contains an immunosuppressive active agent, which is administered in the form of a special galenic formulation for targeted local activity in the intestinal area, its use and a process for the production thereof. The therapies known today for the treatment of Crohn's disease and ulcerative colitis are not very effective. At the end of drug treatment, the patient usually faces surgical intervention. There are numerous preparations for extending and improving the therapeutical possibilities, but until now no preparation has been able to meet the medicinal requirements to a maximum degree. One possibility of local, enteral therapy of inflammatory intestinal affections was opened up with the development and usage of special mesalazine-containing (5-aminosalicylic acid) preparations, which release the active agent in the distal part of the small intestine and in the large intestine.
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The preparations concerned are solid forms of administration, which contain the active agent in crystalline form despite its poor solubility. Web site: http://www.delphion.com/details?pn=US06503883__ •
Phospholipase D polypeptide and DNA sequences Inventor(s): Engebrecht; Joanne (Stony Brook, NY), Frohman; Michael A. (Setauket, NY), Morris; Andrew J. (Mt. Sinai, NY) Assignee(s): Onyx Pharmaceuticals, Inc. (Richmond, CA) Patent Number: 6,379,665 Date filed: March 27, 2000 Abstract: Provided are novel phospholipase D DNA and amino acid sequences. The sequences are useful in methods and compositions for identifying phospholipase D mediator molecules which are in turn useful in therapeutic pharmaceutical compositions for treating rheumatoid arthritis, psoriasis, ulcerative colitis, in wound healing and for treating other diseases or conditions characterized by exhibition of an inflammatory response or in the treatment of cancer and other diseases characterized by pathogenic mitogenicity. Excerpt(s): This invention is in the field of molecular biology and particularly relates to nucleic acid sequences that encode novel phospholipases. The mechanism by which specificity of physiological responses are conferred by a limited number of signal transducing substances, typically enzymes, is poorly understood. Cellular receptors on the surfaces of various cells are involved and initiate multiple signaling pathways. Some of the receptors on neutrophils are known: the PAF receptor, the interleukin-8 receptor and the fMetLeuPhe receptor all belong to the super-family of G-protein-linked receptors. A common feature of these receptors is that they span the cell membrane seven times, forming three extracellular and three intracellular loops and a cytoplasmic carboxy-terminal tail. The third loop and the tail exhibit extensive variability in length and sequence, leading to speculation that these parts are responsible for the selective interaction with the various G-proteins. Many of these G-protein-linked receptors stimulate the activation of three phospholipases, phospholipase C (PLC), phospholipase D (PLD) and phospholipase A.sub.2 (PLA.sub.2). These phospholipases constitute a family of regulatory enzymes which trigger various neutrophilic functions, for example adherence, aggregation, chemotaxis, exocytosis of secretory granules and activation of NADPH oxidase, i.e., the respiratory burst. The main substrates for the phospholipases are membrane phospholipids. The primary substrates for PLC are the inositol containing lipids specifically and typically phosphotidylinositol (PI). PI is phosphorylated by PLC resulting in the formation of PIP, phosphotidylinositol 4phosphate. The primary substrate for PLD and PLA.sub.2 is phosphatidylcholine (PC), a relatively ubiquitous constituent of cell membranes. The activity of cytosolic PLA.sub.2 on PC liberates arachidonic acid, a precursor for the biosynthesis of prostaglandins and leukotrienes and possible intracellular secondary messenger. PLD, on the other hand, catalyzes the hydrolytic cleavage of the terminal phosphate diester bond of glycerophospholipids at the P-O position. PLD activity was originally discovered in plants and only relatively recently discovered in mammalian tissues. PLD has been the focus of recent attention due to the discovery of its activation by fMetLeuPhe in neutrophils. PLD activity has been detected in membranes and in cytosol. Although a 30 kD (kilodalton) and an 80 kD activity have been detected, it has been suggested that these molecular masses represented a single enzyme with varying extents of
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aggregation. See Cockcroft, Biochimica et Biophysica Acta 1113: 135-160 (1992). One PLD has been isolated, cloned and partially characterized. See Hammond, J. Biol. Chem. 270:29640-43 (1995). Biological characterization of PLD1 revealed that it could be activated by a variety of G-protein regulators, specifically PKC (protein kinase C), ADPribosylation factor (ARF), RhoA, Rac1 and cdc-42, either individually or together in a synergistic manner, suggesting that a single PLD participates in regulated secretion in coordination with ARF and in propagating signal transduction responses through interaction with PKC, PhoA and Rac1. Nonetheless, PKC-independent PLD activation has been associated with Src and Ras oncogenic transformation, leaving open the possibility that additional PLDs might exist. See Jiang, Mol. and Cell. Biol. 14:3676 (1994) and Morris, Trends in Pharmacological Sciences 17: 182-85(1996). The difficulty may arise at least in part from the fact that in the phospholipase family enzymes may or may not be activated by, and catalyze, multiple substances, making sorting, tracking and identification by functional activities impractical. Web site: http://www.delphion.com/details?pn=US06379665__ •
Preparation capable of releasing drug at target site in intestine Inventor(s): Ishibashi; Takashi (Sakai, JP), Kubo; Hiroaki (Kobe, JP), Mizobe; Masakazu (Takatsuki, JP), Yoshino; Hiroyuki (Suita, JP) Assignee(s): Tanabe Seiyaku Co., Ltd. (Osaka, JP) Patent Number: 6,638,534 Date filed: January 29, 2001 Abstract: A preparation capable of releasing a medicinal substance at a targeted site in the intestine, wherein the preparation dose not releases medicinal substance in endogastri at all, but can quickly release a medicinal substance when it reaches the desired site in the intestine after a certain period of time from discharge of the preparation from the stomach, and wherein a core material containing a medicinal substance is coated with a mixed film of a hydrophobic organic compound--an enteric polymer. The preparation is useful for a local therapy of inflammatory disease in the intestine such as ulcerative colitis or Crohn's disease, or an oral administrative therapy with a medicinal substance of a peptide which is apt to be decomposed chemically or enzymatically in any site except for a specific site in the intestine such as the large intestine, or with a medicinal substance whose absorption site in the intestine is limited, or the like, because a medicinal substance can be delivered selectively to a specific site in the intestine. Excerpt(s): The present invention relates to a preparation capable of releasing a medicinal substance at a targeted site in the intestine, which can selectively deliver a medicinal substance to the large intestine and the like, and a method for preparation thereof. Selective delivery of a medicinal substance to a specific site in the intestine has been desired in pharmacotherapy, for example, a local therapy for inflammatory disease in the gastrointestinal tract such as ulcerative colitis or Crohn's disease, an oral administrative therapy with a medicinal substance of a peptide which is apt to be decomposed chemically or enzymatically in any site except for a specific site in the intestine such as the large intestine, or with a medicinal substance whose absorption site in intestine is limited, or the like. In order to efficiently realize the selective delivery of a medicinal substance in the intestine, it is necessary to design a preparation considering the physical and physiological environment in the human gastrointestinal tract and the traveling time of the preparation through the gastrointestinal tract. With respect to the
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physical and physiological environment in the gastrointestinal tract, it is recognized that the value of pH in the stomach is usually 1.8 to 4.5 and the value of pH in the intestine is 6.5 to 7.5 in a healthy human. According to the results of the widespread research of Davis et al., in a human, the residence time of a preparation in the stomach is 0.5 to 10 hours and further not only the inter-individual variation thereof is large, but also the residence time is considerably influenced, for example, by a condition of feeding, a size of the preparation to be administered and the like, while the traveling time of a preparation through the small intestine is generally recognized to be 3.+-.1 hours and the variation is relatively small (Journal of Controlled Release, 2, 27-38 (1985)). Web site: http://www.delphion.com/details?pn=US06638534__ •
Prevention and treatment of inflammatory bowel disease Inventor(s): Kink; John A. (Madison, WI), Stafford; Douglas C. (Madison, WI), Worledge; Katherine L. (Madison, WI) Assignee(s): Promega Corporation (Madison, WI) Patent Number: 6,395,273 Date filed: June 10, 1998 Abstract: Methods are described for treating inflammatory bowel disease in animals, including humans. Specific avian polyclonal antibodies directed to TNF are shown to have a beneficial effect in animal models predictive of human therapy for the treatment of colitis. Excerpt(s): The present invention relates to therapeutics for the prevention and treatment of inflammatory bowel disease, and in particular the prevention and treatment of inflammatory bowel disease in humans as well as other animals through the use of avian polyclonal antibody therapy. Inflammatory bowel diseases (IBD) are defined by chronic, relapsing intestinal inflammation of obscure origin. IBD refers to two distinct disorders, Crohn's disease and ulcerative colitis (IC). Both diseases appear to result from the unrestrained activation of an inflammatory response in the intestine. This inflammatory cascade is thought to be perpetuated through the actions of proinflammatory cytolines and selective activation of lymphocyte subsets. In patients with IBD, ulcers and inflammation of the inner lining of the intestines lead to symptoms of abdominal pain, diarrhea, and rectal bleeding. Ulcerative colitis occurs in the large intestine, while in Crohn's, the disease can involve the entire GI tract as well as the small and large intestines. For most patients, IBD is a chronic condition with symptoms lasting for months to years. It is most common in young adults, but can occur at any age. It is found worldwide, but is most common in industrialized countries such as the United States, England, and northern Europe. It is especially common in people of Jewish descent and has racial differences in incidence as well. The clinical symptoms of IBD are intermittent rectal bleeding, crampy abdominal pain, weight loss and diarrhea. Diagnosis of IBD is based on the clinical symptoms, the use of a barium enema, but direct visualization (sigmoidoscopy or colonoscopy) is the most accurate test. Protracted IBD is a risk factor for colon cancer, and treatment of IBD can involve medications and surgery. Some patients with UC only have disease in the rectum (proctitis). Others with UC have disease limited the rectum and the adjacent left colon (proctosigmoiditis). Yet others have UC of the entire colon (universal IBD). Symptoms of UC are generally more severe with more extensive disease (larger portion of the colon involved with disease). Web site: http://www.delphion.com/details?pn=US06395273__
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Substituted nipecotyl derivatives as inhibitors of cell adhesion Inventor(s): de Laszlo; Stephen E. (Rumson, NJ), Gutteridge; Clare E. (Westfield, NJ), Hagmann; William K. (Westfield, NJ), Kamenecka; Theodore M. (North Brunswick, NJ) Assignee(s): Merck & Co., Inc. (Rahway, NJ) Patent Number: 6,403,584 Date filed: June 15, 2001 Abstract: Compounds of Formula I are antagonists of VLA-4 and/or.alpha.sub.4.beta.sub.7, and as such are useful in the inhibition or prevention of cell adhesion and cell-adhesion mediated pathologies. These compounds may be formulated into pharmaceutical compositions and are suitable for use in the treatment of AIDS-related dementia, allergic conjunctivitis, allergic rhinitis, Alzheimer's disease, asthma, atherosclerosis, autologous bone marrow transplantation, certain types of toxic and immune-based nephritis, contact dermal hypersensitivity, inflammatory bowel disease including ulcerative colitis and Crohn's disease, inflammatory lung diseases, inflammatory sequelae of viral infections, meningitis, multiple sclerosis, multiple myeloma, myocarditis, organ transplantation, psoriasis, pulmonary fibrosis, restenosis, retinitis, rheumatoid arthritis, septic arthritis, stroke, tumor metastasis, uveititis, and type I diabetes. Excerpt(s): The compounds of the present invention are antagonists of the VLA-4 integrin ("very late antigen-4"; CD49d/CD29; or.alpha.sub.4.beta.sub.1), the.alpha.4.beta.7 integrin (LPAM-1 and.alpha.sub.4.beta.sub.p), and/or the.alpha.9.beta.1 integrin, thereby blocking the binding of VLA-4 to its various ligands, such as VCAM-1 and regions of fibronectin,.alpha.4.beta.7 to its various ligands, such as MadCAM-1, VCAM-1 and fibronectin, and/or.alpha.9.beta.1 to its various ligands, such as tenascin, osteopontin and VCAM-1. Thus, these antagonists are useful in inhibiting cell adhesion processes including cell activation, migration, proliferation and differentiation. These antagonists are useful in the treatment, prevention and suppression of diseases mediated by VLA-4-,.alpha.4.beta.7 -, and/or.alpha.9.beta.1 binding and cell adhesion and activation, such as AIDS-related dementia, allergic conjunctivitis, allergic rhinitis, Alzheimer's disease, aortic stenosis, asthma, atherosclerosis, autologous bone marrow transplantation, certain types of toxic and immune-based nephritis, contact dermal hypersensitivity, inflammatory bowel disease including ulcerative colitis and Crohn's disease, inflammatory lung diseases, inflammatory sequelae of viral infections, meningitis, multiple sclerosis, myocarditis, organ transplantation, psoriasis, restenosis, retinitis, rheumatoid arthritis, septic arthritis, stroke, tumor metastasis, type I diabetes, and vascular occlusion following angioplasty. The present invention relates to susbstituted cyclic amine derivatives which are useful for the inhibition and prevention of leukocyte adhesion and leukocyte adhesion-mediated pathologies. This invention also relates to compositions containing such compounds and methods of treatment using such compounds. Many physiological processes require that cells come into close contact with other cells and/or extracellular matrix. Such adhesion events may be required for cell activation, migration, proliferation and differentiation. Cell-cell and cell-matrix interactions are mediated through several families of cell adhesion molecules (CAMs) including the selectins, integrins, cadherins and immunoglobulins. CAMs play an essential role in both normal and pathophysiological processes. Therefore, the targetting of specific and relevant CAMs in certain disease conditions without interfering with normal cellular functions is
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essential for an effective and safe therapeutic agent that inhibits cell-cell and cell-matrix interactions. Web site: http://www.delphion.com/details?pn=US06403584__ •
Substituted quinoxaline derivatives as interleukin-8 receptor antagonists Inventor(s): Carson; Kenneth G. (Needham, MA), Connor; David Thomas (Ann Arbor, MI), Li; Jie Jack (Ann Arbor, MI), Low; Joseph Edwin (Brighton, MI), Luly; Jay R. (Wellesley, MA), Miller; Steven Robert (Ann Arbor, MI), Roth; Bruce David (Plymouth, MI), Trivedi; Bharat Kalidas (Farmington Hills, MI) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 6,548,499 Date filed: October 20, 2000 Abstract: Quinoxaline compounds are described as well as methods for the preparation and pharmaceutical compositions of same, which are useful as interleukin-8 (IL-8) receptor antagonists and can be used in the treatment of a chemokine-mediated disease wherein the chemokine binds to an IL-8a (CXCR1) or b (CXCR2) receptor such as a chemokine-mediated disease selected from psoriasis, or atopic distress syndrome, arthritis, inflammatory bowel disease, Crohn's disease, ulcerative colitis, gastric ulcer, septic shock, endotoxic shock, gram-negative sepsis, toxic shock syndrome, stroke, cardiac and renal reperfusion injury, glomerulo-nephritis, or thrombosis, Alzheimer's disease, graft versus host reaction, allograft rejections, or allergic diseases. Excerpt(s): The present invention relates to novel quinoxaline compounds useful as pharmaceutical agents, to methods for their production, to pharmaceutical compositions which include these compounds and a pharmaceutical carrier, and to pharmaceutical methods of treatment. The compounds of the present invention are Interleukin-8 (IL-8) receptor antagonists. More particularly, the compounds of the present invention are useful in the treatment of a chemokine-mediated disease wherein the chemokine binds to an IL-8a (CXCR1) or b (CXCR2) receptor such as, for example, a chemokine-mediated disease selected from psoriasis, or atopic dermatitis, tumor growth and angiogenesis, asthma, chronic obstructive pulmonary disease, adult respiratory distress syndrome, arthritis, inflammatory bowel disease, Crohn's disease, ulcerative colitis, gastric ulcer, septic shock, endotoxic shock, gram-negative sepsis, toxic shock syndrome, stroke, cardiac and renal reperfusion injury, glomerulo-nephritis, or thrombosis, Alzheimer's disease, graft versus host reaction, allograft rejections, or allergic diseases. We have identified a series of quinoxalines that are IL-8 receptor antagonists and which can additionally be used in psoriasis, or atopic dermatitis, disease associated with pathological angiogenesis (i.e. cancer), asthma, chronic obstructive pulmonary disease, adult respiratory distress syndrome, arthritis, inflammatory bowel disease, Crohn's disease, ulcerative colitis, gastric ulcer, septic shock, endotoxic shock, gram-negative sepsis, toxic shock syndrome, stroke, cardiac and renal reperfusion injury, glomerulonephritis, or thrombosis, Alzheimer's disease, graft versus host reaction, allograft rejections, or allergic diseases. or a pharmaceutically acceptable salt thereof. Web site: http://www.delphion.com/details?pn=US06548499__
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Synergistic compositions containing aromatic compounds and terpenoids present in alpinia galanga Inventor(s): Jensen; Nina Worm (Koge, DK), Petersen; Morten Just (Verlose, DK), Weidner; Morten Sloth (Virum, DK) Assignee(s): Eurovita A/S (Karlslunde, DK) Patent Number: 6,566,405 Date filed: August 6, 1999 Abstract: Novel compositions of matter containing aromatic compounds and terpenoids which are present in and may preferably be derived from the plant Alpinia galanga (Zingiberaceae) show synergistic effects with respect to immunomodulation, and they significantly suppress hypersensitivity reactions. Thus they are used for preparing medicaments for these purposes and, more specifically, for the treatment or prevention of IgE mediated allergic reactions and conditions, such as asthma, allergic rhinitis, a topic eczema or anaphylaxis, and autoimmune disorders, such as Crohn's disease, ulcerative colitis, rheumatoid arthritis or psoriasis, as well as for the alleviation of pain. They can for example be formulated into pharmaceuticals, cosmetics or dietary supplements. A method of preparing such compositions from Alpinia galanga is also described. Excerpt(s): The present invention relates to novel compositions of matter containing aromatic compounds and terpenoids which are present in and may preferably be derived from the plant Alpinia galanga (Zingiberaceae), and more specifically to novel pharmaceuticals, cosmetics or dietary supplements containing such compositions. Furthermore the invention relates to the use of the compositions for preparing medicaments for the treatment or prevention of hypersensitivity reactions and diseases associated with hypersensitivity reactions. The invention also relates to a method of preparing such compositions from Alpinia galanga. Alpinia galanga (L.), family Zingiberaceae, commonly known as Greater Galangal or Java Galangal, is cultivated and grows wild in Asia. The herb is rhizomatic, 1.8-2.1 m in height with oblong glabrous leaves and greenish white flowers. The fruits are orange-red capsules. The plant is also known under the name Languas galanga, especially in Thailand, and here it is locally called Katuk karohinee. In relation to the present invention the term "Alpinia galanga" refers to any variety of Alpinia galanga or Languas galanga found anywhere in the world. Web site: http://www.delphion.com/details?pn=US06566405__
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Therapeutic agent for treating ulcerative colitis Inventor(s): Aono; Shunji (Toyonaka, JP), Hattori; Ken-ichi (Kagawa, JP), Kawada; Mitsuhiro (Kagawa, JP) Assignee(s): Teikoku Seiyaku Co., Ltd. (Kagawa, JP) Patent Number: 6,586,022 Date filed: August 9, 2001 Abstract: An ulcerative colitis treating therapeutic agent which is very effective in repairing damaged tissues of ulcerative colitis and yet has no need of fear of side effects as those of steroids is provided. It is an therapeutic agent for treating ulcerative colitis which has peony root, especially, dry powders of peony root, or a Chinese medicine
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formulation containing peony root as an active ingredient. It is also an therapeutic agent for treating ulcerative colitis which has, as an active ingredient, an infused dry extract of peony root, an infused dry extract of a Chinese medicine formulation containing peony root, or especially an infused dry extract of Jia-Wei-Xiao-Yao-San, Dang-GuiShao-Yao-San, Shao-Yao-Gan-Cao-Tang, or Gui-Zhi-Fu-Ling-Wan. Excerpt(s): The present invention relates to a therapeutic agent for treating ulcerative colitis, which contains peony root. More particularly, the invention relates to a therapeutic agent for treating ulcerative colitis, having peony root or a Chinese medicine formulation containing peony root, which is very effective in repairing damaged tissues of ulcerative colitis and yet has no fear of side effects as those of steroids. Ulcerative colitis is a diffuse nonspecific inflammatory disease that only causes inflammation mainly in large intestines, that is, the regions from the rectum to the intestinum cecum and is characterized by continuous lesion. The disease is characterized in that the region of inflammation is localized in mucosa and submucosa, remission and exacerbation are repeated, and it cannot be completely cured. From the characteristics, it is said that patients can be relatively easily diagnosed as ulcerative colitis. With respect to the cause of ulcerative colitis, although there are various theories such as a theory that it is caused by food and life style and a theory that the cause is autoimmunity, the cause has not been convinced yet and the true cause is still unknown. Meanwhile, the enlargement process of inflammation of ulcerative colitis has been uncovered to a considerable extent and its knowledge has been disclosed in literatures, academic meetings, and the like. Ulcerative colitis cannot be treated by etiotropic therapy as a matter of fact and is treated by conservative therapy under the present conditions. Web site: http://www.delphion.com/details?pn=US06586022__ •
Treatment for inflammatory bowel disease with a vcam-1/1gG fusion protein Inventor(s): Burkly; Linda C. (West Newton, MA), Lobb; Roy R. (Westwood, MA) Assignee(s): Biogen, Inc. (Cambridge, MA) Patent Number: 6,482,409 Date filed: September 21, 1998 Abstract: A method for the treatment of inflammatory bowel disease (IBD) is disclosed. The method comprises administration of a VCAM-1/IgG fusion protein. Excerpt(s): The present invention relates to a treatment for inflammatory bowel disease (IBD). More particularly, this invention relates to the use of antibodies recognizing the integrin VLA-4 (very late antigen-4) in the treatment of IBD. Inflammatory bowel disease, or IBD, is a collective term encompassing ulcerative colitis and Crohn's disease (ileitis), which are chronic inflammatory disorders of the gastrointestinal tract. Ulcerative colitis is confined to the large intestine (colon) and rectum, and involves only the inner lining of the intestinal wall. Crohn's disease may affect any section of the gastrointestinal tract (i.e., mouth, esophagus, stomach, small intestine, large intestine, rectum and anus) and may involve all layers of the intestinal wall. Both diseases are characterized by abdominal pain and cramping, diarrhea, rectal bleeding and fever. The symptoms of these diseases are usually progressive, and sufferers typically experience periods of remission followed by severe flareups. Severe side effects are associated with the drugs commonly prescribed for IBD, including nausea, dizziness, changes in blood chemistry (including anemia and leukopenia), skin rashes and drug dependence; and
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the surgical treatments are radical procedures that often profoundly alter the everyday life of the patient. Accordingly, there is a great need for treatments for IBD that are effective yet less severe in their side effects and are less invasive of the IBD sufferer's body and quality of life. Web site: http://www.delphion.com/details?pn=US06482409__ •
Treatment of Inflammatory bowel disease by inhibiting binding and/or signalling through.alpha. 4.beta. 7 and its ligands and madcam Inventor(s): Newman; Walter (Boston, MA), Picarella; Dominic (Boston, MA), Ringler; Douglas J. (Revere, MA) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 6,551,593 Date filed: February 10, 1995 Abstract: The invention relates to the treatment of individuals suffering from a disease associated with leukocyte recruitment to the gastrointestinal tract or other tissues as a result of binding of leukocytes to gut-associated endothelium expressing the molecule MAdCAM (such as inflammatory bowel disease), comprising administering to the individual an effective amount of an antibody which inhibits the binding of leukocytes to endothelial MAdCAM. Excerpt(s): Inflammatory bowel disease (IBD), such as ulcerative colitis and Crohn's disease, for example, can be a debilitating and progressive disease involving inflammation of the gastrointestinal tract affecting an estimated two million people in the United States. Symptoms include abdominal pain, cramping, diarrhea and rectal bleeding. IBD treatments have included anti-inflammatory drugs (such as, corticosteroids and sulfasalazine), immunosuppressive drugs (such as, 6mercaptopurine, cyclosporine and azathioprine) and surgery (such as, colectomy). Podolsky, The New England Journal of Medicine, 325:928-937 (1991) and Podolsky, The New England Journal of Medicine, 325:1008-1016 (1991). Some studies have suggested that the cell adhesion molecule, ICAM-1, mediates leukocyte recruitment to inflammatory sites through adhesion to leukocyte surface ligands, i.e. Mac-1, LFA-1 or.alpha.4.beta.2 (Springer, Nature, 346:425-434 (1990)). In addition, vascular cell adhesion molecule-1 (VCAM-1), recognizing the.alpha.4.beta.1 integrin (VLA-4), has been reported to play a role in in vivo leukocyte recruitment as well (Silber et al., J. Clin. Invest. 93:1554-1563 (1994)). It has been proposed that IBD can be treated by blocking the interaction of ICAM-1 with LFA-1 or Mac-1 or VCAM-1 with.alpha.4.beta.1 (e.g., WO 93/15764). However, these therapeutic targets are likely involved in inflammatory processes in multiple organs, and a functional blockade would likely result in systemic immune dysfunction. Mucosal addressin MAdCAM, a mucosal vascular adhesion molecule, is a 58-66K glycoprotein adhesion receptor for lymphocytes which is distinct from VCAM-1 and ICAM-1 (Briskin et al., Nature, 363:461-463 (1993)). In contrast to VCAM-1 and ICAM-1, MAdCAM is preferentially expressed in the gastrointestinal tract, binds the.alpha.4.beta.7 integrin (also called LPAM-1 and CD49d/CD.sup.-) found on lymphocytes, and participates in the homing of these cells to mucosal sites, such as Peyer's patches in the intestinal wall (Hamann et al., Journal of Immunology, 152:32823293 (1994)). The use of inhibitors to the binding of MAdCAM to the receptor,.alpha.4.beta.7, in the treatment of diseases such as IBD has not been suggested. Web site: http://www.delphion.com/details?pn=US06551593__
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Treatment of inflammatory bowel disease with IFN-.gamma. inhibitors Inventor(s): Ashkenazi; Avi J. (San Mateo, CA), Ward; Rebecca H. R. (San Francisco, CA) Assignee(s): Genentech, Inc. (South San Francisco, CA) Patent Number: 6,558,661 Date filed: February 22, 1994 Abstract: The invention concerns a method for the prevention or treatment of inflammatory bowel disease by administering an interferon-.gamma. inhibitor. The invention further concerns pharmaceutical compositions and bispecific molecules useful in such method. Excerpt(s): The invention concerns the prevention or treatment of inflammatory bowel disease by administering an interferon-gamma (IFN-.gamma.) inhibitor. Inflammatory bowel disease (IBD) is a collective term for ulcerative colitis (UC) and Crohn's disease, which are considered as two different entities, but have many common features and probably share at least some pathologic mechanisms. There is sufficient overlap in the diagnostic criteria for UC and CD that it is sometimes impossible to say which a given patient has; however, the type of lesion typically seen is different, as is the localization. UC mostly appears in the colon, proximal to the rectum, and the characteristic lesion is a superficial ulcer of the mucosa; CD can appear anywhere in the bowel, with occasional involvement of stomach, esophagus and duodenum, and the lesions are usually described as extensive linear fissures. The aetiology of these diseases is unknown and the initial lesion has not been clearly defined; however, patchy necrosis of the surface epithelium, focal accumulations of leukocytes adjacent to glandular crypts, and an increased number of intraepithelial lymphocytes and certain macrophage subsets have been described as putative early changes, especially in Crohn's disease. Web site: http://www.delphion.com/details?pn=US06558661__
Patent Applications on Ulcerative Colitis As of December 2000, U.S. patent applications are open to public viewing.10 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to ulcerative colitis: •
1,3,4-Oxadiazolin-2-one derivatives and drugs containing these derivatives as the active ingredient Inventor(s): Ohmoto, Kazuyuki; (Mishima-gun, JP), Okuma, Motohiro; (Mishima-gun, JP), Sekioka, Tomohiko; (Mishima-gun, JP) Correspondence: Sughrue Mion, Pllc; 2100 Pennsylvania Avenue, N.W.; Washington; DC; 20037; US Patent Application Number: 20030087831 Date filed: May 31, 2002 Abstract: 1The compounds of formula (I) have an elastase inhibitory activity, therefor, they are useful for the treatment and/or prevention of a disease induced by an
10
This has been a common practice outside the United States prior to December 2000.
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abnormal enhancement of degradation of elastin, collagen fiber and/or proteoglycans by elastase, for example, pulmonary emphysema, rheumatoid arthritis, arteriosclerosis, adult respiratory distress syndrome, myocardial infarction, ulcerative colitis and gingivitis. Excerpt(s): (3) a pharmaceutical composition comprising them as active ingredient. Recently, researches and developments concerning elastase inhibitors are becoming active. was disclosed. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
5-Arylsulfonyl-imidazo[1',2':1,6]pyrido[2,3-b]pyrazine-6-amines compounds
and
related
Inventor(s): Kleinman, Edward F.; (Pawcatuck, CT) Correspondence: Pfizer INC.; Patent Department, Ms8260-1611; Eastern Point Road; Groton; CT; 06340; US Patent Application Number: 20030203911 Date filed: April 28, 2003 Abstract: A compound of the formula 1wherein a, X, R.sup.1, R.sup.2, R.sup.3 and R.sup.4 are as defined above, useful in the treatment of respiratory, allergic, rheumatoid, body weight regulation, inflammatory and central nervous system disorders such as asthma, chronic obstructive pulmonary disease, adult respiratory diseases syndrome, shock, fibrosis, pulmonary hypersensitivity, allergic rhinitis, atopic dermatitis, psoriasis, weight control, rheumatoid arthritis, cachexia, crohn's disease, ulcerative colitis, arthritic conditions and other inflammatory diseases, depression, multi-infarct dementia and AIDS. Excerpt(s): This non-provisional patent application is based upon and claims priority from U.S. patent application Ser. No. 09/918,099, filed Jul. 30, 2001, which claims priority from United States non-provisional application Ser. No. 09/489,689, filed Jan. 24, 2000, which claims priority from U.S. provisional patent application No. 60/117,875, filed Jan. 29, 1999. This invention relates to 5-arylsulfonyl-imidazo[1',2':1,6]pyrido[2- ,3b]pyrazine-6-amines and related compounds. The compounds are selective inhibitors of phosphodiesterase type 4 (PDE4) and the production of tumor necrosins factor (TNF), and as such are useful in the treatment of respiratory, allergic, rheumatoid, body weight regulation, inflammatory and central nervous system disorders such as asthma, chronic obstructive pulmonary disease, adult respiratory diseases syndrome, shock, fibrosis, pulmonary hypersensitivity, allergic rhinitis, atopic dermatitis, psoriasis, weight control, rheumatoid arthritis, cachexia, Crohn's disease, ulcerative colitis, arthritic conditions and other inflammatory diseases, depression, multi-infarct dementia, and AIDS. This invention also relates to a method of using such compounds in the treatment of the foregoing diseases in mammals, especially humans, and to pharmaceutical compositions containing such compounds. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Allenic aryl sulfonamide hydroxamic acids as matrix metalloproteinase and tace inhibitors Inventor(s): Delos Santos, Efren Guillermo; (Nanuet, NY), Sandanayaka, Vincent Premaratna; (Northboro, MA) Correspondence: Daniel B. Moran; Five Giralda Farms; Madison; NJ; 07940; US Patent Application Number: 20030130238 Date filed: November 1, 2002 Abstract: Compounds of the formula 1are useful in treating disease conditions mediated by TNF-.alpha., such as rheumatoid arthritis, osteoarthritis, sepsis, AIDS, ulcerative colitis, multiple sclerosis, Crohn's disease, degenerative cartilage loss, graft rejection, cachexia, inflammation, fever, insulin resistance, septic shock, congestive heart failure, inflammatory disease of the central nervous system, inflammatory bowel disease and HIV. Excerpt(s): This invention relates to allenic aryl sulfonamide hydroxamic acids which act as inhibitors of TNF-.alpha. converting enzyme (TACE) and matrix metalloproteinase (MMP). The compounds of the present invention are useful in disease conditions mediated by MMP and TACE, such as rheumatoid arthritis, osteoarthritis, sepsis, AIDS, ulcerative colitis, multiple sclerosis, Crohn's disease, degenerative cartilage loss, graft rejection, cachexia, inflammation, fever, insulin resistance, septic shock, congestive heart failure, inflammatory disease of the central nervous system, inflammatory bowel disease and HIV. TNF-.alpha. converting enzyme (TACE) catalyzes the formation of TNF-.alpha. from membrane bound TNF-.alpha. precursor protein. TNF-.alpha. is a proinflammatory cytokine that is believed to have a role in rheumatoid arthritis [Shire, M. G.; Muller, G. W. Exp. Opin. Ther. Patents 1998, 8(5), 531; Grossman, J. M.; Brahn, E. J. Women's Health 1997, 6(6), 627; Isomaki, P.; Punnonen, J. Ann. Med. 1997, 29, 499; Camussi, G.; Lupia, E. Drugs, 1998, 55(5), 613.] septic shock [Mathison, et. al. J. Clin. Invest. 1988, 81, 1925; Miethke, et. al. J. Exp. Med. 1992, 175, 91.], graft rejection [Piguet, P. F.; Grau, G. E.; et. al. J. Exp. Med. 1987, 166, 1280.], cachexia [Beutler, B.; Cerami, A. Ann. Rev. Biochem. 1988, 57, 505.], anorexia, inflammation [Ksontini, R,; MacKay, S. L. D.; Moldawer, L. L. Arch. Surg. 1998, 133, 558.], congestive heart failure [Packer, M. Circulation, 1995, 92(6), 1379; Ferrari, R.; Bachetti, T.; et. al. Circulation, 1995, 92(6), 1479.], post-ischaemic reperfusion injury, inflammatory disease of the central nervous system, inflammatory bowel disease, insulin resistance [Hotamisligil, G. S.; Shargill, N. S.; Spiegelman, B. M.; et. al. Science, 1993, 259, 87.] and HIV infection [Peterson, P. K.; Gekker, G.; et. al. J. Clin. Invest. 1992, 89, 574; Pallares-Trujillo, J.; Lopez-Soriano, F. J. Argiles, J. M. Med. Res. Reviews, 1995, 15(6), 533.]], in addition to its well-documented antitumor properties [Old, L. Science, 1985, 230, 630.]. For example, research with antiTNF-.alpha. antibodies and transgenic animals has demonstrated that blocking the formation of TNF-.alpha. inhibits the progression of arthritis [Rankin, E. C.; Choy, E. H.; Kassimos, D.; Kingsley, G. H.; Sopwith, A. M.; Isenberg, D. A.; Panayi, G. S. Br. J. Rheumatol. 1995, 34, 334; Pharmaprojects, 1996, Therapeutic Updates 17 (Oct.), au197M2Z.]. This observation has recently been extended to humans as well as described in "TNF-.alpha. in Human Diseases", Current Pharmaceutical Design, 1996, 2, 662. Matrix metalloproteinases (MMPs) are a group of enzymes that have been implicated in the pathological destruction of connective tissue and basement membranes. These zinc containing endopeptidases consist of several subsets of enzymes including collagenases, stromelysins and gelatinases. Of these classes, the gelatinases have been shown to be the MMPs most intimately involved with the growth and spread of tumors. It is known that the level of expression of gelatinase is elevated in malignancies, and that gelatinase can
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degrade the basement membrane which leads to tumor metastasis. Angiogenesis, required for the growth of solid tumors, has also recently been shown to have a gelatinase component to its pathology. Furthermore, there is evidence to suggest that gelatinase is involved in plaque rupture associated with atherosclerosis. Other conditions mediated by MMPs are restenosis, MMP-mediated osteopenias, inflammatory diseases of the central nervous system, skin aging, tumor growth, osteoarthritis, rheumatoid arthritis, septic arthritis, corneal ulceration, abnormal wound healing, bone disease, proteinuria, aneurysmal aortic disease, degenerative cartilage loss following traumatic joint injury, demyelinating diseases of the nervous system, cirrhosis of the liver, glomerular disease of the kidney, premature rupture of fetal membranes, inflammatory bowel disease, periodontal disease, age related macular degeneration, diabetic retinopathy, proliferative vitreoretinopathy, retinopathy of prematurity, ocular inflammation, keratoconus, Sjogren's syndrome, myopia, ocular tumors, ocular angiogenesis/neo-vascularization and corneal graft rejection. For recent reviews, see: (1) Recent Advances in Matrix Metalloproteinase Inhibitor Research, R. P. Beckett, A. H. Davidson, A. H. Drummond, P. Huxley and M. Whittaker, Research Focus, Vol. 1,16-26, (1996), (2) Curr. Opin. Ther. Patents (1994) 4(1): 7-16, (3) Curr. Medicinal Chem. (1995) 2: 743-762, (4) Exp. Opin. Ther. Patents (1995) 5(2): 1087-110, (5) Exp. Opin. Ther. Patents (1995) 5(12): 1287-1196: (6) Exp. Opin. Ther. Patents (1998) 8(3): 281-259. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
ANTISENSE OLIGONUCLEOTIDES TARGETED TO IL-15 Inventor(s): HAMANAKA, SHOJI; (YOKOSUKA, JP), KUBO, HIROYUKI; (CARLSBAD, CA), NOZAWA, IWAO; (CARLSBAD, CA), VEERAPANANE PH.D, DANGE; (SAN DIEGO, CA) Correspondence: Fish & Richardson, PC; 4350 LA Jolla Village Drive; Suite 500; San Diego; CA; 92122; US Patent Application Number: 20030013668 Date filed: July 7, 1999 Abstract: The invention features antisense oligonucleotide molecules that specifically bind polynucleotides encoding IL-15. The present invention provides antisense oligonucleotides capable of inhibiting IL-15 expression, and methods of use thereof to reduce activity of IL-15 in tissues in order to treat diseases such as rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis, chronic liver disease, ulcerative colitis and cell proliferative disorders. Excerpt(s): This application claims priority from U.S. Provisional Application Ser. No. 60/091,873 filed Jul. 7, 1998, the disclosure of which is incorporated herein by reference. This invention relates generally to the field of therapeutic compositions and more specifically to antisense oligonucleotides that bind to interleukin-15 (IL-15 ) polynucleotides and methods of treatment for diseases associated with IL-15. There are a number of diseases known in humans that affect various tissues, including the joints, and particularly the synovium. These include synovial sarcomas, osteoarthritis, bacterial and fungal infections, and inflammatory, autoimmune, and hemorrhagic diseases. Combined, they are a cause of great pain and suffering in the population, with little effective therapy apart from symptomatic treatment with analgesics and antiinflammatory drugs (reviewed by Gardner, 1994 J. Anat. 184:465-76). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Apparatus and method for debilitating or killing microorganisms within the body Inventor(s): Ganz, Robert A.; (Minnetonka, MN), Melgaard, Hans L.; (North Oaks, MN) Correspondence: James V. Harmon; Pillsbury Center, Suite 2000; 220 South Sixth Street; Minneapolis; MN; 55402; US Patent Application Number: 20030191459 Date filed: April 9, 2002 Abstract: A surgical apparatus has a body portion that includes a shaft terminating in a distal head or tip and a means for directing light radiation from the apparatus onto the lining of a body cavity for treating an ailment in a body cavity of a patient as for example a gastrointestinal ailment of a patient such as gastritis, gastric ulcer, duodenal ulcer, gastric cancer, gastric lymphoma, ulcerative colitis, or Crohn's disease as well as for treating diseases of the circulatory system, urogenital systems and other body cavities. The method of use of the apparatus comprises inserting the shaft of the apparatus into a body cavity, e.g., stomach or colon, of the patient to place the distal tip of the shaft in the desired position. The body cavity of the patient is then irradiated with light radiation so as to kill or debilitate microorganisms lining the body cavity without serious destruction of the body tissue of the patient to thereby improve or alleviate one or more of the symptoms of the ailment. A probiotic comprising innocuous bacteria can be administered to the patient to reestablish the growth of normal microbial flora when used in the gastrointestinal tract. Excerpt(s): This invention relates to an apparatus and method for the destruction of micro-organisms on or within a body cavity of a patient through the use of radiation. Infections involving the human gastrointestinal tract are extremely common, involving many millions of people on an annual basis. These infections include bacteria, viruses, and fungi, and are responsible for significant illness, morbidity and, in many cases, death. While the invention has utility in destroying microorganisms in various parts of the body, e.g., the stomach, bowel, lungs, peritoneal cavity, urinary tract, etc., it is particularly useful in the treatment of gastrointestinal infections. It has recently been shown that the most common gastrointestinal infection in the world is due to Helicobacter pylori, a bacterial pathogen that infects the stomach and duodenum. In the United States, for example, Helicobacter pylori is found in approximately 20% of the adult population. It is a chronic gut infection and, once acquired, is notoriously difficult to cure. Most infectious bacteria can be readily destroyed by the human immune system; however, Helicobacter pylori lives in the lumen of the stomach and on the surfaces of the stomach and duodenal cells, making it relatively resistant to a host immune response, even if vigorous. Its position has, however, been taken advantage of in the treatment method and apparatus employed in the present invention. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Benzoic acid derivatives, processes for producing the same and drugs containing the same as the active ingredient Inventor(s): Kobayashi, Kaoru; (Osaka, JP), Maruyama, Takayuki; (Osaka, JP), Tani, Kousuke; (Osaka, JP) Correspondence: Sughrue Mion, Pllc; 2100 Pennsylvania Avenue, N.W.; Washington; DC; 20037; US Patent Application Number: 20030114435 Date filed: August 16, 2002 Abstract: An agent comprising the benzoic acid of formula (I) 1, wherein A, B, R.sup.6, R.sup.7 are carbocyclic ring, heterocyclic ring, etc.; R.sup.1 is hydroxy etc.; R.sup.2, R.sup.3, R.sup.4 are alkyl etc.; R.sup.5, D, E are alkylene, etc.; G is oxygen etc., as active ingredient.The compound of formula (I) is considered to be useful for the treatment and/or prophylaxis of bone diseases, cancer, systemic granuloma, immunological diseases, allergy, atopy, asthma, gumboil, gingivitis, periodontitis, neurocyte death, Alzheimer's diseases, lungs injury, pulmopathy, acute hepatitis, nephritis, myocardial ischemia, Kawasaki disease, ambustion, ulcerative colitis, Crohn's disease, multiple organ failure, sleeping disorder, platelet aggregation, etc. Excerpt(s): The present invention relates to benzoic acid derivatives. , wherein all symbols have the same meanings as hereafter described, a process for the preparation thereof and a pharmaceutical agent comprising the same as active ingredient. Prostaglandin E.sub.2 (abbreviated as PGE.sub.2) has been known as a metabolite in the arachidonic acid cascade. It has been known that PGE.sub.2 possesses cyto-protective activity, uterine contractile activity, a pain-inducing effect, a promoting effect on digestive peristalsis, an awaking effect, a suppressive effect on gastric acid secretion, hypotensive activity, and diuretic activity. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
•
Diagnostic and therapeutic compositions and methods related to GPCR 38, a G protein-coupled receptor (GPCR) Inventor(s): Brown, Joseph P.; (Seattle, WA), Burmer, Glenna C.; (Seattle, WA), Kulander, Bruce G.; (Seattle, WA), Roush, Christine L.; (Seattle, WA) Correspondence: Joshua King; Graybeal Jackson Haley Llp; Suite 350; 155-108th Avenue N.E.; Bellevue; WA; 98004-5901; US Patent Application Number: 20030186336 Date filed: July 26, 2002 Abstract: The present invention comprises systems, methods, compositions and the like, such as diagnostics, medicaments and therapeutics, relating to GPR 38 and Alzheimer's disease and Parkinson's disease, inflammatory bowel diseases including ulcerative colitis and Crohn's disease, Hodgkin's disease, glioblastoma and carcinomas including breast, colon, lung (small cell and adenocarcinoma) pancreatic (small cell and adenocarcinoma), ovarian, and prostate. Such diagnostics and therapeutics include peptide, protein, antibody and nucleic acid based compositions, including agonists, antagonists, probes, antisense and gene therapy compositions. Excerpt(s): The present application claims priority from PCT patent application PCT/US01/45219, filed Nov. 29, 2001, which application claims priority from U.S.
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provisional patent application Ser. No. 60/250,251, filed Nov. 29, 2000, and U.S. provisional patent application Ser. No. 60/250,452, filed Nov. 30, 2000, both of which are presently pending. G protein-coupled receptors (GPCRs) are a large group of proteins that transmit signals across cell membranes. In general terms, GPCRs function somewhat like doorbells. When a molecule outside the cell contacts the GPCR (pushes the doorbell), the GPCR changes its shape and activates "G proteins" inside the cell (similar to the doorbell causing the bell to ring inside the house, which in turn causes people inside to answer the door). In addition, GPCRs are like high-security doorbells because each GPCR responds to only one specific kind of signaling molecule (called its "endogenous ligand"). Part of the GPCR is located outside the cell (the "extracellular domain"), part spans the cell's membrane (the "transmembrane domain"), and part is located inside the cell (the "intracellular domain"). GPCRs are embedded in the outer membrane of a cell and recognize and bind certain types of signaling molecules that are present in the spaces surrounding the cell. GPCRs are used by cells to keep an eye on the cells' own activity and environment. In organisms having many cells, the cells use GPCRs to talk to each other. GPCRs are of great interest to the pharmaceutical industry and other industries. For example, many drugs act by binding to specific GPCRs and initiating their intracellular actions, and diagnostics and therapeutics based on GPCRs are becoming increasingly important. Databases, such as LifeSpan BioScience's GPCR Database, help researchers to compare and contrast different GPCRs so that various GPCR functions can be investigated and established. With greater knowledge about the distribution of GPCRs in human tissues and their involvement in disease processes, researchers can design more diagnostics and more effective drugs with fewer side effects. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Early detection marker for chronic inflammatory associated diseases Inventor(s): Pereira, Heloise Anne; (Edmond, OK) Correspondence: Dunlap, Codding & Rogers P.C.; PO Box 16370; Oklahoma City; OK; 73114; US Patent Application Number: 20030170745 Date filed: March 7, 2003 Abstract: The present invention in one embodiment is an early detection marker for chronic inflammatory-associated diseases, including atherosclerosis, Alzheimer's disease, asthma, rheumatoid arthritis, osteoarthritis, and inflammatory diseases of the bowel such as Crohn's disease, Ulcerative colitis, Irritable bowel syndrome and Inflammatory bowel disease. The method, for example may comprise (1) obtaining a fluid sample from the subject, wherein the subject does not have an acute bacterial or viral infection when the fluid sample is obtained, (2) testing the fluid sample for a circulating or secreted CAP37 protein, and (3) concluding that the subject has a chronic inflammatory-associated disease when the CAP37 protein is detected in the fluid sample. The fluid sample may comprise serum, plasma, or cerebrospinal fluid, for example, or any other body fluid exposed to endothelial, vascular, or neuronal secretions. Excerpt(s): This application claims the benefit of U.S. Serial No. 60/363,114, filed Mar. 8, 2002, which is hereby expressly incorporated herein by reference in its entirety. The present invention relates to, but is not limited to, methods for detecting inflammatoryassociated diseases by detecting CAP37 proteins in a body fluid. Cationic Antimicrobial
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Protein of M.sub.r 37 kDa (CAP37) was originally isolated from granule extracts of human polymorphonuclear leukocytes (PMN) in 1984 (1). The amino acid sequence of PMN-CAP37 revealed its relation to members of the serine protease family that have a conserved catalytic active site consisting of his-57, asp-102 and ser-195 in the charge relay system (2). Of these sites, the conserved histidine and serine of the catalytic triad have been replaced with serine and glycine residues, respectively, rendering CAP37 ineffective as a serine protease (2,3). However, CAP37 has been demonstrated to have a diverse and exciting repertoire of functions. It was first analyzed regarding its bactericidal properties against Gram negative bacteria including, but not limited to, Salmonella typhimurium, Escherichia coli and Pseudomonas aeruginosa (4) and its ability to bind to and neutralize lipopolysaccharide (LPS)(5). Subsequently we showed CAP37 to be a potent chemoattractant for monocytes (6). Additionally, regarding its effects on the monocyte, CAP37 has been reported to stimulate their survival and thrombospondin secretion (7), also to enhance the LPS-stimulated release of prostaglandin E2 (8), interleukin 6 (IL-6)(9) and tumor necrosis factor-alpha (TNF.alpha.)(8-10). To add even further to its extensive range of known functions, CAP37 has been demonstrated to stimulate the reversible contraction of fibroblasts and endothelial cells (7) and to activate endothelial cell protein kinase C (PKC)(11). Recently, CAP37 released from stimulated PMN was reported to be taken up and sequestered in nearby endothelial mitochondria and has been suggested to protect against apoptosis (12). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Indole derivatives, process for preparation of the same and use thereof Inventor(s): Kobayashi, Kaoru; (Mishima-gun, JP), Nambu, Fumio; (Mishima-gun, JP), Torisu, Kazuhiko; (Mishima-gun, JP) Correspondence: Sughrue Mion, Pllc; 2100 Pennsylvania Avenue, N.W.; Washington; DC; 20037; US Patent Application Number: 20030176400 Date filed: December 13, 2002 Abstract: Indole derivatives represented by formula (I): 1(wherein all symbols are described in the description), a process for the preparation of the same and a DP receptor antagonist comprising it as an active ingredient. Since the compounds of formula (I) binds to and are antagonistic to a DP receptor, they are useful in for the prevention and/or treatment of diseases, for example, allergic diseases (allergic rhinitis, allergic conjunctivitis, atopic dermatitis, bronchial asthma, food allergy, etc., systemic mastocytosis; disorders due to systemic mastocyte activation, anaphylactic shock, bronchoconstriction, urticaria, eczema, etc.), diseases accompanied with itching (atopic dermatitis, urticaria, etc.), secondary diseases caused by behaviors (scratching behaviors, beating, etc.) (cataract, retinal detachment, inflammation, infection, sleep disorder, etc.), inflammation, chronic obstructive pulmonary disease, ischemic reperfusion disorder, cerebrovascular disorder, pleuritis complicated by rheumatoid arthritis, ulcerative colitis, and the like. Excerpt(s): The present invention relates to indole derivatives. (wherein all symbols have the same meanings as described below), a process for the preparation of the same and use thereof. Prostaglandin D (hereinafter referred to as "PGD") are known as a metabolite in the arachidonic acid cascade, and are known to have effects of bronchoconstriction, vasodilatation or vasoconstriction and platelet aggregation
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inhibition. PGD is considered to be produced from mast cells, and the increase of PGD concentration has been recognized among systemic mastocytosis patients (New Eng. J. Med., 303, 1400-1404 (1980)). Also, PGD is considered to relate to neuro activities, especially, sleep and hormone secretion. Furthermore, there are reports suggesting participations in platelet aggregation, glycogen metabolism, ocular tension adjustment and the like. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Isoxazolone compounds useful in treating diseases associated with unwanted cytokine activity Inventor(s): Clark, Michael Philip; (Loveland, OH), De, Biswanath; (Cincinnati, OH), Djung, Jane Far-Jine; (Mason, OH), Laughlin, Steven Karl; (Taylor Mill, KY), Natchus, Michael George; (Alpharetta, GA), Tullis, Joshua Spector; (Broomfield, CO) Correspondence: The Procter & Gamble Company; Intellectual Property Division; Winton Hill Technical Center - Box 161; 6110 Center Hill Avenue; Cincinnati; OH; 45224; US Patent Application Number: 20030096814 Date filed: May 7, 2002 Abstract: Isoxazolone compounds having the generic structure: 1are used to treat disease associated with unwanted cytokine activity, including rheumatoid arthritis, osteoarthritis, diabetes, HIV/AIDS, inflammatory bowel disease, Crohn's disease, ulcerative colitis, congestive heart, hypertension, chronic obstructive pulmonary disease, septic shock syndrome, tuberculosis, adult respiratory distress, asthma, atherosclerosis, muscle degeneration, periodontal disease, cachexia, Reiter's syndrome, gout, acute synovitis, anorexia and bulimia nervosa fever, malaise, myalgia and headaches. Excerpt(s): This application claims priority under Title 35, United States Code 119(e) from Provisional Application Serial No. 60/293,889, filed May 24, 2001. The present invention is directed to certain isoxazolone compounds that inhibit the release of inflammatory cytokines such as interleukin-1 (1L-1) and tumor necrosis factor (TNF) from cells. The compounds of the invention, therefore, are useful in treating diseases involving unwanted cytokine activity. Many cytokine-mediated diseases and conditions are associated with excessive or unregulated production or activity of one or more cytokines such as interleukin 1 (IL-1), tumor necrosis factor (TNF), interleukin 6 (IL-6) and interleukin 8 (IL-8). IL-1 and TNF are important proinflammatory cytokines, which along with several other related molecules, mediate inflammatory cellular response in a wide variety of diseases and conditions. Proinflammatory cytokines such as IL-1 and TNF stimulate other inflammatory mediators such as nitric oxide, cyclooxygenase-2, matrix metalloproteinases. The inhibition of these cytokines is consequently both directly and indirectly beneficial in controlling, reducing and alleviating many of these disease states. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method and apparatus for distinguishing crohn's disease from ulcerative colitis and other gastrointestinal diseases by detecting the presence of fecal antibodies to saccharomyces cerevisiae Inventor(s): Boone, James Hunter; (Christiansburg, VA), Lyerly, David Maxwell; (Radford, VA), Wilkins, Tracy Dale; (Riner, VA) Correspondence: Shook, Hardy & Bacon Llp; 1200 Main Street; Kansas City; MO; 641052118; US Patent Application Number: 20030143649 Date filed: October 25, 2002 Excerpt(s): This application claims the benefit of priority to U.S. Provisional Application No. 60/335,812 filed on Oct. 26, 2001, the entirety of the disclosure of which is hereby incorporated by reference. Not Applicable. A method and apparatus for the differentiation of Crohn's disease from other gastrointestinal illnesses, such as ulcerative colitis and irritable bowel syndrome, using the presence of fecal anti-Saccharomyces cerevisiae antibodies (ASCA) as a marker for Crohn's disease are provided. The apparatus includes an enzyme-linked immunoassay or other immunoassay that utilizes antibodies specific to human immunoglobulins for the measurement of total endogenous ASCA in a human fecal sample. The method and apparatus may be used by healthcare providers to distinguish Crohn's disease from other gastrointestinal illnesses, such as ulcerative colitis and irritable bowel syndrome. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method and composition for treatment of inflammatory bowel disease Inventor(s): Bergeron, Raymond J. JR.; (Gainesville, FL) Correspondence: Miles & Stockbridge P.C.; Suite 500; 1751 Pinnacle Drive; Mclean; VA; 22102-3833; US Patent Application Number: 20030211978 Date filed: June 12, 2003 Abstract: A composition in unit dosage form for the inhibition, prevention or treatment of inflammatory bowel disease comprising an effective amount of a compound having the formula: 1and a pharmaceutically acceptable carrier therefor. Also disclosed is a method for the inhibition, prevention or treatment of inflammatory bowel disease comprising administering to a human or non-human mammal in need thereof an effective amount of a compound having the formula: 2 Excerpt(s): The present invention relates to the treatment of inflammatory bowel diseases. Inflammatory bowel disorders or diseases (IBD) encompass a spectrum of overlapping clinical diseases that appear to lack a common etiology. IBD, however, are characterized by chronic inflammation at various sites in the gastrointestinal (GI) tract. Illustrative IBD are regional enteritis (or Crohn's disease), idiopathic ulcerative colitis, idiopathic proctocolitis and infectious colitis. Most hypotheses regarding the pathogenesis of IBD concern the implication of immunologic, infectious and dietary factors. IBD are characterized histopathologically by ulceration, pseudomembranes, radiologically visible lesions, edema and the build-up of inflammatory cells; symptoms involve diarrhea, abdominal pain, weight loss and hypoproteinemia. Descriptions in the literature include Northfield, Drugs, Vol. 14, pages 198-206 (1977); Blaker et al, Eur. J.
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Pediatr., Vol. 139, pages 162-164 (1982); Singleton, The Gastroenterology Annual, pages 268-310 (1983); Saco et al, J. Amer. Acad. Dermatol., Vol. 4, pages 619-629 (1981); Prantera et al, Ital. J. Gastroenterol., Vol. 13, pages 24-27 (1981); Sales et al, Arch. Int. Med., Vol. 143, pages 294-299 (1983); and Ament, Inflammatory Bowel Diseases, Martinus Nijhoff Publ., Boston, Mass., pages 254-268 (1982). Less frequent, but also possible, are mucosal inflammation of other sections of the GI tract, such as duodenitis, jejunitis and proctitis. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method for the preparation of a pharmaceutical composition comprising 5aminosalicylic acid for use in treatment of ulcerative colitis and crohn's disease Inventor(s): Jepsen, Svenn Kluver; (Holte, DK) Correspondence: Steptoe & Johnson Llp; 1330 Connecticut AVE., NW; Washington; DC; 20036; US Patent Application Number: 20030138495 Date filed: October 11, 2002 Abstract: The present invention concerns a new method of preparing granules comprising 5-aminosalicylic acid and a new method of preparing a pharmaceutical composition for the treatment of ulcerative colitis or Crohn's disease by oral administration comprising as active ingredient 5-aminosalicylic acid. Excerpt(s): The present invention relates to a method of preparing a pharmaceutical composition useful for the treatment of ulcerative colitis and Crohn's disease, currently denominated "inflammatory bowel diseases" (IBD). More particular, the invention relates to a new method of producing granules comprising 5-aminosalisylic acid (5ASA) for use in the preparation of solid oral dosage forms. Ulcerative colitis is a chronic inflammatory disease of the colon of unknown etiology. In its acute stages it resembles an infectious disease, but no microorganism has been definitively established as its cause. The disease causes inflammations of the mucosa of the colon, with extension to the submucosa in severe cases. Typically, not only the colon, but also the rectum is attacked, but only rarely is the ileum involved. The ulcer formation and its extent vary with the developmental stage of the disease, but can often be determined macroscopically (sigmoidoscopy and colonoscopy). The related disease, Crohn's disease, also known as regional enteritis or colitis granulomatosa, is most frequently located in the small intestine (small bowel), especially in the ileum, but may also affect the jejunum and any part of the colon, including the rectum. In the latter case the differentiation of Crohn's disease from ulcerative colitis gives rise to great diagnostic problems. Generally, the inflammation differs from that of ulcerative colitis by progressing to layers deeper than the mucosa and affecting the epithelium to a lesser degree. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method for treating inflammation Inventor(s): Blumberg, Hal; (Seattle, WA), Chandrasekher, Yasmin A.; (Mercer Island, WA), Eagan, Maribeth A.; (Seattle, WA), Foster, Donald C.; (Lake Forest Park, WA), Jaspers, Stephen R.; (Edmonds, WA), Kelly, James D.; (Mercer Island, WA), Madden, Karen L.; (Bellevue, WA), Novak, Julia E.; (Bainbridge Island, WA), Sprecher, Cindy A.; (Seattle, WA), Thompson, Penny; (Snohomish, WA), Xu, Wenfeng; (Mukilteo, WA) Correspondence: Shelby J. Walker; Zymogenetics, INC.; 1201 Eastlake Avenue East; Seattle; WA; 98102; US Patent Application Number: 20040005320 Date filed: April 28, 2003 Abstract: A method for treating IL-20 induced inflammation. An antagonist to IL-20 is administered to treat inflammation and associated diseases. The antagonist can be an antibody that binds to IL-20 or its receptor or a soluble receptor that binds to IL-20. Examples of such diseases are adult respiratory disease, psoriasis, eczema, contact dermatitis, atopic dermatitis, septic shock, multiple organ failure, inflammatory lung injury, bacterial pneumonia, inflammatory bowel disease, rheumatoid arthritis, asthma, ulcerative colitis and Crohn's disease. Excerpt(s): The present application is a divisional application of U.S. application Ser. No. 09/746,359, filed Dec. 22, 2000, which claims priority under 35 U.S.C.sctn.119(e) to U.S. Provisional Patent Application 60/171,969, filed Dec. 23, 1999 and U.S. Provisional Application No. 60/213,341 filed Jun. 22, 2000. The teachings of all of the references cited herein are incorporated in their entirety herein by reference. Inflammation normally is a localized, protective response to trauma or microbial invasion that destroys, dilutes, or walls-off the injurious agent and the injured tissue. It is characterized in the acute form by the classic signs of pain, heat, redness, swelling, and loss of function. Microscopically, it involves a complex series of events, including dilation of arterioles, capillaries, and venules, with increased permeability and blood flow, exudation of fluids, including plasma proteins, and leukocyte migration into the area of inflammation. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method for treating inflammatory bowel disease and other forms of gastrointestinal inflammation Inventor(s): Rachmilewitz, Daniel; (Tel Aviv, IL), Raz, Eyal; (Del Mar, CA) Correspondence: Bozicevic, Field & Francis Llp; 200 Middlefield RD; Suite 200; Menlo Park; CA; 94025; US Patent Application Number: 20030130217 Date filed: August 13, 2002 Abstract: The invention provides a method for ameliorating gastrointestinal inflammation, particularly chronic gastrointestinal inflammation such as inflammatory bowel disease (IBD), in a subject. In one embodiment, the method comprises administering an immunomodulatory nucleic acid to a subject suffering from or susceptible to gastrointestinal inflammation. Excerpt(s): This application is a continuation-in-part of U.S. patent application Ser. No. 09/791,500, filed Feb. 22, 2001, which claims the benefit of U.S. Provisional Application
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Serial No. 60/184,256, filed Feb. 23, 2000, which applications are incorporated herein by reference in their entirety. The invention relates to a method for ameliorating inflammation of the gastrointestinal tract, such as that associated with inflammatory bowel disease, in a subject. The method involves administering a nucleic acid comprising an immunomodulatory nucleotide sequence to the subject. The immunomodulatory sequence can be administered alone or together with an additional therapeutic agents. Gastrointestinal inflammation is one of the most common types of inflammatory process which affects humans (for a review, see, e.g., Bamford, FEMS Immunol Med Microbiol 91999);24(2):161-8). Inflammatory bowel disease (IBD), a form of chronic gastrointestinal inflammation, includes a group of chronic inflammatory disorders of generally unknown etiology, e.g., ulcerative colitis (UC) and Crohn's disease (CD). Clinical and experimental evidence suggest that the pathogenesis of IBD is multifactorial involving susceptibility genes and environmental factors (Sartor Am J Gastroenterol. (1997) 92:5S-11S). The interaction of these factors with the immune system leads to intestinal inflammation and dysregulated mucosal immunity against commensal bacteria, various microbial products (e.g., LPS) or antigens (Mayer et al. Current concept of IBD: Etiology and pathogenesis. In "Inflammatory Bowel Disease" 5.sup.th edition 2000, Kirsner J B editor. W. B. Sanunders Company, pp 280-296; for a discussion of IBD in children see, e.g., Walker-Smith, Postgrad Med J (2000) 76(898):46972). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Methods and compositions for treating inflammatory bowel diseases relating to human tumor necrosis factor-gamma-beta Inventor(s): Ni, Jian; (Germantown, MD), Rosen, Craig A.; (Laytonsville, MD), Wei, Ping; (Brookeville, MD), Yu, Guo-Liang; (Berkeley, CA), Zhang, Jun; (San Diego, CA) Correspondence: Human Genome Sciences Inc; 9410 Key West Avenue; Rockville; MD; 20850 Patent Application Number: 20030198640 Date filed: December 6, 2002 Abstract: The present invention encompasses methods for detection, diagnosis, prevention, treatment, and/or amelioration of inflammatory bowel diseases and disorders using TNF-gamma-.beta. and its receptors DR3 and TR6. In particular the invention encompasses methods of using TNF-gamma-.beta., DR3 and TR6 polypeptides, as well as antibodies, and antagonists thereto, in the diagnosis, prognosis and treatment of ulcerative colitis and/or Crohn's disease. Methods of screening for antagonists of the TNF-gamma-.beta. polypeptide, together with therapeutic uses of such antagonists are also disclosed. Excerpt(s): This application, which claims benefit under 35 U.S.C.sctn.119(e) of U.S. Provisional Application No. 60/336,695, filed Dec. 7, 2001, is a Continuation-In-Part of U.S. patent application Ser. No. 10/226,294, filed Aug. 23, 2002; which in turn claims the benefit of priority under 35 U.S.C.sctn.119(e) based on U.S. Provisional Application No. 60/314,381, filed Aug. 24, 2001, and is a Continuation-In-Part of U.S. patent application Ser. No. 09/899,059, filed Jul. 6, 2001; which in turn claims the benefit of priority under 35 U.S.C.sctn.119(e) based on U.S. Provisional Application Nos. 60/278,449 and 60/216,879, filed Mar. 26, 2001 and Jul. 7, 2000 respectively, and is a Continuation-InPart of U.S. patent application Ser. No. 09/559,290, filed Apr. 27, 2000; which in turn claims the benefit of priority under 35 U.S.C.sctn.119(e) based on U.S. Provisional
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Application Nos. 60/180,908, 60/134,067, 60/132,227 and 60/131,963, filed Feb. 8, 2000, May 13, 1999, May 3, 1999 and Apr. 30, 1999 respectively, and is a Continuation-In-Part of U.S. patent application Ser. No. 09/246,129, filed Feb. 8, 1999; which in turn claims the benefit of priority under 35 U.S.C.sctn.119(e) based on U.S. Provisional Application No. 60/074,047, filed Feb. 9, 1998, and is a Continuation-In-Part of U.S. patent application Ser. No. 09/131,237, filed Aug. 7, 1998; which in turn is a Continuation-In-Part of U.S. patent application Ser. No. 09/005,020, filed Jan. 9, 1998, now abandoned; which in turn is a Continuation-In-Part of U.S. patent application Ser. No. 08/461,246, filed Jun. 5, 1995, now abandoned; which in turn is a Continuation-In-Part of PCT/US94/12880 filed Nov. 7, 1994. The contents of each of the above-identified applications and their associated sequence listings are hereby incorporated by reference in their entireties. The present invention encompasses methods for diagnosis and treatment of inflammatory bowel diseases and disorders using a novel member of the tumor necrosis factor (TNF) family of cytokines. In particular the invention encompasses methods of using TNFgamma-.beta., and/or its receptors DR3 and TR6, in the diagnosis, prognosis and treatment of inflammatory bowel diseases and disorders. Furthermore, the invention encompasses methods of using homomultimeric and heteromultimeric polypeptide complexes comprising TNF-gamma-.beta., and/or its receptors DR3 and TR6, in the diagnosis, prognosis and treatment of inflammatory bowel diseases and disorders. Also encompassed by the invention are methods of using TNF-gamma-.beta., and/or its receptors DR3 and TR6, and/or homomultimeric or heteromultimeric polypeptide complexes containing TNF-gamma-.beta., and/or its receptors DR3 and TR6, in the diagnosis, prognosis and treatment of diseases and/or disorders associated with inflammatory bowel diseases and disorders. Also encompassed by the invention are methods of using TNF-gamma-.beta., and/or its receptors DR3 and TR6, and/or homomultimeric or heteromultimeric polypeptide complexes containing TNF-gamma.beta., and/or its receptors DR3 and TR6, in the diagnosis, prognosis and treatment of diseases and/or disorders associated with aberrant interferon gamma secretion and/or activity, including, for example, inflammatory bowel disease. This invention encompasses methods of using polynucleotides, polypeptides encoded by the polynucleotides, antibodies that bind the polypeptides, and antagonists of such polypeptides in the detection, diagnosis, prevention, treatment, and/or amelioration of inflammatory bowel disease. The present invention further encompasses inhibiting the production and function of the polypeptides of the present invention for prevention, treatment, and/or amelioration of inflammatory bowel disease. The cytokine known as tumor necrosis factor-.alpha. (TNF.alpha.; also termed cachectin) is a protein secreted primarily by monocytes and macrophages in response to endotoxin or other stimuli as a soluble homotrimer of 17 kD protein subunits (Smith, R. A. et al., J. Biol. Chem. 262:6951-6954 (1987)). A membrane-bound 26 kD precursor form of TNF has also been described (Kriegler, M. et al., Cell 53:45-53 (1988)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods of treating ulcerative colitis with chimeric anti-TNF antibodies Inventor(s): Daddona, Peter; (Menlo Park, CA), Ghraveb, John; (Downingtown, PA), Knight, David; (Berwyn, PA), Le, Junming; (Jackson Heights, NY), Siegel, Scott; (Westborough, MA), Vilcek, Jan; (New York, NY) Correspondence: Hamilton, Brook, Smith & Reynolds, P.C.; 530 Virginia Road; P.O. Box 9133; Concord; MA; 01742-9133; US Patent Application Number: 20030198641 Date filed: March 4, 2003 Abstract: Anti-TNF antibodies, fragments and regions thereof which are specific for human tumor necrosis factor-.alpha. (TNF.alpha.) and are useful in vivo diagnosis and therapy of a number of TNF.alpha.-mediated pathologies and conditions, as well as polynucleotides coding for murine and chimeric antibodies, methods of producing the antibody, methods of use of the anti-TNF antibody, or fragment, region or derivative thereof, in immunoassays and immunotherapeutic approaches are provided. Excerpt(s): This application is a continuation of U.S. application Ser. No. 09/756,398, filed Jan. 8, 2001, which is a divisional of U.S. application Ser. No. 09/133,119, filed Aug. 12, 1998, now U.S. Pat. No. 6,277,969, issued Aug. 21, 2001, which is a divisional of U.S. application Ser. No. 08/570,674, filed Dec. 11, 1995, now abandoned, which is a continuation-in-part of U.S. application Ser. No. 08/324,799, filed Oct. 18, 1994, now U.S. Pat. No. 5,698,195, issued Dec. 16, 1997, which is a continuation-in-part of U.S. application Ser. Nos. 08/192,102, now U.S. Pat. No. 5,656,272, issued Aug. 12, 1997, Ser. No. 08/192,861, now U.S. Pat. No. 5,919,452, issued Jul. 6, 1999, and Ser. No. 08/192,093, now U.S. Pat. No. 6,284,471, issued Sep. 4, 2001, all filed on Feb. 4, 1994 which are continuations-in-part of U.S. application Ser. No. 08/010,406, filed Jan. 29, 1993, now abandoned, and U.S. application Ser. No. 08/013,413, filed Feb. 2, 1993, now abandoned, which is a continuation-in-part of U.S. application Ser. No. 07/943,852, filed Sep. 11, 1992, now abandoned, which is a continuation-in-part of U.S. application Ser. No. 07/853,606, filed Mar. 18, 1992, now abandoned, which is a continuation-in-part of U.S. application Ser. No. 07/670,827, filed Mar. 18, 1991, now abandoned. Each of the above applications are entirely incorporated herein by reference. The present invention in the field of immunology and medicine relates to anti-tumor necrosis factor (TNF) antibodies, anti-TNF peptides and nucleic acids encoding therefor, and to pharmaceutical and diagnostic compositions and production, diagnostic and therapeutic methods thereof, and to methods for treating human TNF-mediated pathologies. Monocytes and macrophages secrete cytokines known as tumor necrosis factors (TNF.alpha.) and tumor necrosis factor-.beta. (TNF.beta.) in response to endotoxin or other stimuli. TNF.alpha. is a soluble homotrimer of 17 kD protein subunits (Smith, et al., J. Biol. Chem. 262:6951-6954 (1987)). A membrane-bound 26 kD precursor form of TNF also exists (Kriegler, et al., Cell 53:45-53 (1988)). For reviews of TNF, see Beutler, et al., Nature 320:584 (1986), Old, Science 230:630 (1986), and Le, et al., Lab. Invest. 56:234. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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N-arylsulfonyl aryl aza-bicyclic derivatives as potent cell adhesion inhibitors Inventor(s): Chang, Linda L.; (Wayne, NJ), Hagmann, William K.; (Westfield, NJ), Lin, Linus S.; (Westfield, NJ), Mumford, Richard A.; (Red Bank, NJ), Shah, Shrenik K.; (Metuchen, NJ) Correspondence: Merck And CO Inc; P O Box 2000; Rahway; NJ; 070650907 Patent Application Number: 20020193399 Date filed: March 13, 2002 Abstract: Compounds of Formula I are antagonists of VLA-4 and/or alpha4/beta7, and as such are useful in the inhibition or prevention of cell adhesion and cell-adhesion mediated pathologies. These compounds may be formulated into pharmaceutical compositions and are suitable for use in the treatment of AIDS-related dementia, allergic conjunctivitis, allergic rhinitis, Alzheimer's disease, asthma, atherosclerosis, autologous bone marrow transplantation, certain types of toxic and immune-based nephritis, contact dermal hypersensitivity, inflammatory bowel disease including ulcerative colitis and Crohn's disease, inflammatory lung diseases, inflammatory sequelae of viral infections, meningitis, multiple sclerosis, multiple myeloma, myocarditis, organ transplantation, psoriasis, pulmonary fibrosis, restenosis, retinitis, rheumatoid arthritis, septic arthritis, stroke, tumor metastasis, uveititis, and type I diabetes. Excerpt(s): The compounds of the present invention are antagonists of the VLA-4 integrin ("very late antigen-4"; CD49d/CD29; or.alpha.sub.4.beta.sub.1- ), the.alpha.sub.4.beta.sub.7 integrin (LPAM-1 and.alpha.sub.4.beta.sub.p), and/or the.alpha.sub.9.beta.sub.1 integrin, and are useful in the treatment, prevention and suppression of diseases mediated by VLA-4-,.alpha.sub.4.beta.sub.7-, and/or.alpha.sub.9.beta.sub.1-binding and cell adhesion and activation. The present invention relates to potent substituted N-arylsulfonylated-proline derivatives which are useful for the inhibition and prevention of leukocyte adhesion and leukocyte adhesionmediated pathologies. This invention also relates to compositions containing such compounds and methods of treatment using such compounds. Many physiological processes require that cells come into close contact with other cells and/or extracellular matrix. Such adhesion events may be required for cell activation, migration, proliferation and differentiation. Cell-cell and cell-matrix interactions are mediated through several families of cell adhesion molecules (CAMs) including the selectins, integrins, cadherins and immunoglobulins. CAMs play an essential role in both normal and pathophysiological processes. Therefore, the targeting of specific and relevant CAMs in certain disease conditions without interfering with normal cellular functions is essential for an effective and safe therapeutic agent that inhibits cell-cell and cell-matrix interactions. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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NKT cell-activating agents containing alpha-glycosylceramides Inventor(s): Kawano, Tetsu; (Chiba, JP), Koezuka, Yasuhiko; (Gunma, JP), Taniguchi, Masaru; (Chiba, JP) Correspondence: Stephen A. Bent; Foley & Lardner; Washington Harbour; 3000 K Street, N.W., Suite 500; Washington; DC; 20007-5143; US Patent Application Number: 20030139351 Date filed: January 2, 2003
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Abstract: An objective of the present invention is to provide NKT cell-activating agents, therapeutic agents for autoimmune diseases (for example, systemic lupus erythematosus, systemic sclerosis, ulcerative colitis, encephalomyelitis, multiple sclerosis and human type I diabetes), and abortifacients. The medicinal compositions according to the present invention comprise.alpha.-glycosylceramides of the following formula (I), or a salt or a solvate thereof as an active ingredient. 1 Excerpt(s): The present invention relates to NKT cell-activating agents, therapeutic agents for autoimmune diseases and agents for inducing abortion. It has been revealed that intermediate TCR cells (TCR.sup.int cells), which express T-cell receptors (TCRs) intermediately, are related to natural killer (NK) cells in terms of their features, for example, showing a large granular lymphocyte (LGL)-like morphology, constantly expressing IL-2R.beta.-chains, and having perforin granules, but they are clearly different from NK cells in terms of having TCRs (Watanabe, H. et al., J. Immunol., 155, 2972 (1995)). Furthermore, among the TCR.sup.int cells activated by interleukin 12 (IL12), NK 1.1-expressing NK 1.1.sup.+TCR.sup.int (NKT) cells have been shown to be important effector cells in controlling hematogenous metastases of tumors to the liver and lung in mice (Hashimoto, W. et al., J. Immunol., 154, 4333 (1995); Anzai, R. et al., Immunol., 88, 82 (1996)). These data suggest that the NKT cells may play an important role in eradicating cancer cells, parasites, protozoans, and intracellular infectious bacteria such as Listeria monocytogenes and Micobacterium tubeculosis (Seki, S. et al., Clin. Immunol., 28, 1069 (1996)). The NKT cells are also known to be closely associated with acute rejection in bone marrow transplantation (Yankelevich, B. et al., J. Immunol., 142, 3423 (1989)) and with controlling of IgE antibody production by controlling Th1/Th2 differentiation of helper T cells (Yoshimoto, T. et al., J. Exp. Med., 179, 1285 (1994)). Thus, the NKT cells are a group of new cells that are currently attracting enormous attention. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Novel phospholipase D polypeptide and DNA sequences Inventor(s): Engebrecht, Joanne; (Stony Brook, NY), Frohman, Michael A.; (Setauket, NY), Morris, Andrew J.; (Mt. Sinai, NY) Correspondence: Gregory Giotta, PH.D.; Vice President & Chief Legal Counsel; Onyx Pharmaceuticals, INC.; 3031 Research Drive; Richmond; CA; 94806; US Patent Application Number: 20030124108 Date filed: April 30, 2002 Abstract: Provided are novel phospholipase D DNA and amino acid sequences. The sequences are useful in methods and compositions for identifying phospholipase D mediator molecules which are in turn useful in therapeutic pharmacuetical compositions for treating rheumatoid arthritis, psoriasis, ulcerative colitis, in wound healing and for treating other diseases or conditions characterized by exhibition of an inflammatory response or in the treatment of cancer and other diseases characterized by pathogenic mitogenicity. Excerpt(s): This invention is in the field of molecular biology and particularly relates to nucleic acid sequences that encode novel phospholipases. The mechanism by which specificity of physiological responses are conferred by a limited number of signal transducing substances, typically enzymes, is poorly understood. Cellular receptors on the surfaces of various cells are involved and initiate multiple signaling pathways. Some
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of the receptors on neutrophils are known: the PAF receptor, the interleukin-8 receptor and the fMetLeuPhe receptor all belong to the super-family of G-protein-linked receptors. A common feature of these receptors is that they span the cell membrane seven times, forming three extracellular and three intracellular loops and a cytoplasmic carboxy-terminal tail. The third loop and the tail exhibit extensive variability in length and sequence, leading to speculation that these parts are responsible for the selective interaction with the various G-proteins. Many of these G-protein-linked receptors stimulate the activation of three phospholipases, phospholipase C (PLC), phospholipase D (PLD) and phospholipase A.sub.2 (PLA.sub.2). These phospholipases constitute a family of regulatory enzymes which trigger various neutrophilic functions, for example adherence, aggregation, chemotaxis, exocytosis of secretory granules and activation of NADPH oxidase, i.e., the respiratory burst. The main substrates for the phospholipases are membrane phospholipids. The primary substrates for PLC are the inositol containing lipids, specifically and typically phosphotidylinositol (PI). PI is phosphorylated by PLC resulting in the formation of PIP, phosphotidylinositol 4phosphate. The primary substrate for PLD and PLA.sub.2 is phosphatidylcholine (PC), a relatively ubiquitous constituent of cell membranes. The activity of cytosolic PLA.sub.2 on PC liberates arachidonic acid, a precursor for the biosynthesis of prostaglandins and leukotrienes and possible intracellular secondary messenger. PLD, on the other hand, catalyzes the hydrolytic cleavage of the terminal phosphate diester bond of glycerophospholipids at the P-O position. PLD activity was originally discovered in plants and only relatively recently discovered in mammalian tissues. PLD has been the focus of recent attention due to the discovery of its activation by fMetLeuPhe in neutrophils. PLD activity has been detected in membranes and in cytosol. Although a 30 kD (kilodalton) and an 80 kD activity have been detected, it has been suggested that these molecular masses represented a single enzyme with varying extents of aggregation. See Cockcroft, Biochimica et Biophysica Acta 1113: 135-160 (1992). One PLD has been isolated, cloned and partially characterized. See Hammond, J. Biol. Chem. 270:29640-43 (1995). Biological characterization of PLD1 revealed that it could be activated by a variety of G-protein regulators, specifically PKC (protein kinase C), ADPribosylation factor (ARF), RhoA, Rac1 and cdc-42, either individually or together in a synergistic manner, suggesting that a single PLD participates in regulated secretion in coordination with ARF and in propagating signal transduction responses through interaction with PKC, PhoA and Rac1. Nonetheless, PKC-independent PLD activation has been associated with Src and Ras oncogenic transformation, leaving open the possibility that additional PLDs might exist. See Jiang, Mol. and Cell. Biol. 14:3676 (1994) and Morris, Trends in Pharmacological Sciences 17: 182-85(1996). The difficulty may arise at least in part from the fact that in the phospholipase family enzymes may or may not be activated by, and catalyze, multiple substances, making sorting, tracking and identification by functional activities impractical. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Novel synergistic compositions containing aromatic compounds and terpenoids present in Alpinia galanga Inventor(s): Jensen, Nina Worm; (Koge, DK), Petersen, Morten Just; (Verlose, DK), Weidner, Morten Sloth; (Virum, DK) Correspondence: Darby & Darby P.C.; Post Office Box 5257; New York; NY; 10150-5257; US Patent Application Number: 20030157204 Date filed: January 2, 2003 Abstract: Novel compositions of matter containing aromatic compounds and terpenoids which are present in and may preferably be derived from the plant Alpinia galanga (Zingiberaceae) show synergistic effects with respect to immunomodulation, and they significantly suppress hypersensitivity reactions. Thus they are used for preparing medicaments for these purposes and, more specifically, for the treatment or prevention of IgE mediated allergic reactions and conditions, such as asthma, allergic rhinitis, atopic eczema or anaphylaxis, and autoimmune disorders, such as Crohn's disease, ulcerative colitis, rheumatoid arthritis or psoriasis, as well as for the alleviation of pain. They can for example be formulated into pharmaceuticals, cosmetics or dietary supplements. A method of preparing such compositions from Alpinia galanga is also described. Excerpt(s): The present invention relates to novel compositions of matter containing aromatic compounds and terpenoids which are present in and may preferably be derived from the plant Alpinia galanga (Zingiberaceae), and more specifically to novel pharmaceuticals, cosmetics or dietary supplements containing such compositions. Furthermore the invention relates to the use of the compositions for preparing medicaments for the treatment or prevention of hypersensitivity reactions and diseases associated with hypersensitivity reactions. The invention also relates to a method of preparing such compositions from Alpinia galanga. Alpinia galanga (L.), family Zingiberaceae, commonly known as Greater Galangal or Java Galangal, is cultivated and grows wild in Asia. The herb is rhizomatic, 1.8-2.1 m in height with oblong glabrous leaves and greenish white flowers. The fruits are orange-red capsules. The plant is also known under the name Languas galanga, especially in Thailand, and here it is locally called Katuk karohinee. In relation to the present invention the term "Alpinia galanga" refers to any variety of Alpinia galanga or Languas galanga found anywhere in the world. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Nuclear envelope protein recognized by atypical p-ANCA in patients with inflammatory bowel disease and autoimmune liver diseases Inventor(s): Terjung, Birgit; (Swisttal, DE), Worman, Howard J.; (New York, NY) Correspondence: Cooper & Dunham Llp; 1185 Avenue OF The Americas; New York; NY; 10036; US Patent Application Number: 20030003518 Date filed: June 15, 2001 Abstract: The present invention is directed to the molecular characterization of the nuclear antigen recognized by atypical p-antineutrophil cytoplasmic antibodies (p-
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ANCA) in order to better diagnose patients with inflammatory bowel diseases such as ulcerative colitis (UC), and autoimmune liver diseases such as primary sclerosing cholangitis (PSC) and autoimmune hepatitis (AIH). Molecular characterization of the target antigen comprises preparing cytoplasmic and nuclear extracts of human neutrophils, human HL-60 and murine 32D myeloid cells. Proteins should then be resolved by 1 and 2 dimensional gel electrophoresis and reactive proteins can then be detected by immunoblotting with sera from individuals, making certain to have both normal and disease controls. Atypical p-ANCA should then be affinity purified against the reactive protein and investigated for their immunofluorescence pattern using confocal microscopy. One could then detect the antigen that atypical p-ANCA can recognize and use that antigen to detect the prescence of atypical p-antineutrophil cytoplasmic antibodies so as to diagnose patients with inflammatory bowel diseases such as ulcerative colitis (UC), and autoimmune liver diseases such as sclerosing cholangitis (PSC) and autoimmune hepatitis (AIH). Excerpt(s): Throughout this application, various publications are referenced by author and date. Full citations for these publications may be found listed alphabetically at the end of the specification immediately preceding the claims. The disclosures of these publications in their entireties are hereby incorporated by reference into this application in order to more fully describe the state of the art as known to those skilled therein as of the date of the invention described and claimed herein. Atypical "antineutrophil cytoplasmic antibodies" (ANCA) are present in patients with ulcerative colitis (UC), primary sclerosing cholangitis (PSC), and autoimmune hepatitis (AIH) ANCA represent a family of heterogenous autoantibodies directed against constituents of neutrophilic granulocytes. These autoantibodies have become valuable seromarkers for the diagnostic and therapeutic management of patients with systemic vasculitides such as Wegner granulomatosis and microscopic polyangiitis, in which they recognize well defined cytoplasmic antigens such as proteinase 3 and myeloperoxidase. Two well established ANCA staining patterns can be distinguished on ethanol-fixed neutrophils: a difuse cytoplasmic fluorescence pattern (c-ANCA) and a fine homogeneous labeling of the perinuclear cytoplasm (p-ANCA). Autoantibodies that are similar to p-ANCA in patients with systemic vasculitides are detected in individuals with chronic inflammatory bowel diseases (IBD) such as ulcerative colitis or autoimmune liver disorders such as primary sclerosing cholangitis (PSC) and autoimmune hepatitis (AIH). Contrary to systemic vasculitides, the role of ANCA in these disorders is not clear. Various cytoplasmic proteins such as bactericidal/permeability increasing protein, catalase, cathepsin G, enolase, or lactoferrin have been proposed as putative target antigens of ANCA in these disorders, but reactivity to these proteins has only been detected in less than thirty five percent of cases. The predominant target antigen of ANCA in IBD and autoimmune liver disorders has not been identified. Since their target antigens are unknown, p-ANCA in patients with IBD or autoimmune liver disorders are generally referred to as atypical p-ANCA. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Pharmaceutical composition and method of modulating cholinergic function in a mammal Inventor(s): Coe, Jotham W.; (Niantic, CT), Sands, Steven B.; (Stonington, CT) Correspondence: Pfizer Inc; 150 East 42nd Street; 5th Floor - Stop 49; New York; NY; 10017-5612; US Patent Application Number: 20030008892 Date filed: March 25, 2002 Abstract: A pharmaceutical composition and method of modulating cholinergic function in a mammal comprising administration of a NRPA compound or a pharmaceutically acceptable salt thereof; and an anti-emetic/anti-nausea agent or a pharmaceutically acceptable salt thereof; and a pharmaceutically acceptable carrier. The NRPA compound and the anti-emetic/anti-nausea agent are present in amounts that render the composition effective modulating cholinergic function or in the treatment of a diorder or condition selected from inflammatory bowel disease (including but not limited to ulcerative colitis, pyoderma gangrenosum and Crohn's disease), irritable bowel syndrome, spastic dystonia, chronic pain, acute pain, celiac sprue, pouchitis, vasoconstriction, anxiety, panic disorder, depression, bipolar disorder, autism, sleep disorders, jet lag, amyotrophic lateral sclerosis (ALS), cognitive dysfunction, hypertension, bulimia, anorexia, obesity, cardiac arrythmias, gastric acid hypersecretion, ulcers, pheochromocytoma, progressive supranuclear palsy, chemical dependencies and addictions (e.g., dependencies on, or addictions to nicotine (and/or tobacco products), alcohol, benzodiazepines, barbiturates, opioids or cocaine), headache, migraine, stroke, traumatic brain injury (TBI), obsessive-compulsive disorder (OCD), psychosis, Huntington's chorea, tardive dyskinesia, hyperkinesia, dyslexia, schizophrenia, multiinfarct dementia, age-related cognitive decline, epilepsy, including petit mal absence epilepsy, senile dementia of the Alzheimer's type (AD), Parkinson's disease (PD), attention deficit hyperactivity disorder (ADHD) and Tourette's Syndrome. The method of using these compositions is also disclosed. Excerpt(s): The present invention relates to pharmaceutical compositions for modulating cholinergic function in a mammal comprising a nicotinic receptor partial agonist compound in combination with an anti-emetic/anti-nausea agent and a pharmaceutically acceptable carrier. The nicotinic receptor partial agonists (NRPAs) included herein are aryl fused azapolycyclic compounds. NRPAs are not limited to those described here. The term NRPA refers to all chemical compounds which bind at neuronal nicotinic acetylcholine specific receptor sites in mammalian tissue and elicit a partial agonist response. A partial agonist response is defined here to mean a partial, or incomplete functional effect in a given functional assay. Additionally, a partial agonist will also exhibit some degree of antagonist activity by its ability to block the action of a full agonist (Feldman, R. S., Meyer, J. S. & Quenzer, L. F. Principles of Neuropsychopharmacology, 1997; Sinauer Assoc. Inc.). The present invention may be used to treat mammals (e.g. humans) for inflammatory bowel disease (including but not limited to ulcerative colitis, pyoderma gangrenosum and Crohn's disease), irritable bowel syndrome, spastic dystonia, chronic pain, acute pain, celiac sprue, pouchitis, vasoconstriction, anxiety, panic disorder, depression, bipolar disorder, autism, sleep disorders, jet lag, amyotrophic lateral sclerosis (ALS), cognitive dysfunction, hypertension, bulimia, anorexia, obesity, cardiac arrythmias, gastric acid hypersecretion, ulcers, pheochromocytoma, progressive supranuclear palsy, chemical dependencies and addictions (e.g., dependencies on, or addictions to nicotine (and/or tobacco products), alcohol, benzodiazepines, barbiturates, opioids or cocaine), headache, migraine, stroke,
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traumatic brain injury (TBI), obsessive-compulsive disorder (OCD), psychosis, Huntington's chorea, tardive dyskinesia, hyperkinesia, dyslexia, schizophrenia, multiinfarct dementia, age-related cognitive decline, epilepsy, including petit mal absence epilepsy, senile dementia of the Alzheimer's type (AD), Parkinson's disease (PD), attention deficit hyperactivity disorder (ADHD) and Tourette's Syndrome with a decrease in the incidence and severity of unwanted side effects such as nausea and/or stomach upset. The present invention also relates to the combination use of NRPAs and anti-emetic/anti-nausea agents resulting in modulation of cholinergic function without nausea. The combination will provide an improved treatment paradigm than NRPAs alone. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Pharmacological composition containing yeast cell wall fraction Inventor(s): Nakamura, Tomohiko; (Takasaki-shi, JP), Shirasu, Yoshiharu; (Takasaki-shi, JP), Wakabayashi, Hideyuki; (Takasaki-shi, JP) Correspondence: Venable, Baetjer, Howard And Civiletti, Llp; P.O. Box 34385; Washington; DC; 20043-9998; US Patent Application Number: 20030118607 Date filed: October 10, 2002 Abstract: The present invention provides a pharmacological composition as a composition as a raw material capable of preventing or treating the symptoms of inflammatory bowel diseases such as ulcerative colitis, constipation, allergic diseases such as atopic dermatitis, and so on, and which has little side effect and thereby safe, high water dispersibility, and can be ingested easily.A yeast cell wall fraction, which comprises yeast extracts residue and being superior in water dispersibility and swelling properties, is used as an active constituent. As a yeast cell wall fraction, a yeast cell wall fraction obtained with a simple operation of water cleansing of yeast cell after alkali processing yields superior effects for preventing or treating the symptoms of inflammatory bowel diseases such as ulcerative colitis, constipation, allergic diseases such as atopic dermatitis, and so on, as well as such yeast cell wall fraction without foreign taste and odor characteristic to autolysis and suitable for ingestion. Excerpt(s): The present invention generally relates to a pharmacological composition containing cell residue obtained by removing soluble cell substance from enzymegenated yeast, preferably cell residue obtained by conducting water cleansing after alkali treatment, and having as its active constituent a yeast cell wall fraction containing abundant protein and dietary fiber. Particularly, the present invention relates to an agent and/or a food product having as its active constituent the aforementioned yeast cell wall fraction and capable of preventing and/or treating the symptoms of inflammatory bowel diseases such as ulcerative colitis, constipation, allergic diseases such as atopic dermatitis, and so on. Conventionally, as technology directed to a pharmacological composition having as its active constituent yeast or a yeast cell component substance, known are a manufacturing method of a polysaccharide ester sulfate compound and the alkali metal saline thereof having a anti-digestive ulcer agent effect and an anti-arterial sclerosis effect, obtained by sulfating a yeast cell wall in a basic organic solution with chlorosulphonic acid or sulfur trioxide, or sulfating a yeast cell wall by blending it with cooled and levigated strong sulfuric acid and thereafter making it an alkali salt (Japanese Patent Application Laid-Open No. 49-48894); a manufacturing method of a polysaccharide ester sulfate compound and the alkali metal saline thereof
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obtained by sulfating a yeast cell wall in a basic organic solution with chlorosulphonic acid or sulfur trioxide, or sulfating a yeast cell wall by blending it with cooled and levigated strong sulfuric acid and thereafter making it an alkali salt (Japanese Patent Application Laid-Open No. 56-31955); a manufacturing method of a new physiologically active substance peptide mannan A which extracts peptide mannan A from a yeast cell belonging to Saccharomyces and ingests peptide mannan A from such extract (Japanese Patent Laid-Open Publication No. 49-69808); a manufacturing method of a compound protein SP-1 having an anti-ulcer effect and containing amino acids and mannose by making the pepsin act upon the yeast cell wall (Japanese Patent Application Laid-Open No. 62-39527); an anti-allergic agent having as its active constituent mannan deriving from yeast and the like (Japanese Patent Application Laid-Open No.63-119427); an antiulcer agent having as its active constituent dried brewer's yeast with no concern of side effects as it is a natural product (Japanese Patent Application Laid-Open No. 1-313434); a nutrition supplement composition to be administered to mammals and containing a sufficient amount of.beta.-glucan deriving from yeast for supplying a fiber source in foods, fecal-increasing agent, and short-chain fatty acid, and which improves the digestion in mammals, decreases the serum cholesterol level, and fortifies the decrease in weight (Japanese Patent Application Laid-Open No. 4-505997); food, beverage and medical product containing magnesium supplement material which connotes magnesium salt within a yeast cell wall prepared by eluting and separating intercellular cell constituents (Japanese Patent Application Laid-Open No. 9-107919); an inhibitor of antibody-producing cell containing yeast-related polymer, and a composition such as food or medical product for autoimmune disease containing this inhibitor of antibodyproducing cell (Japanese Patent Laid-Open Publication No. 9-188626); and a skin condition improving composition suitable for preventing and treating the likes of atopic dermatitis and containing protease hydrolysate of brewer's yeast and diuretic (Japanese Patent Laid-Open Publication No. 9-227390). Further, conventionally, as technology directed to making the autolytic residue of yeast tasteless and odorless, known are a method of improving the flavor of brewer's yeast by moisture distillation and organic solvation of brewer's yeast (Japanese Patent Application Laid-Open No. 63-22177), a method of decolorizing and deodorizing yeast extract residue, or yeast autolytic residue, wherein yeast extract residue is processed with alkali and acid, high concentration ozone treatment is conducted thereafter, and ethanol treatment is further implemented (Japanese Patent Application Laid-Open No. 4-248968); a method of reducing the foreign taste and odor characteristic to yeast by conducting acid treatment and heat treatment to yeast or a yeast-processed product (Japanese Patent Application Laid-Open No. 6-70751); and a method of making a yeast autolytic insoluble substance tasteless and odorless by suspending a yeast autolytic insoluble substance in ethanol, carrying the stirring treatment under alkaline conditions and eluting the causative agent of foreign taste and odor thereby, and eliminating the eluted material pursuant to centrifugation and eliminating the foreign taste and odor characteristic to a yeast autolytic insoluble substance thereby (Japanese Patent Application Laid-Open No. 9-103266). In addition, as technology directed to the treatment method of yeast cells and yeast cell walls, known is a manufacturing method of a seasoning wherein yeast cells are crushed with a highpressure spray-impact homogenizer, hot water extraction is conducted thereto, and centrifugation is performed to the yeast cell walls which could not be made into particulates (Japanese Patent Application Laid-Open No. 9-117263). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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PLAP polypeptides and methods of producing and using same Inventor(s): Chopra, Ashok K.; (Galveston, TX), Peterson, Johnny W.; (Dickinson, TX), Saini, Shamsher S.; (Galveston, TX), Wood, Thomas G.; (Houston, TX) Correspondence: Mark B. Wilson; Fulbright & Jaworski L.L.P.; Suite 2400; 600 Congress Avenue; Austin; TX; 78701; US Patent Application Number: 20030166548 Date filed: June 19, 2002 Abstract: Synthetic milittin and related peptides derived from the sequence of human phospholipase A.sub.2-activating protein (PLAP), free from the contaminating phospholipase A.sub.2 (PLA.sub.2) and/or present when the peptides are purified from natural sources, show inhibitory activity against PLA.sub.2. Inhibition of this enzyme, responsible for the hydrolysis of arachiodonate, an important precursor of eicosanoids, should lead to a decrease in the inflammatory response. In addition to their use as antiinflammatory therapeutics, compositions containing the synthetic peptides may also be useful therapeutic tools for diagnosing inflammatory diseases (e.g., Crohn's disease, ulcerative colitis, rheumatoid arthritis). Excerpt(s): This application claims priority from U.S. Serial No. 60/049,316, filed Jun. 11, 1997. The present invention relates generally to the fields of diagnosing and treating inflammatory diseases. More particularly, it concerns the uses of synthetic peptide and peptide analog inhibitors of phospholipase A.sub.2. Inflammation is normally a basic host protective mechanism that increases resistance to microorganisms and other foreign antigens. Inflammatory responses are mediated in part by the eicosanoids, C.sub.20 products of the cyclooxygenase and lipooxygenase metabolism of arachidonic acid. The eicosanoids include proinflammatory prostaglandins (e.g., PGE.sub.2) and leukotrienes (e.g., LTB.sub.4). The level of arachidonic acid, itself, is mediated by the action of phospholipase A.sub.2 (PLA.sub.2) a lipophilic enzyme that hydrolyzes arachidonic acid from the sn-2 position of phospholipids located in cell membranes. PLA.sub.2 enzyme activity is increased by a eukaryotic cell protein referred to as phospholipase A.sub.2-activating protein (PLAP), which was initially cloned from murine BC.sub.3H.sub.1 cells (Clark, 1991). Murine PLAP is reported to increase PLA.sub.2 enzyme activity (Bomalaski et al, 1994). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Pyridone-fused azabicyclic- or cytisine derivatives, their preparation and their use in addiction therapy Inventor(s): O'Neill, Brian T.; (Old Saybrook, CT) Correspondence: Paul H. Ginsburg; Pfizer INC.; 20th Floor; 235 East 42nd Street; New York; NY; 10017-5755; US Patent Application Number: 20030065173 Date filed: February 14, 2001 Abstract: Pyridone-fused azabicyclic compounds of the formula 1and their pharmaceutically acceptable salts and prodrugs, wherein R.sup.1, R.sup.2 and R.sup.3 are defined below, intermediates and methods for their preparation. Compositions and methods for using compounds of the formula I in the treatment of neurological and mental disorders related to a decrease in cholinergic function such as nicotine addiction,
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Huntington's Chorea, tardive dyskinesia, hyperkinesia, mania, dyslexia, schizophrenia , analgesia, attention deficit disorder (ADD), multi-infarct demetia, age related cognitive decline, epilepsy, neurological and mental disorders related to a decrease in cholinergic function, senile dementia of the Alzheimer's type, Parkinson's disease, attention deficit hyperactivity disorder (ADHD), anxiety, obesity, Tourette's Syndrome and ulcerative colitis. Excerpt(s): This invention relates to azabicyclic compounds. More particularly it relates to pyridone-fused azabicyclic compounds of the formula I below Compounds of formula I are useful in the treatment of addictive disorders such as the use of tobacco or other nicotine containing products and also for the treatment or prevention of withdrawal symptoms caused by cessation of chronic or long term use of tobacco products. These compounds are also useful in the treatment of Huntington's Chorea, tardive dyskinesia, hyperkinesia, mania, dyslexia, schizophrenia, analgesia, attention deficit disorder (ADD), multi-infarct demetia, age related cognitive decline, epilepsy, neurological and mental disorders related to a decrease in cholinergic function such as Huntington's Chorea, tardive dyskinesia, hyperkinesia, mania, dyslexia, schizophrenia, analgesia, attention deficit disorder (ADD), multi-infarct demetia, age related cognitive decline, epilepsy, neurological and mental disorders related to a decrease in cholinergic function, senile dementia of the Alzheimer's type, Parkinson's disease, attention deficit hyperactivity disorder (ADHD), anxiety, obesity, Tourette's Syndrome and ulcerative colitis. The compounds of this invention may also be used in combination with a antidepressants such as imipramine in order to treat both the cognitive decline and depression associated with AD; in combination with serotonin uptake inhibitors such as Zoloft to treat both the cognitive decline and depression associated with AD; in combination with muscarinic agonists in order to stimulate both central muscarinic and nicotinic receptors; in combination with neurotrophic factors such as NGF in order to maximize cholinergic enhancement; in combination with agents which slow or arrest AD such as amyloid or tau inhibitors. Substances which can deliver pharmacologically relevant amounts of nicotine to the central nervous system are among the most abused substances known. These include, but not are not limited to tobacco cigarettes, and "chewing tobacco" (see J. E. Henningfield, Ph.D, New England Journal of Med., 1196, 1995). Cigarette smoking has been tied to increased risk for lung cancer, emphysema and heart disease and it is estimated 400,000 people will die in 1995 from the combined effects of nicotine abuse in the United States (see J. A. Califano, Jr., New England Journal of Med. 1214, 1995). Nicotine is a highly addicting drug with 40% of those who try smoking later becoming physically dependent upon it. Attempts to quit the use of nicotine, such as in smoking, have been largely ineffective with >80% of such attempts ending in failure. Most attempts to quit end in failure in the first week due to intense withdrawal and craving symptoms. An effective therapy should aid in the cessation or lessening of tobacco use, prevent withdrawal. etc prevent withdrawal symptoms, relieve craving and, simultaneously, antagonize the reinforcing effects of nicotine obtained through smoking. Currently, few therapies are available for smoking cessation and most involve replacement of cigarettes with nicotine in the form of a patch or gum. A high rate of relapse and low overall success in ending nicotine use is evidence of the need for additional and more effective therapies for treatment of nicotine addiction than the nicotine patch or gum. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Remedies for inflammatory bowel diseases Inventor(s): Hirota, Yasushi; (Fukui, JP) Correspondence: Sughrue Mion, Pllc; 2100 Pennsylvania Avenue, N.W.; Washington; DC; 20037; US Patent Application Number: 20030212115 Date filed: March 25, 2003 Abstract: Prophylactic and/or therapeutic drugs against ulcerative colitis, which include five-member heterocyclic compounds represented by the formula (I) or these nontoxic salts as active principle, 1(wherein Z represents the group containing.alpha.aminocarbonyl group, R.sup.1 represents (1) substituted alkyl, alkenyl or alkynyl groups, (2) OH, (3) amino, (4) alkylamino, (5) dialkylamino, etc., X and Y represent oxygen atom, sulfur atom or substituted nitrogen atom.) Excerpt(s): The present invention relates to medicines of ulcerative colitis. medicines of ulcerative colitis, which include five-member heterocyclic compounds represented by the formula (I) (all signs in the formula represent the same meanings as postscripts.) and have inhibitory activity against elastase or these nontoxic salts as active principle. Human neutrophil elastase (HNE) is a kind of serine protease, and protein proteinase that is secreted from neutrophils by various inflammatory stimulus and takes a part in connective tissue biolysis. HNE activity is regulated by alpha1-proteinase inhibitor that is inhibitory factor in vivo, and the symptom of tissue destruction appears when unbalance between the enzyme and the inhibitor arise. For example, it is well known that it is involved in pulmonary emphysema, atherosclerosis and arthritis, etc. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Stimulating neutrophil function to treat inflammatory bowel disease Inventor(s): Dieckgraefe, Brian; (Chesterfield, MO), Korzenik, Joshua; (St. Louis, MO) Correspondence: Banner & Witcoff; 1001 G Street N W; Suite 1100; Washington; DC; 20001; US Patent Application Number: 20030035801 Date filed: October 1, 2002 Abstract: Immune stimulatory amounts of hematopoietic colony stimulating factors are administered to patients with inflammatory bowel disease. The factors include G-CSF and GM-CSF. These factors induce and maintain remission of the disease and its manifestations, whether within the intestine or without. Excerpt(s): This application claims the benefit of provisional application Serial No. 60/119,842 filed Feb. 12, 1999. The disclosure of the provisional application is expressly incorporated by reference herein. Crohn's disease persists as an enigma: without a deciphered etiology and without adequate therapy. Prevailing explanations of the pathogenesis of Crohn's disease (Crohn's Disease) hold that the characteristic chronic intestinal inflammation results from an aberrant, activated immune response generated against ubiquitous bacteria or bacterial products that gain access to the lamina propria, perhaps through a more permeable intestinal barrier. The abnormal reaction has been suggested to be mediated principally by T-cells enhanced by an intrinsic imbalance in pro-inflammatory and contra-inflammatory mediators. Thus, most therapy aims to counteract that inflammatory state with increasingly potent and sophisticated immune
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suppressants. Current therapy, mostly directed at suppressing the inflammatory process, remains inadequate both for the treatment of flares and maintenance of remission. Steroids can be effective in short term use but produce dependency in a significant proportion of patients. While certain antibiotics appear promising, data are limited. Thus there is a need in the art for effective method for treating inflammatory bowel diseases. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Therapeutic and diagnostic methods for ulcerative colitis and associated disorders Inventor(s): Das, Kiron M.; (Basking Ridge, NJ) Correspondence: Perkins Coie Llp; Post Office Box 1208; Seattle; WA; 98111-1208; US Patent Application Number: 20030236182 Date filed: February 5, 2003 Abstract: This invention relates to the field of therapy and diagnostic methods for ulcerative colitis. Specifically, the method comprises administering a compound or recombinant protein that inhibits interaction between CEP and human tropomyosin. Also included in the invention are methods to screen for drugs useful in treating ulcerative colitis and diagnostic methods for detecting diseases associated with an autoanticen response to hTM in affected tissue. Excerpt(s): This Application is a Continuation of U.S. patent application Ser. No. 09/779,689 filed Feb. 8, 2001, and now pending, which claims priority to U.S. Provisional Patent Application Ser. No. 60/181,356, filed Feb. 8, 2000, now expired. U.S. patent application Ser. Nos. 09/779,689 and 60/181,356 are incorporated herein by reference. Priority to these applications is claimed under 35 U.S.C.sctn. 120. Various scientific and scholarly articles are referenced throughout the specification. These articles are incorporated by reference herein to describe the state of the art to which this invention pertains. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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TNF receptor 2 related protein variant Inventor(s): Lal, Preeti G.; (Santa Clara, CA), Warren, Bridget A.; (Cupertino, CA) Correspondence: Incyte Genomics, INC.; 3160 Porter Drive; Palo Alto; CA; 94304; US Patent Application Number: 20030068619 Date filed: July 27, 2001 Abstract: The invention provides a cDNA which encodes a TNFR2PV. It also provides for the use of the cDNA, fragments, complements, and variants thereof and of the encoded protein, portions thereof and antibodies thereto for diagnosis and treatment of cancer and immune disorders, particularly cancer of the prostate, ovary, breast, and brain, or an inflammatory disorder, including rheumatoid arthritis, asthma, and ulcerative colitis. The invention additionally provides expression vectors and host cells for the production of the protein and a transgenic model system. Excerpt(s): This invention relates to a cDNA which encodes a TNF receptor 2 related protein variant and to the use of the cDNA and the encoded protein in the diagnosis and
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treatment of cancers and immune disorders. Phylogenetic relationships among organisms have been demonstrated many times, and studies from a diversity of prokaryotic and eukaryotic organisms suggest a more or less gradual evolution of molecules, biochemical and physiological mechanisms, and metabolic pathways. Despite different evolutionary pressures, the proteins of nematode, fly, rat, and man have common chemical and structural features and generally perform the same cellular function. Comparisons of the nucleic acid and protein sequences from organisms where structure and/or function are known accelerate the investigation of human sequences and allow the development of model systems for testing diagnostic and therapeutic agents for human conditions, diseases, and disorders. Cytokines are a diverse class of extracellular signaling molecules that regulate survival, growth, differentiation, and effector function in a variety of cells. Cytokines include families of signaling molecules such as growth factors, colony-stimulating factors, interleukins, lymphokines, monokines, and interferons. Cytokines are produced by cells that are widespread throughout the body and act in a paracrine or autocrine manner to carry out roles which often involve fighting infection and mediating tissue healing. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Topical formulations for delivery of interleukin-11 Inventor(s): Bedrosian, Camille L.; (Belmont Hills, MA), Keith, James C. JR.; (Andover, MA), Schendel, Paul F.; (Wayland, MA), Schwerschlag, Ullrich S.; (Beverly Farms, MA), Warne, Nicholas W.; (Andover, MA) Correspondence: Mintz, Levin, Cohn, Ferris,; Glovsky And Popeo, P.C.; One Financial Center; Boston; MA; 02111; US Patent Application Number: 20030147849 Date filed: February 7, 2003 Abstract: Provided by the present invention are topical formulations of Interleukin-11 and methods for treating a variety of disorders, including inflammatory bowel diseases (e.g., Crohn's disease, ulcerative colitis, indeterminate colitis, and infectious colitis), mucositis (e.g., oral mucositis, gastrointestinal mucositis, nasal mucositis, and proctitis), necrotizing enterocolitis, inflammatory skin disorders (e.g., psoriasis, atopic dermatitis, and contact hypersensitivity), aphthous ulcers, pharyngitis, esophagitis, peptic ulcers, gingivitis, periodontitis, and ocular diseases (e.g., conjunctivitis, retinitis, and uveitis). Excerpt(s): This is a continuation-in-part of U.S. patent application Ser. No. 09/179,026 filed Oct. 26, 1998, which is a continuation-in-part of U.S. patent application Ser. No. 08/892,407, filed Jul. 15, 1997, now U.S. Pat. No. 5,948,402, which is a divisional of U.S. patent application Ser. No. 08/495,724, filed Jun. 27, 1995, now U.S. Pat. No. 5,679,339, issued Oct. 21, 1997. The present invention relates generally to novel compositions and methods for topical delivery of interleukin-11 (IL-11). In preferred embodiments, patients are treated employing topical delivery of recombinant human IL-11 for inflammatory bowel diseases (e.g., Crohn's disease, ulcerative colitis, indeterminate colitis, and infectious colitis), mucositis (e.g., oral mucositis, gastrointestinal mucositis, nasal mucositis, and proctitis), necrotizing enterocolitis, inflammatory skin disorders (e.g., psoriasis, atopic dermatitis, and contact hypersensitivity), aphthous ulcers, pharyngitis, esophagitis, peptic ulcers, gingivitis, periodontitis, and ocular diseases (e.g., conjunctivitis, retinitis, and uveitis). Inflammatory responses include a broad range of host reaction to a variety of insults, such as injury, infection, or rejection. It is the overproduction of mediators that is believed to be associated with a broad range of
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disorders, including AIDS, arthritis (rheumatoid arthritis, osteoarthritis, spondyloarthropathies), antibiotic-induced diarrheal diseases, multiple sclerosis, osteoporosis, gingivitis, peptic ulcer disease, esophagitis, diabetes, retinitis, uveitis, reperfusion injury after myocardial infarction, cerebral vascular accident, aphthous ulcers (oral), atherosclerosis, tumor metastases, asthma, preeclampsia, pancreatitis, psoriasis, infertility and allergic disorders such as rhinitis, conjunctivitis, and urticaria. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Treatment for inflammatory bowel disease with a fibronectin polypeptide Inventor(s): Burkly, Linda C.; (West Newton, MA), Lobb, Roy R.; (Westwood, MA) Correspondence: Louis Myers; Fish & Richardson P.C.; 225 Franklin Street; Boston; MA; 02110-2804; US Patent Application Number: 20030095969 Date filed: September 23, 2002 Abstract: A method for the treatment of inflammatory bowel disease (IBD) is disclosed. The method comprises administration of an antibody, polypeptide or other molecule recognizing VLA-4, a surface molecule expressed on most types of white blood cells and involved in leukocyte adhesion to endothelium and other tissus in the gut. Excerpt(s): This application is a continuation-in-part of Lobb U.S. Ser. No. 08/373,857, filed Jan. 18, 1995, which is a continuation-in-part of Lobb U.S. Ser. No. 08/284,603, filed Aug. 11, 1994, and of PCT/US93/00924 filed Feb. 2, 1993, which is the continuation-inpart of Lobb U.S. Ser. No. 07/835,139, filed Feb. 12, 1992, all of which are incorporated by reference. The present invention relates to a treatment for inflammatory bowel disease (IBD). More particularly, this invention relates to the use of antibodies recognizing the integrin VLA-4 (very late antigen-4 ) in the treatment of EBD. Inflammatory bowel disease, or IBD, is a collective term encompassing ulcerative colitis and Crohn's disease (ileitis), which are chronic inflammatory disorders of the gastrointestinal tract. Ulcerative colitis is confined to the large intestine (colon) and rectum, and involves only the inner lining of the intestinal wall. Crohn's disease may affect any section of the gastrointestinal tract (i.e., mouth, esophagus, stomach, small intestine, large intestine, rectum and anus) and may involve all layers of the intestinal wall. Both diseases are characterized by abdominal pain and cramping, diarrhea, rectal bleeding and fever. The symptoms of these diseases are usually progressive, and sufferers typically experience periods of remission followed by severe flareups. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Treatment of inflammatory bowel disease Inventor(s): Pfirrmann, Rolf W.; (Lucerne, CH), Redmond, H. Paul; (Wilton, IE) Correspondence: Rothwell, Figg, Ernst & Manbeck, P.C.; 1425 K Street, N.W.; Suite 800; Washington; DC; 20005; US Patent Application Number: 20030119824 Date filed: December 19, 2002 Abstract: Patients suffering from inflammatory bowel disease such as Crohn's disease or ulcerative colitis are treated either orally or intravenously with methylol transfer
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agents, such as taurolidine and/or taurultam. These agents can be used in combination with other drugs thereby allowing the use of smaller amounts of the other drugs and limiting unwanted side effects. Excerpt(s): The present application is a continuation of application Ser. No. 09/753,679, filed Jan. 4, 2001, which claims the benefit of U.S. Provisional Application No. 60/174,608, filed Jan. 5, 2000. Inflammatory bowel disease (IBD) is of unknown etiology, although immunological mechanisms play a significant role. The two major disorders involved are ulcerative colitis and Crohn's disease. Both diseases are chronic relapsing disorders. The exact pathogenesis of IBD is unknown. Various factors such as environmental, genetic, smoking and infectious agents have been suggested. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Treatment of inflammatory bowel disease with IFN-gamma inhibitors Inventor(s): Ashkenazi, Avi J.; (San Mateo, CA), Ward, Rebecca H.R.; (San Francisco, CA) Correspondence: Merchant & Gould PC; P.O. Box 2903; Minneapolis; MN; 55402-0903; US Patent Application Number: 20030012787 Date filed: July 12, 2002 Abstract: The invention concerns a method for the prevention or treatment of inflammatory bowel disease by administering an interferon-.gamma. inhibitor. The invention further concerns pharmaceutical compositions and bispecific molecules useful in such method. Excerpt(s): The invention concerns the prevention or treatment of inflammatory bowel disease by administering an interferon-gamma (IFN-.gamma.) inhibitor. Inflammatory bowel disease (IBD) is a collective term for ulcerative colitis (UC) and Crohn's disease, which are considered as two different entities, but have many common features and probably share at least some pathologic mechanisms. There is sufficient overlap in the diagnostic criteria for UC and CD that it is sometimes impossible to say which a given patient has; however, the type of lesion typically seen is different, as is the localization. UC mostly appears in the colon, proximal to the rectum, and the characteristic lesion is a superficial ulcer of the mucosa; CD can appear anywhere in the bowel, with occasional involvement of stomach, esophagus and duodenum, and the lesions are usually described as extensive linear fissures. The aetiology of these diseases is unknown and the initial lesion has not been clearly defined; however, patchy necrosis of the surface epithelium, focal accumulations of leukocytes adjacent to glandular crypts, and an increased number of intraepithelial lymphocytes and certain macrophage subsets have been described as putative early changes, especially in Crohn's disease. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Treatment of inflammatory bowel disease with vitamin d compounds Inventor(s): Cantorna, Margherita T; (State College, PA) Correspondence: Andrus Sceales Starke & Sawall; Suite 1100; 100 East Wisconsin Avenue; Milwaukee; WI; 53202-4178; US Patent Application Number: 20030188756 Date filed: August 19, 2002 Abstract: A method of treating inflammatory bowel disease, particularly ulcerative colitis and Crohn's disease, is disclosed. The method involves administering a vitamin D compound in an amount effective to treat the disease. The administration of a vitamin D compound also prevents the development of or delays the onset of inflammatory bowel disease in susceptible individuals. Excerpt(s): This invention relates to vitamin D compounds, and more particularly to the use of vitamin D compounds to treat inflammatory bowel disease. The natural hormone, 1.alpha.,25-dihydroxyvitamin D.sub.3 and its analog 1.alpha.,25dihydroxyvitamin D.sub.2 are known to be highly potent regulators of calcium homeostasis in animals and humans, and their activity in cellular differentiation has also been established, Ostrem et al., Proc. Natl. Acad. Sci. USA, 84, 2610 (1987). Many structural analogs of these metabolites have been prepared and tested, including 1.alpha.-hydroxyvitamin D.sub.3, 1.alpha.-hydroxyvitamin D.sub.2, various side chain homologated vitamins and fluorinated analogs. Some of these compounds exhibit an interesting separation of activities in cell differentiation and calcium regulation. This difference in activity may be useful in the treatment of a variety of diseases such as renal osteodystrophy, vitamin D-resistant rickets, osteoporosis, psoriasis, and certain malignancies. Inflammatory bowel diseases (IBD) are immune mediated diseases of unknown etiology affecting the gastrointestinal (GI) tract. There are at least two distinct forms of IBD, ulcerative colitis and Crohn's disease. IBD are chronic recurring illnesses most commonly involving inflammation of the terminal ileum and colon, although these diseases can also affect many sites throughout the alimentary tract. Clearly, genetic factors predispose individuals to development of IBD (Podolosky 1991). In addition, the environment contributes to IBD development, and there is reason to believe that vitamin D may be an environmental factor which affects IBD. Vitamin D from sunlight exposure is less in areas where IBD occurs most often, as IBD is most prevalent in northern climates such as North America and Northern Europe (Podolosky 1991, Sonnenberg et al. 1991). A major source of vitamin D results from its manufacture via a photolysis reaction in the skin, and vitamin D available from sunlight exposure is significantly less in northern climates, and especially low during the winter (Clemens et al. 1982, DeLuca 1993). Dietary intake of vitamin D is problematic since there are few foods which are naturally rich in vitamin D. Weight loss occurs in 65-75% of patients diagnosed with Crohn's disease and 1862% of patients with ulcerative colitis (Fleming 1995, Geerling et al. 1998). Vitamin deficiencies in general and vitamin D deficiency in particular have been shown to occur in IBD patients (Andreassen et al. 1998, Kuroki et al. 1993). To date the possible association between vitamin D status and the incidence and severity of IBD in humans or animals has not been studied. The anecdotal information suggests that vitamin D status could be an environmental factor affecting the prevalence rate for IBD and that the correlation warrants investigation. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Treatment of ulcerative colitis with tropomyosin isoforms and monoclonal antibodies to tropomyosin isoforms Inventor(s): Das, Kiron M.; (Basking Ridge, NJ) Correspondence: Perkins Coie Llp; Post Office Box 1208; Seattle; WA; 98111-1208; US Patent Application Number: 20030198635 Date filed: May 1, 2003 Excerpt(s): This Application is a Continuation of U.S. patent application Ser. No. 09/046,049 filed Mar. 23, 1998, and now pending and which is incorporated herein by reference. Priority to this application is claimed under 35 U.S.C.sctn. 120. This invention pertains to a method for treating ulcerative colitis. Specifically, the method comprises orally or rectally administering to a human having ulcerative colitis a therapeutically effective amount of an antibody which binds to a tropomyosin isoform associated with ulcerative colitis. In another embodiment, the invention pertains to a method for treating ulcerative colitis in a human which comprises the steps of (a) obtaining from a human a colon epithelial cell extract containing a tropomyosin isoform associated with ulcerative colitis; (b) purifying the tropomyosin isoform until the tropomyosin isoform is substantially homogeneous; (c) developing an antibody which binds to the tropomyosin isoform; and (d) orally or rectally administering to a human having ulcerative colitis a therapeutically effective amount of the antibody to bind to the tropomyosin isoform associated with ulcerative colitis. In yet another embodiment, the invention pertains to a method for treating ulcerative colitis in a human which comprises orally administering to the human a therapeutically effective amount of a tropomyosin isoform associated with ulcerative colitis. The disclosures referred to herein to illustrate the background of the invention and to provide additional detail with respect to its practice are incorporated herein by reference and, for convenience, are numerically referenced in the following text and respectively grouped in the appended bibliography. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Use of il-18 inhibitors Inventor(s): Chvatchko, Yolande; (Confignon, CH), Dinarello, Charles; (Boulder, CO), Kim, Soo-Hyun; (Denver, CO), Novick, Daniela; (Rehovot, IL), Plater-Zyberk, Christine; (Geneva, CH), Rubinstein, Menachem; (Givat Shmuel, IL), Van Deventer, Santer; (Haarlem, NL) Correspondence: David S Resnick; Nixon Peabody; 101 Federal Street; Boston; MA; 02110; US Patent Application Number: 20030157094 Date filed: January 24, 2003 Abstract: The invention relates to the use of inhibitors of IL-18 in the preparation of a medicament for treatment and/or prevention of liver injury. The invention further relates to the use of IL-18 inhibitors in the preparation of a medicament for treatment and/or prevention of arthritis, in particular rheumatoid arthritis. In addition to this, the invention relates to the use of inhibitors of IL-18 in the preparation of a medicament for treatment and/or prevention of inflammatory bowel diseases, in particular of Crohn's disease and ulcerative colitis.
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Excerpt(s): The present invention relates to the therapeutical use of IL-18 inhibitors in several pathological conditions. More specifically, the invention relates to the treatment and/or prevention of arthritis, to the treatment and/or prevention of liver diseases and to the treatment and/or prevention of inflammatory bowel diseases (IBD). In 1989, an endotoxin-induced serum activity that induced interferon-.gamma. (IFN-.gamma.) obtained from mouse spleen cells was described (Micallef et al., 1996). This serum activity functioned not as a direct inducer of IFN-.gamma. but rather as a co-stimulant together with IL-2 or mitogens. An attempt to purify the activity from post-endotoxin mouse serum revealed an apparently homogeneous 50-55 kDa protein. Since other cytokines can act as co-stimulants for IFN-.gamma. production, the failure of neutralizing antibodies to IL-1, IL4, IL-5, IL-6, or TNF to neutralize the serum activity suggested it was a distinct factor. In 1995, the same scientists demonstrated that the endotoxin-induced co-stimulant for IFN-.gamma. production was present in extracts of livers from mice preconditioned with P. acnes (Novick et al., 1992). In this model, the hepatic macrophage population (Kupffer cells) expand and in these mice, a low dose of bacterial lipopolysaccharide (LPS), which in non-preconditioned mice is not lethal, becomes lethal. The factor, named IFN-.gamma.-inducing factor (IGIF) and later designated interleukin-18 (IL-18), was purified to homogeneity from 1,200 grams of P. acnes-treated mouse livers. Degenerate oligonucleotides derived from amino acid sequences of purified IL-18 were used to clone a murine IL-18 cDNA (Novick et al., 1992). IL-18 is an 18-19 kDa protein of 157 amino acids, which has no obvious similarities to any peptide in the databases. Messenger RNAs for IL-18 and interleukin12 (IL-12) are readily detected in Kupffer cells and activated macrophages. Recombinant IL-18 induces IFN-gamma more potently than does IL-12, apparently through a separate pathway (Novick et al., 1992). Similar to the endotoxin-induced serum activity, IL-18 does not induce IFN-.gamma. by itself, but functions primarily as a co-stimulant with mitogens or IL-2. IL-18 enhances T cell proliferation, apparently through an IL-2dependent pathway, and enhances Th1 cytokine production in vitro and exhibits synergism when combined with IL-12 in terms of enhanced IFN-.gamma. production (Maliszewski et al., 1990). Neutralizing antibodies to mouse IL-18 were shown to prevent the lethality of low-dose LPS in P. acnes pre-conditioned mice. Others had reported the importance of IFN-.gamma. as a mediator of LPS lethality in preconditioned mice. For example, neutralizing anti-IFN-.gamma. antibodies protected mice against Shwartzman-like shock (Fantuzzi et al., 1998), and galactosamine-treated mice deficient in the IFN-.gamma. receptor were resistant to LPS-induced death (Bym, 1990). Hence, it was not unexpected that neutralizing antibodies to murine IL-18 protected P. acnes-preconditioned mice against lethal LPS (Novick et al., 1992). Antimurine IL-18 treatment also protected surviving mice against severe hepatic cytotoxicity. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
USE OF PARASITIC BIOLOGICAL AGENTS FOR PREVENTION AND CONTROL OF AUTOIMMUNE DISEASES Inventor(s): ELLIOTT, DAVID E.; (IOWA CITY, IA), WEINSTOCK, JOEL V.; (IOWA CITY, IA) Correspondence: Palmer & Dodge, Llp; Kathleen M. Williams; 111 Huntington Avenue; Boston; MA; 02199; US Patent Application Number: 20030039666 Date filed: December 11, 1998
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Abstract: The invention relates to a method of treating an excessive immune response including an aberrant/enhanced Th1 response by administering a helminthic parasite preparation in an amount sufficient to reduce the excessive immune response in an individual. This invention is generally directed to autoimmune diseases which involve an excessive immune response or an aberrant/enhanced Th1 response. More specifically, the present invention is directed to the treatment of Crohn's disease and ulcerative colitis, both known as IBD. While the present invention discloses specific information about the treatment of IBD, the disclosure is in no way limiting. Additionally, rheumatoid arthritis, type 1 diabetes mellitus, lupus erythematosis, sarcoidosis and multiple sclerosis can be treated by the methods and compositions disclosed therein. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/070,147, filed Dec. 31, 1997. This invention relates to the prevention and/or treatment of a condition or disease state in an individual which results from an excessive immune response. Parasites are living entities that dwell on or in other creatures during some part of their life cycles, drawing nourishment from the host. Parasites that inhabit the intestines have a complex interplay with the mucosal immune system. They must establish a tranquil relationship with host mucosal defenses to survive. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Keeping Current In order to stay informed about patents and patent applications dealing with ulcerative colitis, you can access the U.S. Patent Office archive via the Internet at the following Web address: http://www.uspto.gov/patft/index.html. You will see two broad options: (1) Issued Patent, and (2) Published Applications. To see a list of issued patents, perform the following steps: Under “Issued Patents,” click “Quick Search.” Then, type “ulcerative colitis” (or synonyms) into the “Term 1” box. After clicking on the search button, scroll down to see the various patents which have been granted to date on ulcerative colitis. You can also use this procedure to view pending patent applications concerning ulcerative colitis. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.
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CHAPTER 7. BOOKS ON ULCERATIVE COLITIS Overview This chapter provides bibliographic book references relating to ulcerative colitis. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on ulcerative colitis include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.
Book Summaries: Federal Agencies The Combined Health Information Database collects various book abstracts from a variety of healthcare institutions and federal agencies. To access these summaries, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. You will need to use the “Detailed Search” option. To find book summaries, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer. For the format option, select “Monograph/Book.” Now type “ulcerative colitis” (or synonyms) into the “For these words:” box. You should check back periodically with this database which is updated every three months. The following is a typical result when searching for books on ulcerative colitis: •
Clinician's Guide to Inflammatory Bowel Disease Source: Thorofare, NJ: SLACK Incorporated. 2003. 336 p. Contact: Available from SLACK Incorporated. 6900 Grove Road, Thorofare, NJ 080869447. (856) 848-1000. Fax (856) 853-5991. Website: www.slackbooks.com. PRICE: $44.95; plus shipping and handling. ISBN: 556425546. Order number: 75546. Summary: Although the term inflammatory bowel disease (IBD) describes a wide range of inflammatory states, it generally refers to ulcerative colitis (UC) and Crohn's disease. This handbook presents an up to date guide on selected topics in IBD, focusing on those clinically important areas that have undergone recent changes or discoveries. The book offers 18 chapters: epidemiology, imaging in IBD, clinical features of UC, clinical features of Crohn's disease, postoperative recurrence of Crohn's disease, extraintestinal manifestations of IBD, cancer in IBD, complications of the ileal pouch-anal anastomosis,
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nutritional support considerations, pregnancy and fertility with IBD, indications for surgery in IBD, surgical therapy for IBD, medical therapy for Crohn's disease, medical therapy for UC, disease modifiers in IBD, evaluation of the patient suspected of having IBD, special considerations for pediatric and adolescent patients with IBD, and the medical approach to the patient with IBD. Each chapter includes references and a subject index concludes the volume. •
Understanding Crohn Disease and Ulcerative Colitis Source: Jackson, MS: University Press of Mississippi. 2000. 116 p. Contact: Available from University Press of Mississippi. 3825 Ridgewood Road, Jackson, MS 39211-6492. (601) 432-6205. Fax (601) 432-6217. E-mail:
[email protected]. PRICE: $28.00 plus shipping and handling. ISBN: 1578062039. Summary: Crohn's disease and ulcerative colitis, together known as inflammatory bowel disease (IBD), are chronic illnesses of unknown origin. Written from a patient's perspective, this book provides timely information about how to obtain and maintain the highest quality of life possible while living with IBD. The inflammation within the intestinal tract leads to some or all of these clinical symptoms: diarrhea (with or without blood), abdominal pain, fever, and fatigue. The disease is characterized by periods of flareup and remission. Some individuals, especially those who have ulcerative colitis, may have one acute episode in their lifetime. But most people with IBD have recurrent periods of illness. Even in the absence of clinical symptoms there is usually radiological and laboratory evidence of the disease. Current medical treatments reduce symptoms, but do not cure either disease. Because of the unpredictable nature of the disease process, quality of life can be severely impaired. Besides providing basic information, this book describes various medical, surgical, nutritional, and even spiritual treatments. The authors also look at the special situations of IBD in children and in the elderly, and at issues surrounding IBD and reproductive function (in men and in women). The authors stress that patients with IBD can do much to improve their emotional and psychological capabilities for facing the disease, and thus can actively improve their quality of life. The book concludes with appendices of information resources, a glossary of terms, and a subject index.
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Contemporary Diagnosis and Management of Ulcerative Colitis and Proctitis Source: Newtown, PA: Handbooks in Health Care. 1995. 173 p. Contact: Available from Handbooks in Health Care. 9 Pheasant Run, Newtown, PA 18940. (215) 860-9600. PRICE: $9.95 plus $2 shipping (as of 1995). ISBN: 1884065082. Summary: In this handbook, the author provides readers with a detailed overview of the diagnosis and management of ulcerative colitis and proctitis. Fourteen chapters cover epidemiology; etiology, pathogenesis, and pathophysiology; clinical presentation, diagnostic evaluation, and differential diagnosis; commonly used drugs for ulcerative colitis and ulcerative proctitis; potential new drugs and novel therapeutic approaches; the management of ulcerative proctitis; the management of distal ulcerative colitis, leftsided ulcerative colitis, and mild to moderate pancolitis; the management of fulminant ulcerative colitis and toxic megacolon; surgical management; associated extraintestinal disorders; colon cancer surveillance; pregnancy and nursing; the pediatric patient and the elderly patient; and psychosocial and quality of life issues. Each chapter includes figures and tables where appropriate, and brief references; a subject index concludes the handbook.
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Managing Your Child's Crohn's Disease or Ulcerative Colitis Source: New York, NY: MasterMedia Limited. 1996. 163 p. Contact: Available from Crohn's and Colitis Foundation of America, Inc. 386 Park Avenue South, 17th Floor, New York, NY 10016-8804. (800) 932-2423 or (212) 685-3440. Fax (212) 779-4098. E-mail:
[email protected]. PRICE: $16.95 (members) or $21.95 (nonmembers). Also available from MasterMedia Limited. 17 East 89th Street, New York, NY 10128. (800) 334-8232 or (212) 546-7650. PRICE: $21.95. ISBN: 1571010238. Summary: This book about Crohn's disease and ulcerative colitis provides current information so that parents and children can learn how to handle these inflammatory bowel diseases (IBD). Interviews with children coping with these illnesses add a special insight to the book. Sixteen chapters are presented in three sections: diagnosing IBD, the treatment of IBD, and living with IBD. Topics include symptoms, the first visit to the gastroenterologists, laboratory tests, the causes of IBD, pediatric gastroenterology, surgery, the role of diet, treating slow growth through nutrition, psychosocial factors, school, camp, play and recreation, family life, and pregnancy. The final chapter provides a series of common questions and answers for young patients. The book concludes with a resource section that provides information about the Crohn's and Colitis Foundation of America (CCFA), about the National Digestive Diseases Information Clearinghouse (NDDIC), a guide to medications used in the treatment of IBD, a glossary of terms, and a Children's Legacy Scroll of Honor.
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Challenges in Inflammatory Bowel Disease Source: Malden, MA: Blackwell Science, Inc. 2001. 294 p. Contact: Available from Blackwell Science, Inc. 350 Main Street, Commerce Place, Malden, MA 02148. (800) 215-1000 or (617) 388-8250. Fax (617) 388-8270. E-mail:
[email protected]. Website: www.blackwell-science.com. PRICE: $145.95. ISBN: 0632051698. Summary: This book offers an approach to the subject of inflammatory bowel disease (IBD) that highlights current areas of controversy. Divided into six sections, the book covers epidemiology; etiology and pathogenesis; diagnosis and assessment; management; surveillance for colorectal cancer; long-term complications; and prognosis. The 23 chapters cover topics including chances in the incidence of IBS, the differences between familial disease and sporadic disease, the role of genetics, controversies in histopathological diagnosis, diagnostic tools, the use of mesalazine, nutritional therapy, antibiotics in treating Crohn's disease, immunosuppression and immunomodulation, the surgical management of ulcerative colitis, the causes and treatment of ileoanal pouch dysfunction, the recognition of dysplasia, cancer surveillance in colitis, the case against surveillance for colorectal cancer, growth retardation in children with IBD, osteopenia, and prognosis in IBD. Each chapter includes references and a subject index concludes the text.
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Inflammatory Bowel Disease. 5th ed Source: Saint Louis, MO: W.B. Saunders Company. 1999. 832 p. Contact: Available from W.B. Saunders Company. Book Order Fulfillment Department, 11830 Westline Industrial Drive, Saint Louis, MO 63146-9988. (800) 545-2522. Fax (800) 568-5136. E-mail:
[email protected]. Website: www.wbsaunders.com. PRICE: $145.00 plus shipping and handling. ISBN: 0721676162.
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Summary: This comprehensive textbook describes all the latest scientific and clinical advances in the field of inflammatory bowel disease (IBD), including etiology and pathogenesis, evaluation and classification, medical and surgical therapies, and patient care management. Specific topics include homeostasis of the bowel in health and disease, the intestinal epithelium, the epidemiology of IBD, the genetics of Crohn's disease and ulcerative colitis, the pathogenesis of IBD, differential diagnosis, idiopathic IBD in the elderly, psychosocial factors in IBD, fertility and pregnancy in IBD, gastrointestinal malignancies in IBD, the other colitides (collagenous, lymphocytic, diversion, ischemic infections, clostridium difficile), endoscopy and radiography in IBD, medical therapy in IBD, the nutritional aspects of dealing with IBD, indications for surgery, the surgical management of patients with IBD, enterostomal care for patients with IBD, and prognostic considerations in IBD. The textbook integrates new therapeutic guidelines on the principles of induction, maintenance, and sustained control of remissions as well as discussions of current indications for surgery, the latest surgical technologies, and possible consequences of surgery. Each chapter is written by authorities in the field and includes illustrations and extensive references. The text concludes with a detailed subject index. •
Advanced Therapy of Inflammatory Bowel Disease Source: Hamilton, Ontario: B.C. Decker Inc. 2001. 670 p. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This is the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). The editors note that most readers of the text will be experienced digestive disease specialists who have already made the correct diagnosis and are now looking for another opinion regarding a new or controversial treatment modality. The text includes 138 chapters, each written by experts in the field, arranged in eleven categories: introduction, diagnostic methodology, proctosigmoiditis, ulcerative colitis, surgery for UC, complications of IBD, Crohn's disease, surgery for Crohn's disease, patient support services, behavioral therapy, and special situations. The latter sections cover IBD genetics, managing patients' concerns, lifestyle issues, the role of the IBD nurse advocate, the Crohn's and Colitis Foundation of America, pediatrics and family support, nutritional consultation and guidance, insurance and disability advocacy issues, sexual adjustments and body image, the role of clergy, psychiatric complications of IBD, stress management, behavioral pain management, fitness program, alternative patient care methods, fertility and pregnancy in IBD, colitis in the elderly, radiation enterocolitis, colitis and enteritis in immunocompromised individuals, lymphoma in IBD, and Behcet's disease. Each chapter includes a list of references and a list of supplemental reading suggestions, and is illustrated with black and white photographs, figures, and tables. A detailed subject index concludes the volume. Accompanying the text is a CD ROM version of the entire volume, with search features that enable increased access to the information in the text.
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Inflammatory Bowel Disease: A Guide for Patients and Their Families. 2nd ed Source: Philadelphia, PA: Lippincott-Raven Publishers. 1999. 235 p.
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Contact: Available from Crohn's and Colitis Foundation of America. 386 Park Avenue South, 17th Floor, New York, NY 10016-8804. (800) 932-2423. Fax (212) 779-4098. E-mail:
[email protected]. Website: www.ccfa.org. PRICE: $17.00 for members; $22.00 for nonmembers; plus shipping and handling. ISBN: 0397517718. Summary: This text is the official patient guide of the Crohn's and Colitis Foundation of America (CCFA). The text was written specifically for people with inflammatory bowel disease (IBD) and their families, physicians, and other health care professionals. IBD is the collective term for ulcerative colitis and Crohn's disease. Ulcerative colitis is an inflammatory disease of the large intestine (the colon), that is characterized by inflammation and ulceration of its inner lining. By contrast, Crohn's disease can affect any area of the gastrointestinal tract, including the small intestine, and there can be areas of normal intestine as well. The guide provides an extensive overview of IBD, including types, distinguishing features, and complications. Fourteen chapters discuss the anatomy and function of the digestive system, the cause of IBD, ulcerative colitis, Crohn's disease, extraintestinal complications, IBD and pregnancy, diet and nutrition, medical and surgical therapies, IBD in children and adolescents, special considerations for older patients, the emotional impact of IBD, alternative medicine, and the role of the CCFA. Each chapter is written by an expert in the field; most conclude with a list of references. The book also contains a glossary of medical terms, a glossary of surgical terms, and a subject index.
Book Summaries: Online Booksellers Commercial Internet-based booksellers, such as Amazon.com and Barnes&Noble.com, offer summaries which have been supplied by each title’s publisher. Some summaries also include customer reviews. Your local bookseller may have access to in-house and commercial databases that index all published books (e.g. Books in Print). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “ulcerative colitis” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “ulcerative colitis” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “ulcerative colitis” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •
Advanced Therapy of Inflammatory Bowel Disease (Book with CD-ROM) by Theodore M. Bayless (Editor), et al (2000); ISBN: 1550091220; http://www.amazon.com/exec/obidos/ASIN/1550091220/icongroupinterna
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Chronic inflammatory bowel disease by James L. Achord; ISBN: 0846301547; http://www.amazon.com/exec/obidos/ASIN/0846301547/icongroupinterna
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Contemporary Diagnosis and Management of Ulcerative Colitis and Proctitis by Mark A. Peppercorn; ISBN: 1884065449; http://www.amazon.com/exec/obidos/ASIN/1884065449/icongroupinterna
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Coping With Crohn's Disease and Ulcerative Colitis (Coping) by Christina Potter (2003); ISBN: 0823939626; http://www.amazon.com/exec/obidos/ASIN/0823939626/icongroupinterna
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Crohn's Disease & Ulcerative Colitis by Fred Saibil, Fredric G. Saibil (1997); ISBN: 1552091147; http://www.amazon.com/exec/obidos/ASIN/1552091147/icongroupinterna
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Crohn's Disease & Ulcerative Colitis: Everything You Need to Know (Your Personal Health) by Fred, Md. Saibil, Fredric G. Saibil (2003); ISBN: 1552977714; http://www.amazon.com/exec/obidos/ASIN/1552977714/icongroupinterna
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Crohn's Disease and Ulcerative Colitis by Canadian Medical Association, Fred Saibil; ISBN: 1552635430; http://www.amazon.com/exec/obidos/ASIN/1552635430/icongroupinterna
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Crohn's Disease and Ulcerative Colitis: Surgical Management by Devinder Kumar, John Alexander-Williams; ISBN: 0387197303; http://www.amazon.com/exec/obidos/ASIN/0387197303/icongroupinterna
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Diet Management for Ulcerative Colitis; Menus, Recipes, and Methods of Food Preparation for Anti-Inflammatory Treatment. by Map Hanson; ISBN: 0398023077; http://www.amazon.com/exec/obidos/ASIN/0398023077/icongroupinterna
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Everything You Need to Know About Crohn's Disease and Ulcerative Colitis (Need to Know Library) by Sandra Giddens, Owen Giddens (2003); ISBN: 0823939960; http://www.amazon.com/exec/obidos/ASIN/0823939960/icongroupinterna
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Histopathologic spectrum of regional enteritis and ulcerative colitis by N. Karle Mottet; ISBN: 0721665705; http://www.amazon.com/exec/obidos/ASIN/0721665705/icongroupinterna
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Inflammatory Bowel Disease by F. T. De Dombal (Editor) (1994); ISBN: 0192613545; http://www.amazon.com/exec/obidos/ASIN/0192613545/icongroupinterna
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Inflammatory Bowel Disease by Richard P. MacDermott, William Stenson (Editor); ISBN: 0838540694; http://www.amazon.com/exec/obidos/ASIN/0838540694/icongroupinterna
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Inflammatory Bowel Disease by Joseph B. Kirsner, Roy G. Shorter (Editor); ISBN: 0812110927; http://www.amazon.com/exec/obidos/ASIN/0812110927/icongroupinterna
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Inflammatory Bowel Disease, Volume II by Hugh J. Freeman (Editor), et al; ISBN: 0849355230; http://www.amazon.com/exec/obidos/ASIN/0849355230/icongroupinterna
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Inflammatory Bowel Disease: A Clinical Approach by Henry D. Janowitz, Henry D. Janowtiz; ISBN: 0195078306; http://www.amazon.com/exec/obidos/ASIN/0195078306/icongroupinterna
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Inflammatory Bowel Disease: A Guide for Patients and Their Families by Sktephen B. Hanauer, Joseph B. Kirsner; ISBN: 0890049505; http://www.amazon.com/exec/obidos/ASIN/0890049505/icongroupinterna
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Inflammatory Bowel Disease: Basic Research and Clinical Implications (Falk Symposium, No 46) by H. Goebell, et al (1989); ISBN: 0746200676; http://www.amazon.com/exec/obidos/ASIN/0746200676/icongroupinterna
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Inflammatory Bowel Disease: Current Status and Future Approach: Proceedings (International Congress Series, No 775) by Richard P. MacDermott (Editor); ISBN: 0444810013; http://www.amazon.com/exec/obidos/ASIN/0444810013/icongroupinterna
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Inflammatory Bowel Disease: Proceedings by International Symposium on Etiopathogenesis and Treatment of Inflammat, et al; ISBN: 0860083640; http://www.amazon.com/exec/obidos/ASIN/0860083640/icongroupinterna
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Inflammatory Bowel Disease: Tenth International Berzelius Symposium Sponsored by the Swedish Society of Medicine by Gunnar Jarnerot (Editor) (1987); ISBN: 0881673188; http://www.amazon.com/exec/obidos/ASIN/0881673188/icongroupinterna
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Inflammatory Bowel Diseases 1986 by Daniel Rachmilewitz (Editor) (1986); ISBN: 0898387965; http://www.amazon.com/exec/obidos/ASIN/0898387965/icongroupinterna
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Inflammatory Bowel Diseases 1986 (1986); ISBN: 9024726123; http://www.amazon.com/exec/obidos/ASIN/9024726123/icongroupinterna
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Managing Your Child's Crohn's Disease and Ulcerative Colitis by Keith J. Benkov, Harland S. Winter; ISBN: 1571010238; http://www.amazon.com/exec/obidos/ASIN/1571010238/icongroupinterna
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Mucosal Ulcerative Colitis by David G. Jagelman (Editor); ISBN: 0879932449; http://www.amazon.com/exec/obidos/ASIN/0879932449/icongroupinterna
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People Not Patients: A Source Book for Living With Inflammatory Bowel Disease by Penny Steiner, et al; ISBN: 0961549505; http://www.amazon.com/exec/obidos/ASIN/0961549505/icongroupinterna
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Psychotherapy in chronic ulcerative colitis by Aaron Karush; ISBN: 072165293X; http://www.amazon.com/exec/obidos/ASIN/072165293X/icongroupinterna
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Straight from the Gut: Living With Crohn's Disease & Ulcerative Colitis (PatientCentered Guides) by Cliff Kalibjian (2003); ISBN: 059650005X; http://www.amazon.com/exec/obidos/ASIN/059650005X/icongroupinterna
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The 2002 Official Patient's Sourcebook on Ulcerative Colitis: A Revised and Updated Directory for the Internet Age (Official Patient Guides Series) by Icon Health Publications, Inc. Staff Icon Group International (Compiler) (2002); ISBN: 0597834091; http://www.amazon.com/exec/obidos/ASIN/0597834091/icongroupinterna
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The Clinician's Guide to Ulcerative Colitis and Crohn's Disease by P. P. Jewell, et al; ISBN: 0443048037; http://www.amazon.com/exec/obidos/ASIN/0443048037/icongroupinterna
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The Crohn's Disease and Ulcerative Colitis Fact Book by Crohn's & Colitis Foundation (Editor), et al; ISBN: 0684179679; http://www.amazon.com/exec/obidos/ASIN/0684179679/icongroupinterna
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The Daily Telegraph: Crohn's Disease and Ulcerative Colitis (The Daily Telegraph) by Fred Saibil; ISBN: 1841196711; http://www.amazon.com/exec/obidos/ASIN/1841196711/icongroupinterna
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The First Year---Crohn's Disease and Ulcerative Colitis: An Essential Guide for the Newly Diagnosed by Jill Sklar, Manuel Sklar; ISBN: 1569245320; http://www.amazon.com/exec/obidos/ASIN/1569245320/icongroupinterna
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The Good Gut Guide: Help for Ibs, Ulcerative Colitis, Crohn's Disease, Diverticulitis, Food Allergies, Other Gut Problems by Stephanie Zinser, R. John Nicholls (2003); ISBN: 0007138059; http://www.amazon.com/exec/obidos/ASIN/0007138059/icongroupinterna
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The surgical management of ulcerative colitis by Frank Couper Walker; ISBN: 0407405003; http://www.amazon.com/exec/obidos/ASIN/0407405003/icongroupinterna
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Treating Ibd: A Patient's Guide to the Medical and Surgical Management of Inflammatory Bowel Disease by Lawrence J. Brandt (Editor), et al; ISBN: 0881675326; http://www.amazon.com/exec/obidos/ASIN/0881675326/icongroupinterna
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Ulcerative Colitis (Bailliere's Clinical Gastroenterology) by P. Gibson; ISBN: 0702023108; http://www.amazon.com/exec/obidos/ASIN/0702023108/icongroupinterna
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Ulcerative Colitis (Clinical Gastroenterology Monograph Series) by Michael J. Goodman, Marshall Sparberg; ISBN: 047148895X; http://www.amazon.com/exec/obidos/ASIN/047148895X/icongroupinterna
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Ulcerative Colitis and Crohn's Colitis, by Joseph Barnett, Kirsner; ISBN: 0812104803; http://www.amazon.com/exec/obidos/ASIN/0812104803/icongroupinterna
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Ulcerative colitis and Crohn's disease : and other diseases of the alimentary system in childhood; ISBN: 0806715111; http://www.amazon.com/exec/obidos/ASIN/0806715111/icongroupinterna
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Ulcerative Colitis: Focus on Topical Treatment by Stephen B. Hanauer, Philippe Marteau (2000); ISBN: 2742002898; http://www.amazon.com/exec/obidos/ASIN/2742002898/icongroupinterna
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Understanding Crohn Disease and Ulcerative Colitis by Jon Zonderman, et al; ISBN: 1578062039; http://www.amazon.com/exec/obidos/ASIN/1578062039/icongroupinterna
The National Library of Medicine Book Index The National Library of Medicine at the National Institutes of Health has a massive database of books published on healthcare and biomedicine. Go to the following Internet site, http://locatorplus.gov/, and then select “Search LOCATORplus.” Once you are in the search area, simply type “ulcerative colitis” (or synonyms) into the search box, and select “books only.” From there, results can be sorted by publication date, author, or relevance. The following was recently catalogued by the National Library of Medicine:11 •
A comparison of clinical findings and morphologic changes in the peripheral blood in patients with chronic ulcerative colitis. Author: Farmer, Richard G. (Richard Gilbert),; Year: 1967; [Minneapolis] 1960
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Anemia of nontropical sprue and chronic ulcerative colitis studied with radioiron and radiochromium. Author: Giuliani, Emilio R. (Emilio Romolo),; Year: 1968; [Minneapolis] 1962
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Chronic ulcerative colitis; a lifelong study. Author: Bargen, Jacob Arnold,; Year: 1969; Springfield, Ill., Thomas [c1969]
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In addition to LOCATORPlus, in collaboration with authors and publishers, the National Center for Biotechnology Information (NCBI) is currently adapting biomedical books for the Web. The books may be accessed in two ways: (1) by searching directly using any search term or phrase (in the same way as the bibliographic database PubMed), or (2) by following the links to PubMed abstracts. Each PubMed abstract has a "Books" button that displays a facsimile of the abstract in which some phrases are hypertext links. These phrases are also found in the books available at NCBI. Click on hyperlinked results in the list of books in which the phrase is found. Currently, the majority of the links are between the books and PubMed. In the future, more links will be created between the books and other types of information, such as gene and protein sequences and macromolecular structures. See http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Books.
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Diet management for ulcerative colitis; menus, recipes, and methods of food preparation for anti-inflammatory treatment. Author: Hanson, Map.; Year: 1967; Springfield, Ill., Thomas [c1971]
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Ileostomy in ulcerative colitis: a long-term study of the results of conventional (Brooke's) and continent (Kock's) ileostomy in 161 patients Author: Valkamo, Erkki.; Year: 1972; Helsinki: [s.n.], 1981
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Inflammatory bowel disease Author: Korelitz, Burton I.,; Year: 1978; Littleton, Mass.: PSG Pub. Co., 1982; ISBN: 0884163105 http://www.amazon.com/exec/obidos/ASIN/0884163105/icongroupinterna
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Inflammatory bowel disease in children and adolescents Author: Kelts, Drew G. (Drew Goddard),; Year: 1971; Chicago: Year Book Medical Publishers, 1980
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Inflammatory bowel diseases Author: Allan, R. N. (Robert Norman); Year: 1971; Edinburgh; New York: Churchill Livingstone, 1983; ISBN: 0443023409 http://www.amazon.com/exec/obidos/ASIN/0443023409/icongroupinterna
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Surgical management of inflammatory bowel disease Author: Beart, Robert W.; Year: 1961; Chicago, Ill.: Year Book Medical, 1980; ISBN: 0815199031 http://www.amazon.com/exec/obidos/ASIN/0815199031/icongroupinterna
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Symposium on inflammatory bowel disease Author: Winship, Daniel H.,; Year: 1960; Philadelphia: Saunders, 1980
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The role of pantothenic acid and coenzyme A in the etiology of chronic ulcerative colitis and granulomatous colitis. Author: Sayed, Judith Ellestad.; Year: 1952; [Minneapolis] 1975
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The surgical management of ulcerative colitis. Author: Walker, Frank C. (Frank Couper); Year: 1971; New York, Appleton-Century-Crofts; London, Butterworth [c1969]
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Treatment of chronic ulcerative colitis. Author: Goligher, J. C. (John Cedric); Year: 1969; Chicago, Year Book Medical Publishers, 1965
Chapters on Ulcerative Colitis In order to find chapters that specifically relate to ulcerative colitis, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and ulcerative colitis using the “Detailed Search” option. Go to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find book chapters, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Book Chapter.” Type “ulcerative colitis” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on ulcerative colitis: •
Use of Probiotics in Inflammatory Bowel Disease Source: in Williams, C.N., et al., eds. Trends in Inflammatory Bowel Disease Therapy 1999. Boston, MA: Kluwer Academic Publishers. 2000. p. 252-258. Contact: Available from Kluwer Academic Publishers. Customer Service Deparment, P.O. Box 358, Accord Station, Hingham, MA 02018-0358. (781) 871-6600. Fax (781) 6819045. E-mail:
[email protected]. Website: www.wkap.nl. PRICE: 145.00 plus shipping and handling. ISBN: 0792387627.
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Summary: A body of evidence from clinical and experimental observations indicates a role for intestinal microflora in the pathogenesis of inflammatory bowel disease (IBD). Probiotics are defined as 'living organisms, which upon ingestion in certain numbers, exert health benefits beyond inherent basic nutrition.' This chapter on the use of probiotics in IBD is from a monograph that reprints the presentations given at the Trends in Inflammatory Bowel Disease Therapy Symposium, held in Vancouver, British Columbia, Canada, in August 1999. The general objective of the conference was to provide an update in the etiology, pathogenesis, and treatment of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and CD. In this chapter, the authors review recent evidence supports the potential role of probiotics in IBD therapy. The authors' experience focuses on the use of a new probiotic preparation (VSL number 3) containing 300 billion per gram of viable lyophilized (freeze dried) bacteria of four strains of lactobacilli, three strains of bifidobacteria, and one strain of Streptococcus salivarius subspecies thermophilus. Twenty patients received 6 grams a day of VSL3 for 12 months and were periodically assessed. Microbiological determination showed a significant increase in concentration of lactobacilli, bifidobacteria, and Streptococcus salivarius subspecies thermophilus, fecal pH was significantly reduced, and the great majority of patients (75 percent) remained in remission. Subsequent efficacy of this new oral probiotic preparation was tested versus placebo in 40 patients with chronic relapsing pouchitis. Of the 20 patients who received placebo, all relapsed, whereas 17 of the 20 patients treated with VSL3 were still in remission after 9 months. All these 17 patients, after suspension of the treatment, had a relapse within 4 months. A controlled study evaluating the efficacy of treatment with antibiotics and probiotics versus mesalazine in the prevention of postoperative recurrence in patients with Crohn' disease is now in progress. The authors conclude that these findings suggest that probiotics may be of therapeutic benefit in maintenance treatment of IBD. 4 figures. 27 references. •
Steroid Unresponsiveness in Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 133-137. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: Although systemic glucocorticoid treatment is associated with a large number and sometimes severe side effects, this is still the first and most useful therapeutic tool in treating patients with both acute ulcerative colitis (UC) and Crohn's disease (CD). In these clinical situations, glucocorticoids are both rapidly acting, within 48 hours, and effective, with a response rate of about 80 percent. Unresponsiveness to steroid treatment leads to the need for therapeutic decisions including surgical resection or the use of immunosuppressive drugs. This chapter on steroid unresponsiveness is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with CD and UC, together known as inflammatory bowel disease (IBD). When a patient presents with steroid resistance, it is important to rule out false causes of refractoriness, such as bile-salt malabsorption, bacterial overgrowth, and coexistent irritable bowel syndrome. It also is important to detect the existence of viral or bacterial gastrointestinal infections that may enhance the synthesis of inflammatory mediators perpetuating the disease process. The molecular basis of genuine steroid resistance is unclear but an understanding will allow earlier diagnosis and treatment. Therapeutic alternatives to steroids should be individualized; the author
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outlines a personal schematic approach in a patient care algorithm. 2 figures. 12 references. •
Clinical Features, Course, and Laboratory Findings in Ulcerative Colitis Source: in Lichtenstein, G.R. The Clinician's Guide to Inflammatory Bowel Disease. Thorofare, NJ: SLACK Incorporated. 2003. p. 27-39. Contact: Available from SLACK Incorporated. 6900 Grove Road, Thorofare, NJ 080869447. (856) 848-1000. Fax (856) 853-5991. Website: www.slackbooks.com. PRICE: $44.95; plus shipping and handling. ISBN: 556425546. Order number: 75546. Summary: Although the term inflammatory bowel disease (IBD) describes a wide range of inflammatory states, it generally refers to ulcerative colitis (UC) and Crohn's disease. This chapter is from a handbook that presents an up to date guide on selected topics in IBD, focusing on those clinically important areas that have undergone recent changes or discoveries. In this chapter, the authors discuss the clinical features, course, and laboratory findings in ulcerative colitis (UC). Written in an outline format for ease of access, the chapter covers an assessment of disease severity, classification systems, ulcerative proctitis, and ulcerative colitis. Each of the latter two sections covers symptoms, physical examination, laboratory features, and expected clinical course. The section on UC also considers extraintestinal manifestations. 4 tables. 19 references.
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Inflammatory Bowel Diseases Source: in Bonci, L. American Dietetic Association Guide to Better Digestion. Hoboken, NJ: John Wiley and Sons, Inc. 2003. p. 74-98. Contact: Available from John Wiley and Sons, Inc. Customer Care Department, One Wiley Drive, Somerset, NJ 08875. (800) 762-2974 or (317) 572-3993. Fax (317) 572-4002. Website: www.wiley.com. PRICE: $14.95 plus shipping and handling. ISBN: 0471442232. Summary: Coping with a gastrointestinal disorder, whether it is irritable bowel syndrome (IBS), gas (flatulence), constipation, heartburn, or another condition, can be embarrassing and debilitating. While medical treatments and prescriptions can offer relief, one of the most important ways patients can help themselves is in their dietary choices. This chapter on inflammatory bowel disease (IBD) is from a book that describes how patients can self-manage their digestive disorders through dietary choices. IBD includes Crohn's disease and ulcerative colitis, both of which result in inflammation of different parts of the digestive tract. In this chapter, the author defines IBD and its possible causes, then discusses the symptoms of the condition, the diagnostic tests that are used to confirm IBD, treatment options, surgical options, medications that are commonly used for symptom management, the use of nutritional supplements, the impact of diet on IBD symptoms, foods and supplements that may be bothersome, and specific eating recommendations for ulcerative colitis and for Crohn's disease. A final section discusses short bowel syndrome (when the small bowel cannot function because of disease, or when it has been surgically removed). 9 figures.
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How and Why the Digestive System Malfunctions in People with Crohn Disease or Ulcerative Colitis Source: in Zonderman, J. and Vender, R.S. Understanding Crohn Disease and Ulcerative Colitis. Jackson, MS: University Press of Mississippi. 2000. p. 29-35.
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Contact: Available from University Press of Mississippi. 3825 Ridgewood Road, Jackson, MS 39211-6492. (601) 432-6205. Fax (601) 432-6217. E-mail:
[email protected]. PRICE: $28.00 plus shipping and handling. ISBN: 1578062039. Summary: Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD), are chronic illnesses of unknown origin. This chapter on digestive system malfunction in IBD is from a book that provides timely information about how to obtain and maintain the highest quality of life possible while living with IBD. The authors offer a patient's perspective on coping with IBD. They describe the major pathology of the intestinal tract in a person with CD or UC as chronic inflammation. Inflammation is characterized by four conditions: heat, redness, pain, and swelling. In IBD, inflammation occurs in the inside of the gastrointestinal tract and the inflammatory process also damages the cellular structure of the intestine. In UC, the inflammation affects only the mucosa; in CD, the inflammation can go through the mucosa and involve the full thickness of the bowel wall. Depending on where in the gastrointestinal tract the inflammation occurs, effects include malabsorption of nutrients, bleeding, diarrhea, fever, and pain. The chapter offers statistics on IBD, discusses the possible genetic component in the disease, and considers the role of the immune system. •
Recent Developments in the Diagnosis and Management of Paediatric Inflammatory Bowel Disease Source: in Williams, C.N., et al., eds. Trends in Inflammatory Bowel Disease Therapy 1999. Boston, MA: Kluwer Academic Publishers. 2000. p. 87-95. Contact: Available from Kluwer Academic Publishers. Customer Service Deparment, P.O. Box 358, Accord Station, Hingham, MA 02018-0358. (781) 871-6600. Fax (781) 6819045. E-mail:
[email protected]. Website: www.wkap.nl. PRICE: 145.00 plus shipping and handling. ISBN: 0792387627. Summary: Inflammatory bowel disease (IBD) in the pediatric age group presents many challenges to the health care team. This chapter on the diagnosis and management of pediatric IBD is from a monograph that reprints the presentations given at the Trends in Inflammatory Bowel Disease Therapy Symposium, held in Vancouver, British Columbia, Canada, in August 1999. The general objective of the conference was to provide an update in the etiology, pathogenesis, and treatment of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD). In this chapter, the authors describe advances in three areas: serological (blood) tests to screen for IBD and to distinguish between forms of colitis; Doppler sonography (ultrasound) to demonstrate disease activity; and pharmacogenomics to optimize therapy with azathioprine and 6 mercaptopurine. In mild cases, the nonspecific symptoms of IBD may be mistaken for a functional bowel disorder, delaying the diagnosis. Improved serological assays allow clinicians to screen for IBD. Not uncommonly, children and adolescents with CD show few symptoms yet present with anorexia (lack of appetite) and growth failure. The availability of the noninvasive Doppler ultrasound to demonstrate subclinical inflammation in such cases is of great benefit to their management. The authors also discuss the importance of detecting and treating osteopenia (subnormally mineralized bone); the lifelong prevention of osteoporosis (loss of bone density) is a goal that must being in childhood, a time of rapid bone growth and increasing density. 2 figures. 3 tables. 15 references.
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Life-Style Issues and Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 531-533. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: Inflammatory bowel diseases (IBDs), ulcerative colitis(UC), and Crohn's disease (CD) are chronic diseases that can afflict patients at various times of their lives. This chapter on lifestyle issues is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with CD and Ulcerative Colitis (UC). The author of this chapter, a practicing gastroenterologist specializing in IBD, and an IBD patient for almost 30 years, shares his experiences so other practitioners will be able to gain insight into living and functioning with IBD and how treating physicians, can become more effective practitioners for this unique group of patients. As with any chronic illness, treating only the symptoms and complications of these diseases may not meet all of the needs of the individual patient. The success or failure of a particular treatment plan also may be dependent on the ability of the family, or support system, to understand the situation and become the surrogate nurse for these patients. The author stresses that the lifestyle issues that need to be addressed in the individual patient are dependent upon the stage of that patient in life. Each of four stages are then discussed: children and adolescents, young adulthood, adulthood, and elderly patients. The author challenges physicians to take on the role of patient advocate, to learn about and use potential referral sources, and to address their own prejudices against patients with chronic diseases. Accessing support from organizations such as the CCFA (Crohn's and Colitis Foundation of America) is also encouraged. 4 references.
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Inflammatory Bowel Disease Nurse Advocate Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 535-537. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: Many patients with Crohn's disease (CD) or ulcerative colitis (UC) report frequent encounters with health care providers who know little about inflammatory bowel disease (IBD) and how to manage it. The position of the Inflammatory Bowel Disease Nurse Advocate at the Johns Hopkins Hospital is designed to address this problem. This chapter describing the IBD nurse advocate is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). The primary goal of this position is to responsibly address the multidisciplinary needs of this unique patient population. The author describes the essential and complementary skills needed for this position, primary responsibilities, measuring role impact, the use of telecommunication, and community outreach. Patients ranked effective communication of health-related information second to clinical skill as the most crucial element of outpatient care. Responding to patient perception, the 'advocate' model prioritizes the essentials of improved communication, patient
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education, and accessibility to the health care system. Using a collaborative approach, the IBD Nurse Advocate functions as a 'physician extender.' This approach to practice promotes productivity and effective use of personnel, and has a positive impact on patient outcomes. One figure reprints a customized intake form for patients with IBD. 1 figure. 3 references. •
Nonsteroidal Anti-Inflammatory Drugs, Enterocolonic Ulceration, and Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 625-629. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: Nonsteroidal antiinflammatory drugs (NSAIDs) cause damage through the gastrointestinal tract. This chapter on NSAIDS, enterocolonic (small bowel) ulceration and inflammatory bowel disease (IBD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as IBD. The authors outline an approach to treatment of the damage of NSAIDs to the small bowel and the management of patients with IBD who require NSAIDs. The authors caution that the use of NSAIDs in patients with IBD is challenging because the drugs may cause relapse of disease. Specific issues addressed include iron deficiency anemia, hypoalbuminemia (reduced levels of protein in the blood), strictures (narrowing of the intestine), NSAID induced colon damage, and the use of NSAIDs in patients with IBD. Rarely, NSAIDs actually cause colitis, but their use is associated with an enhanced risk of appendicitis in the elderly and diverticular complications (fistulae and abscesses). 6 references.
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Role of Nutrition in the Treatment of Inflammatory Bowel Disease Source: in Williams, C.N., et al., eds. Trends in Inflammatory Bowel Disease Therapy 1999. Boston, MA: Kluwer Academic Publishers. 2000. p. 207-216. Contact: Available from Kluwer Academic Publishers. Customer Service Deparment, P.O. Box 358, Accord Station, Hingham, MA 02018-0358. (781) 871-6600. Fax (781) 6819045. E-mail:
[email protected]. Website: www.wkap.nl. PRICE: $145.00 plus shipping and handling. ISBN: 0792387627. Summary: Nutritional management (diet therapy) is used as a therapeutic tool in inflammatory bowel disease (IBD). This chapter on the role of nutrition in the treatment of IBD is from a monograph that reprints the presentations given at the Trends in Inflammatory Bowel Disease Therapy Symposium, held in Vancouver, British Columbia, Canada, in August 1999. The general objective of the conference was to provide an update in the etiology, pathogenesis, and treatment of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD). In this chapter, the author stresses that the nutritional approach to IBD has a common target: to avoid the use of steroids or other immunosuppressive drugs, by influencing metabolic routes involved in the inflammatory response. There is no evidence that either parenteral (outside the digestive tract, i.e., intravenous) or enteral (inside the digestive tract, i.e., gastrostomy or nasogastric tube feeding) nutrition has any primary therapeutic effect on the outcome of patients with severe UC. The research on the nutritional approach to the maintenance treatment of UC has show little or no effect. Greatest interest in the
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nutritional approach in IBD has centered on the possibility of using chemically defined enteral formula diets as primary treatment in CD. Some diets have been shown to induce remission in active CD. Compared to steroid induced remission (80 percent of cases), enteral nutrition resulted in remission levels of 60 to 65 percent. The authors note that enteral nutrition appears particularly effective in children and adolescents (a population that should be especially protected from steroid side effects) in moderate first and subsequent attacks, and possibly as maintenance treatment in clincally inactive disease. In addition, enteral (or in some cases parenteral) nutrition should be used as adjuvant therapy to prevent or reverse nutritional deficiencies whatever primary treatment is used. 98 references. •
How Can We Predict Prognosis in Inflammatory Bowel Disease? Source: Jewell, D.P.; Warren, B.F.; Mortensen, N.J., eds. Challenges in Inflammatory Bowel Disease. Malden, MA: Blackwell Science, Inc. 2001. p.269-284. Contact: Available from Blackwell Science, Inc. 350 Main Street, Commerce Place, Malden, MA 02148. (800) 215-1000 or (617) 388-8250. Fax (617) 388-8270. E-mail:
[email protected]. Website: www.blackwell-science.com. PRICE: $145.95. ISBN: 0632051698. Summary: Patients who have recently been diagnosed with inflammatory bowel disease (IBD) will have many questions for their physicians regarding the clinical course and prognosis of their disease. This chapter on prognosis is from a book that offers an approach to the subject of IBD that highlights current areas of controversy. The authors review the literature concerning the clinical course of ulcerative colitis and Crohn's disease and how physicians can predict prognosis. Topics include prognosis following the first attack of ulcerative colitis, risk for relapse, the need for colectomy, the risk of progression of proctitis and proctosigmoiditis to more extensive disease, relapse of specific Crohn's disease patterns, the need for surgery, the role of smoking, and the role of oral contraceptives. 3 tables. 95 references.
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Current Controversies in the Surgical Management of Ulcerative Colitis Source: Jewell, D.P.; Warren, B.F.; Mortensen, N.J., eds. Challenges in Inflammatory Bowel Disease. Malden, MA: Blackwell Science, Inc. 2001. p.157-165. Contact: Available from Blackwell Science, Inc. 350 Main Street, Commerce Place, Malden, MA 02148. (800) 215-1000 or (617) 388-8250. Fax (617) 388-8270. E-mail:
[email protected]. Website: www.blackwell-science.com. PRICE: $145.95. ISBN: 0632051698. Summary: Proctocolectomy with permanent ileostomy is curative for ulcerative colitis. Since its introduction 50 years ago, subsequent surgical developments have been aimed at avoiding a permanent ileostomy. This chapter on the surgical management of ulcerative colitis is from a book that offers an approach to the subject of inflammatory bowel disease (IBD) that highlights current areas of controversy. The authors note that colectomy with ileorectal anastomosis and restorative proctocolectomy are well accepted but controversies remain on the relative indications for these procedures. In addition there is some controversy on the indications for surgery against continued medical treatment and questions relating to technical aspects of the procedures. The authors discuss emergency and elective surgeries separately. 74 references.
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Psychotherapy for Inflammatory Bowel Disease: New Prospects Source: in Williams, C.N., et al., eds. Trends in Inflammatory Bowel Disease Therapy 1999. Boston, MA: Kluwer Academic Publishers. 2000. p. 185-193. Contact: Available from Kluwer Academic Publishers. Customer Service Deparment, P.O. Box 358, Accord Station, Hingham, MA 02018-0358. (781) 871-6600. Fax (781) 6819045. E-mail:
[email protected]. Website: www.wkap.nl. PRICE: 145.00 plus shipping and handling. ISBN: 0792387627. Summary: Psychotherapeutic approaches to inflammatory bowel disease (IBD) have come in two historical ways. In the first, psychoanalysis assumed a model of psychogenic etiology (cause) and aimed for cure. A second wave aimed to improve coping and reduce the psychosocial consequences of IBD. This chapter on psychotherapy for inflammatory bowel disease (IBD) is from a monograph that reprints the presentations given at the Trends in Inflammatory Bowel Disease Therapy Symposium, held in Vancouver, British Columbia, Canada, in August 1999. The general objective of the conference was to provide an update in the etiology, pathogenesis, and treatment of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and CD. In this chapter, the author reports on two new psychotherapeutic approaches for IBD. Supportive expressive (SE) group psychotherapy was originally described for women with metastatic breast cancer. An adaptation for use in IBD has been tested in four 20 week groups (n = 30). The group discussion is grounded in major IBD concerns including uncertainty, personal control and burden on others, physician-patient relationship, medication concern, and body image. The expressive aspect of SE refers to facing the challenges and limitations imposed by illness honestly, and expressing the feelings that result. The supportive aspect of SE refers to the emphasis on interpersonal support as a buffer against the negative psychosocial consequences of disease. Results demonstrate that among those who complete the group (n = 24), improvement in maladaptive coping behaviors occurs concurrently with improvement in IBD related quality of life in subjects who improve with therapy (67 percent). A second approach to psychotherapy follows from recent data suggesting that a personality trait which results in stress vulnerability (insecure attachment) may be relevant to disease course in a biologically identified subgroup of UC patients. The author describes the model of interaction between individual differences in stress response and biological subtypes of UC which predicted this finding. These data, pending replication, imply that screening of UC patients to identify stress-vulnerable individuals may be useful. The author also discusses the selective application of psychotherapy to modify an interpersonal style which increases stress vulnerability, with respect to therapeutic technique and goals. 2 figures. 36 references.
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Management of Severe Ulcerative Colitis Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 143-147. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: Severe or fulminant ulcerative colitis (UC) is a potentially fatal disease that was associated with a 30 percent mortality rate prior to the introduction of corticosteroids and, in steroid-refractory cases, early surgery. During recent years, the trend has changed from saving lives to improving the quality of life of patients by
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saving colons or using modern surgical methods. This chapter on the management of severe UC is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and UC, together known as inflammatory bowel disease (IBD). The author discusses the etiology, differential diagnosis, and definition of severe UC. Patients with definite or strongly suspected severe colitis must be admitted to the hospital for intensive treatment. The mainstay of the medical treatment is corticosteroids, taken orally with nothing except small sips of water, and total parenteral nutrition (TPN, outside the gastrointestinal tract). Usually, corticosteroids are administered intravenously in severe colitis, but even in acute colitis, corticosteroids given orally are absorbed completely but somewhat more slowly than those administered intravenously. Colonoscopy, rather than food challenge, is relied on to improve decision making in patients with incomplete or poor response to treatment. The author discusses the indications for using antibiotics, 5 aminosalicylic acid (5 ASA), and immunosuppressives. Beyond the drug therapy, the patient must be monitored carefully. Three or 4 days after initiating therapy, a sigmoidoscopy is of further help in monitoring the response and a biopsy helps to rule out cytomegalovirus. Assessment of response is made mainly on clinical and laboratory grounds, although repeat plain abdominal radiography during ongoing treatment can show signs of impending perforation or definite toxic dilatation that requires surgery. 1 table. 10 references. •
Risk Factors and Prevalence of Bone Disease in Inflammatory Bowel Disease Source: in Williams, C.N., et al., eds. Trends in Inflammatory Bowel Disease Therapy 1999. Boston, MA: Kluwer Academic Publishers. 2000. p. 147-162. Contact: Available from Kluwer Academic Publishers. Customer Service Deparment, P.O. Box 358, Accord Station, Hingham, MA 02018-0358. (781) 871-6600. Fax (781) 6819045. E-mail:
[email protected]. Website: www.wkap.nl. PRICE: 145.00 plus shipping and handling. ISBN: 0792387627. Summary: The prevalence rates of decreased bone mineral density (BMD) in patients with inflammatory bowel disease (IBD) range from 40 to 50 percent. The choice of therapies available for the induction of remission in Crohn's disease is becoming increasingly complex. This chapter on the risk factors and prevalence of bone disease in IBD is from a monograph that reprints the presentations given at the Trends in Inflammatory Bowel Disease Therapy Symposium, held in Vancouver, British Columbia, Canada, in August 1999. The general objective of the conference was to provide an update in the etiology, pathogenesis, and treatment of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and CD. In this chapter, the author notes that osteoporosis (a condition of bone thinning), as defined by a BMD Z score of minus 2.5, has been reported in a range of 2 to 30 percent of patients. There is a definite lack of data reporting the fracture incidence rate among patients with IBD. Fractures are a hard endpoint and the main morbidity associated with osteopenia (subnormally mineralized bone) of any cause. Osteoporosis which places subjects at risk for fractures has been a term applied to histomorphometric diagnoses, radiological diagnoses, and most recently to BMD diagnoses. The author notes recent research demonstrating that there is an increased rate of fractures at the hip, ribs and forearm among patients with IBD compared with an age, gender, and geographically matched cohort drawn from the general population. The author discusses risk factors for the development of osteoporosis and fractures in patients with IBD. Measurable risk factors, such as BMD or serum (blood) and urine markers of bone resorption and formation, are discussed in the context of patients with IBD. Patients who are physically inactive, are underweight or
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malnourished, have active disease and have used chronic or recurrent courses of corticosteroids, have a positive history of an osteoporosis associated fracture in a first degree relative, or hae irregular menses should be screened for osteoporosis. For all other patients, each physician will have to develop the criteria he or she wants to follow in terms of deciding who to screen. 1 table. 110 references. •
Induction of Remission in Ulcerative Colitis Source: in Williams, C.N., et al., eds. Trends in Inflammatory Bowel Disease Therapy 1999. Boston, MA: Kluwer Academic Publishers. 2000. p. 107-116. Contact: Available from Kluwer Academic Publishers. Customer Service Deparment, P.O. Box 358, Accord Station, Hingham, MA 02018-0358. (781) 871-6600. Fax (781) 6819045. E-mail:
[email protected]. Website: www.wkap.nl. PRICE: 145.00 plus shipping and handling. ISBN: 0792387627. Summary: Therapy for acute ulcerative colitis (UC) begins with an assessment of disease extent, severity and the response to prior treatments. This chapter on the induction of remission in UC is from a monograph that reprints the presentations given at the Trends in Inflammatory Bowel Disease Therapy Symposium, held in Vancouver, British Columbia, Canada, in August 1999. The general objective of the conference was to provide an update in the etiology, pathogenesis, and treatment of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD). In this chapter, the author describes care for patients with mild, moderate and severe UC. Mild to moderate activity can be treated with oral mesalamine in the setting of extensive colitis, or topical mesalamine or topical corticosteroids for distal disease. The dose response is relevant for oral mesalamine, but is less important for topical therapy. Moderate to severe extensive colitis requires corticosteroid therapy whereas distal disease can still be treated with topical mesalamine or topical corticosteroids. Severe to fulminant colitis requires hospitalization and parenteral corticosteroids. Significant improvement is anticipated within 3 to 5 days of initiating steroids at doses comparable to 40 to 60 milligrams of prednisolone or 200 to 400 milligrams of hydrocortisone. Patients who do not respond within 7 days are unlikely to improve. Failure to improve on parenteral steroids is indication for either colectomy or treatment with cyclosporin. Cyclosporin will provide prompt improvement in approximately 70 to 80 percent of patients within 3 to 5 days. Failure to respond with a reduction in bowel movements, cessation of bleeding and transfusion requirements, and reduction in erythrocyte sedimentation rate within a week implies treatment failure and is an indication of colectomy. Total parenteral nutrition (TPN, usually intravenous therapy) is adjunctive rather than primary therapy for patients with severe colitis who should be allowed t eat as long as they have an appetite. Narcotic analgesia (painkillers) is contraindicated, as are nonsteroidal antiinflammatory agents (NSAIDs). The author notes that the roles of topical mesalamine, infliximab, and heparin in the setting of fulminant (rapid, sudden, severe) disease or toxic megacolon have not been established. 60 references.
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Guide for Patients and Their Families To Manage the Emotional Impact of Inflammatory Bowel Disease Source: in Stein, S.H. and Rood, R.P. Inflammatory Bowel Disease: A Guide for Patients and Their Families. 2nd ed. Philadelphia, PA: Lippincott-Raven Publishers. 1999. p. 111122. Contact: Available from Crohn's and Colitis Foundation of America. 386 Park Avenue South, 17th Floor, New York, NY 10016-8804. (800) 932-2423. Fax (212) 779-4098. E-mail:
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[email protected]. Website: www.ccfa.org. PRICE: $17.00 for members; $22.00 for nonmembers; plus shipping and handling. ISBN: 0397517718. Summary: This chapter is from a text written specifically for people with inflammatory bowel disease (IBD), which is the collective term for ulcerative colitis and Crohn's disease. Ulcerative colitis is an inflammatory disease of the large intestine (the colon), that is characterized by inflammation and ulceration of its inner lining. By contrast, Crohn's disease can affect any area of the gastrointestinal tract, including the small intestine. In this chapter, the author provides a guide to help patients and their families manage the emotional impact of IBD. Readers learn how they can have a good life and adjust to their sporadic symptoms. The author focuses on self management skills that can address the decreased ability to anticipate one's state of health on a particular day. The author also helps readers determine how their obligations and interactions with other people will change because of their illness. Readers are encouraged to obtain information about IBD to better understand options for treatment and everyday living. The author stresses that by changing one's expectations and attitudes, IBD can be tolerated and even integrated into other strategies and goals of life. •
Adherence Issues in Management of Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 9-11. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on adherence issues is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). UC and CD are chronic, recurring conditions requiring life-long management. Most often, patients take their medicines when they are sick, but nonadherence is a common phenomenon with disease in remission. Many clinicians incorrectly assume that their patients follow prescribed therapeutic recommendations. The degree of adherence that patients are able to achieve early in the course of disease may decrease markedly after 1 to 2 years. Once remission has been established, patients often enter a 'honeymoon' phase of maintenance therapy. After a period of time, they may tire of taking their medications. Thus, during the transition from therapeutic to maintenance therapy, education regarding the importance of continued adherence to prevent relapse of disease or complications is vital. Failure to comply with recommended maintenance regimens increases the risk of recurrent active disease, possible hospitalization, or steroid exposure and the consequences of prolonged steroid use. It is worth considering that nonadherence also is associated with the risk of extraintestinal manifestations of IBD that parallel gastrointestinal disease activity, and may also be an important factor regarding long term cancer risks. Furthermore, the issue of compliance is not limited to medicines but includes lifestyle modifications (smoking cessation, dietary restrictions) and other follow-up care (surveillance colonoscopies and monitoring blood tests for certain medications). Patterns of nonadherence include under or overconsuming medication, taking doses at inappropriate intervals, or administering medication incorrectly (as in enema therapy). Factors that influence long-term adherence include those related to the health care provider, the patient, and also the medication itself. The author concludes that physicians cannot support patient compliance alone; a team approach using the strengths, knowledge, and experience of
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nurses, social workers, and pharmacists, and the patients themselves, will ultimately lead to the best medical care. 1 table. 7 references. •
Aminosalicylates Therapy for Ulcerative Colitis Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 123-126. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on aminosalicylates therapy for ulcerative colitis is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). The author cautions that careful attention is necessary in interpreting clinical trials of the aminosalicylates in UC, because of variations in its indications (active disease versus maintenance), therapeutic end points and indices, and duration of treatment. Oral aminosalicylates are the primary maintenance therapy to prevent relapse of colitis after remission has been achieved. There are practical considerations that differentiate sulfasalazine from the non sulfa containing aminosalicylates. There is dose-related efficacy for the maintenance effects of all oral aminosalicylates. With sulfasalazine, the maintenance dose of 2 grams per day is often selected as the best 'balance' between efficacy and side effects. This has led to previous recommendations to reduce the active dose down to 2 grams per day as a maintenance dose. Unfortunately, this precludes use of a more efficacious maintenance dose. In contrast, in the absence of dose-related side effects with mesalamine, the optimal maintenance dose (with respect to efficacy) is the same as the inductive dose. The only constraints are cost and patient compliance. Typically, administration of oral aminosalicylates on a twice-daily schedule is recommended, to enhance compliance. Because of variations in gastric emptying and colonic motility among patients, there is no rationale to require administration of oral mesalamine compounds in more than two doses per day. 10 references.
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Arthritis Associated with Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 279-282. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on arthritis associated with inflammatory bowel disease (IBD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as IBD. Arthritis is a relatively common complication of UC and CD, affecting 10 to 20 percent of patients. Arthritis may predate the bowel disease and may be severe enough to warrant treatment in its own right, perhaps with nonsteroidal anti-inflammatory drugs (NSAIDs). This may, itself, exacerbate the underlying bowel disease. In this chapter, the different forms of arthritis associated with IBD are identified and their management discussed in terms of their prognosis, possible modes of treatment, and when expert help should be sought. With the exception of ankylosing
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spondylitis (AS, fusion of the vertebral facet joints), the IBD associated joint disease is largely non deforming and non progressive, and so can be managed symptomatically, although the use of NSAIDs should be avoided. Management involves judicious use of physical treatments (rest, range of movement exercises, and physiotherapy) in addition to pharmacological treatments. Patients with AS or persistent or erosive peripheral joint disease should be referred to a rheumatologist. 2 tables. 6 references. •
Cancer Prevention Strategies in Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 257-261. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on cancer prevention strategies in inflammatory bowel disease (IBD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflamatory bowel disease (IBD). Ulcerative colitis is associated with an increased risk of developing colorectal cancer (CRC). The risk of CRC is approximately 7 to 14 percent at 25 years of disease. Crohn's disease has a similar ageadjusted increased risk of developing CRC. The risks of developing CRC inUC correlate with increased disease duration and increased disease extent. Neoplasia (new tissue, which can include dysplasia, polyps, or cancer) usually is first evident after approximately 8 years of disease and is more likely to occur among patients with pancolitis than those with left-sided colitis. When cancer occurs in UC, it is more commonly found in the rectosigmoid. For CD, the increased risk is associated with disease duration and extent of 'at risk mucosa' as well. Patients with limited cecal disease are at limited risk for developing CRC and isolated ileal disease does not appear to increase the risk of CRC. The author reviews the pitfalls and benefits of dysplasia surveillance and offers suggestions for the clinical approach to patient counseling, surveillance timing, biopsy site and number, adenoma like masses, and the presence of pseudopolyps. Preventing or removing CRC at an early stage in UC patients is as advantageous as diagnosing early CRC in the general population. 2 figures. 12 references.
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Cholangiocarcinoma in the Inflammatory Bowel Disease Patient Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 311-315. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on cholangiocarcinoma (biliary tract cancer) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). Cholangiocarcinoma (CC) is a dreaded complication of PSC due to its poor prognosis (median survival of 5 months) and limited treatment options. In the general population, CCs are rare tumors but occur in 5 to 15 percent of patients with primary sclerosing cholangitis (PSC). The major risk factor
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for CC development is chronicity of PSC. This duration of disease is somewhat difficult to prove as the precise onset of PSC is often uncertain. Most CC patients have already developed cirrhosis and have longstanding Ulcerative Colitis (UC). Its detection in the setting of PSC necessitates a high index of clinical suspicion in addition to serial assessments of serum biliary biochemistry and possible imaging with CT scan of the abdomen and ERCP with tissue sampling of dominant strictures. Early detection of potentially curable CC remains the challenge, and no proven technique exists. Serum IL-6 concentration and PET scanning may prove to be helpful in this regard. The only definitive treatment is surgical resection as the prognosis following liver transplantation remains unacceptably poor. Neoadjuvant therapy with chemoradiation may offer some benefit in reducing tumor bulk and increasing the proportion of patients suitable for curative resection. Palliative therapy aims to relieve the symptoms of biliary obstruction and optimize quality of life. Endoscopic stricture dilation and biliary stent placement is possible in the majority of patients and highly successful in effecting biliary decompression. A multidisciplinary approach optimizes the treatment strategy in the management of patients with CC. •
Crohn's Disease and Ulcerative Colitis Source: in King, J.E., ed. Mayo Clinic on Digestive Health. Rochester, MN: Mayo Clinic. 2000. p. 99-114. Contact: Available from Mayo Clinic Health Information. 5505 36th Street, SE, Grand Rapids, MI 49512. (800) 291-1128. Website: www.mayoclinic.com. PRICE: $14.95 plus shipping and handling. ISBN: 1893005046. Summary: This chapter on Crohn's disease and ulcerative colitis (the two most common inflammatory bowel diseases, IBD) is from a comprehensive guidebook from the Mayo Clinic that focuses on a variety of digestive symptoms, including heartburn, abdominal pain, constipation, and diarrhea, and the common conditions that are often responsible for these symptoms. Written in nontechnical language, the book includes practical information on how the digestive system works, factors that can interfere with its normal functioning, and how to prevent digestive problems. This chapter first reviews the key signs and symptoms of IBD, including diarrhea, abdominal pain and cramping, blood in the stool (feces), fatigue, reduced appetite, weight loss, and fever. The authors note that although these diseases often cannot be cured, they can be treated. There are several therapies that may drastically reduce the patient's symptoms, and possibly even bring about a long term remission. The chapter outlines the differences between the two diseases (Crohn's disease can strike anywhere from the mouth to the anus; ulcerative colitis is typically limited to the colon and rectum), reviews theories about the causes of these problems, and offers classification systems to determine if the disease is mild, moderate or severe. Diagnostic tests used to confirm the presence of IBD include blood tests, X rays, and colonoscopy (which can include biopsy). Medications can effectively reduce symptoms in most people with IBD; drugs used include antiinflammatory drugs (sulfasalazine, mesalazine, olsalazine, corticosteroids), immunosuppressants (such as azathioprine, methotrexate, and cyclosporine), antibiotics (notably metronidazole and ciprofloxacin), nicotine patches, antidiarrheals, laxatives, pain relievers, iron supplements, and vitamin B12 injections. The chapter concludes with suggestions for lifestyle modifications that can help people cope with IBD and a section explaining the surgical options that may be used for IBD that is not responsive to other treatments. 1 figure.
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Cutaneous Manifestations of Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 271-274. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on cutaneous (skin) manifestations of inflammatory bowel disease (IBD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as IBD. Pyoderma gangrenosum is an idiopathic inflammatory skin disease manifested clinically by painful ulceration with characteristic purple borders. These ulcers most commonly present in an otherwise healthy patient as a single self-limited lesion of the lower extremities. Although a significant number of pyoderma gangrenosum lesions may resolve spontaneously after many months, the debility from pain and the potential of a superimposed local and systemic infection in such a necrotic wound prompts the institution of early therapeutic intervention (based on immunosuppressive therapy). Another condition, erythema nodosum (EN) is a reactive septal panniculitis (a chronic inflammation of subcutaneous fat) characterized by extremely painful, nonulcerating erythematous (reddened) nodules on pretibial (shin) areas. The vast majority of cases affect young women, and the triggering or underlying disease remains unknown. When a cause is identified, a preceding streptococcal infection is a common association. Other infections, sarcoidosis, drugs, rheumatologic disease, and IBD also can be associated with erythema nodosum. In contrast to pyoderma gangrenosum, the activity of erythema nodosum tends to reflect that of the associated intestinal disease. Erythema nodosum usually resolves spontaneously, and while waiting for resolution most cases will respond to nonsteroidal antiinflammatory drugs. Cutaneous CD is an unusual but potentially very debilitating complication of IBD. The most common presentation of cutaneous CD is perineal involvement secondary to enterocutaneous fistulae, and the clinical features of this presentation are draining sinuses, ulcerations, plaques, and nodules. The activity of the perineal disease tends to closely parallel that of the intestinal disease. Treatment involves combination immunosuppressive and antiinflammatory therapy. The author also discusses vasculitis, dermatosis arthritis syndrome, Sweet's syndrome, necrolytic migratory erythema, and other IBD associated mucous membrane disorders. 31 references.
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Dietary Recommendations for Active and Inactive Ulcerative Colitis Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 161-164. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on dietary recommendations for active and inactive ulcerative colitis (UC) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and UC, together known as inflammatory bowel disease (IBD). This chapter discusses the role of diet and nutritional support in ulcerative colitis (UC) in which the catabolic effect
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(breakdown or loss of body tissue) of inflammation, impaired nutrient absorption, and gastrointestinal (GI) dysfunction can rapidly lead to malnutrition. Inactive UC is a chronic disorder and may be associated with malnutrition, specific elemental deficiencies, and specific food intolerances. Patients may not eat enough to meet their nutritional requirements because of anorexia, drug side effects (eg, nausea, headache, and anorexia), food-induced diarrhea, or pain. In lactose intolerant people, production of hydrogen produces bloating, nausea, and flatulence and unabsorbed short-chain fatty acids produce diarrhea. Lactose intolerance may be primary (racial or congenital) or secondary (eg, due to bacterial overgrowth or intestinal mucosal disease or injury). The incidence of UC is not increased in lactose intolerant people, and the incidence of lactose intolerance is not increased in patients with UC. In UC in remission, lactose restriction is important to control symptoms only in those patients documented to have lactose intolerance, presumably on a genetic basis. Active UC involves pathologic and physiologic changes both within the colonic mucosa and systemically. The colonic mucosa is inflamed and associated with loss of fluid, electrolytes, proteins and immunoglobulins, albumin (protein), and hemoglobin (red blood cells). Systemic manifestations of fever and anorexia are associated with reduced oral intake of nutrients. However, the body is in a catabolic state, with increased nutritional requirements and increased energy needs as a result of fever, associated infections, and steroid therapy. In these situations, nutritional support is essential. In such cases, parental or enteral nutrition not only may be of value but may be essential in patient management. 2 tables. 10 references. •
Gallstone Management in Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 317-320. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on gallstone (cholelithiasis) management in inflammatory bowel disease (IBD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and Ulcerative Colitis (UC), together known as IBD. The association between IBD and hepatobiliary (liver, gallstone, bile ducts) disorders has been well established. Both CD and chronic Ulcerative Colitis (UC) can affect the liver and biliary system. Indeed, hepatobiliary involvement in patients with IBD varies from the asymptomatic state to the development of symptomatic complications related to chronic liver injury. Gallstones represent one of the most frequently encountered clinical hepatobiliary problems in patients with IBD especially those with Crohn's disease. In this chapter, the authors present an overview of the management of gallbladder stones and biliary sludge in patients with IBD. A summary of the epidemiology and pathogenesis of gallstones and biliary sludge in these patients is provided to guide therapeutic decisionmaking, which should aim not only to address symptomatic stones but also to prevent their development. Precipitating factors or conditions including prolonged fasting, total parenteral nutrition (TPN), and use of the drugs ceftriazone or octreotide must be avoided. Patients with symptomatic sludge or complications should have cholecystectomy (removal of the gallbladder). In poor surgical candidates, alternative interventions include oral agents for bile acid dissolution and percutaneous cholecystostomy. 1 figure. 1 table. 8 references.
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Growth and Nutritional Problems in Pediatric Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 245-249. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on growth and development in pediatric inflammatory bowel disease (IBD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflamatory bowel disease (IBD). IBD is recognized increasingly as a common diagnosis in the pediatric age group, accounting for approximately 25 percent of all patients with IBD, with CD outnumbering UC by approximately 4 to 1. A small but notable fraction of IBD cases are being diagnosed during infancy. As in adults, a wide variety of gastrointestinal manifestations and extraintestinal complications are commonly encountered in children and adolescents with CD. In view of the added metabolic requirements for growth, children are more likely to suffer from malnutrition and micronutrient deficiencies than adults. Further-more, growth failure is a complication unique to the pediatric age group, which occurs in up to half of the cases of CD and in about 10 percent of those with UC. Although medications often achieve symptomatic relief, malnutrition and growth failure commonly persist, particularly in pediatric CD. The goal of completely suppressing disease activity and minimizing daily steroid use is detailed in another chapter on therapy of CD in children and adolescents. Growth failure may be the presenting complaint, at times in the absence of gastrointestinal symptoms. The combination of short stature and delayed puberty is often more disturbing to the patient than all other symptoms. Thus, nutritional therapy represents a very important adjunctive to effective medical or surgical management strategies for many children, particularly when their disease is accompanied by growth failure. In this chapter, the extent of nutritional problems in pediatric IBD is reviewed, along with an evidence-based review of the role of nutritional therapy in IBD. 2 figures. 17 references.
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Hematologic Problems in Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 325-327. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on hematologic (blood) problems in inflammatory bowel disease (IBD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and Ulcerative Colitis (UC), together known as IBD. The hematologic abnormalities encountered in the management of inflammatory bowel disease (IBD) are varied and range from overt (obvious) and occult (hidden) gastrointestinal bleeding to an increased risk for thromboembolic (blood clotting) complications. Blood disorders are prevalent: anemia is present in more than 50 percent of patients, and a decreased serum iron level is found in over one-third of patients. Iron loss, defective iron transport, insufficient erythropoietin production, and even inhibition of marrow colony formation all have been described.
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Much of the pathophysiology associated with these abnormalities now is seen as either a direct or derivative consequence of the inflammatory cell responses that characterize the inflammatory bowel disorders. Effective clinical management arises from recognizing these relationships and adapting the overall advances in inflammation and immune modulation to these specific clinical settings. •
Infectious Agents as Aggravating Factors in Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 95-98. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on infectious agents as aggravating factors is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). When patients present with diarrhea, one of the first questions is whether it is an infection or an attack of IBD. Initial symptoms may be very similar, including diarrhea (with or without blood), abdominal pain or cramps, fever, and even arthralgias (pain in the joints). Clinical features that favor infection are acute onset of diarrhea (often greater than 10 bowel movements per day) and fever early in the course. Conversely, IBD usually has a more insidious onset, fewer than 6 bowel movements daily, and early fever is uncommon. Colonoscopic features can suggest infection or UC, but are rarely diagnostic. Mucosal biopsy, however, can be useful in distinguishing acute self-limited colitis or infectious-type colitis from IBD. However, to further complicate matters, infections sometimes can precipitate IBD, and intercurrent (happening at the same time) infections can mimic or induce flares of IBD. This chapter considers infections that mimic IBD, including amebic colitis and chronic infectious colitides (including Entamoeba histolytica and Yersinia); and infections that aggravate IBD, including Campylobacter jejuni, Salmonella, Shigella, Escherichia coli, Clostricium difficile, Cytomegalovirus, Herpes simplex virus, parasites, and mycobacterium. 1 table. 22 references.
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Insurance and Disability Advocacy Issues in Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 555-559. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on insurance and disability advocacy issues is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). The author stresses that physicians can be good advocates for their patients with IBD. The key to being a good advocate is to be knowledgeable about the issues and to be able to offer facts and guidance to patients with their many insurance and disability related issues. The author discusses the vulnerable age peak for obtaining insurance; changing employment; benefits programs including Medicare, Medicaid, high risk insurance pools, and Family and Medical
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Leave; and disability programs, including Social Security disability benefits, the Americans with Disabilities Act (ADA), and education issues for children with IBD. The chapter offers a list of tips for patients. Do not let current health insurance coverage lapse. If the patient does not have health insurance, look into the options available to obtain it. Have regular visits with the doctor, as insurers look favorably on patients who have regular visits, and this will also help the patient to stay well. Take medication as prescribed, because the condition likely will not improve on its own, even if the use of medication temporarily disallows eligibility to an insurance plan. If possible, choose a job with group insurance and portable benefits. For parents of children with IBD, anticipate their need for modified coverage prior to their eighteenth birthday. Determine with the insurance agent or benefits representative what the best options are for the teenager prior to turning 18 so that no lapse in coverage occurs. •
Lymphoma in Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 645-648. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on lymphoma (a tumor of the lymphoid tissue, usually malignant) in inflammatory bowel disease (IBD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as IBD. Lymphoma may either mimic or complicate ulcerative colitis UC and CD, and the understanding of this relationship is of importance to physicians. There is significant overlap between the symptoms, signs, and the radiologic and endoscopic appearance of intestinal lymphoma and IBD. Small intestinal lymphoma may mimic CD and colonic lymphoma may mimic both colitis and colonicadnocarcinoma (cancer). The authors conclude that intestinal lymphomas are uncommon but both intestinal and extraintestinal lymphomas appear to be of increased incidence in chronic inflammatory bowel disease states, including IBD. The relationship between immune modifying therapy used in IBD and the development of lymphoma remains controversial. The differential diagnosis between IBD and lymphoma, either complicating IBD or occurring independently, is difficult. Most intestinal lymphomas diagnosed in the setting of IBD have been unanticipated and were found incidentally at the time of surgery performed for IBD indications or only subsequently in the histopathology of the resected specimen. Intestinal lymphoma also may complicate IBD; therefore, awareness of its association, clues to its presence, and knowledge of appropriate diagnostic investigations (and their shortcomings) are critical to patient management. 10 references.
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Managing Inflammatory Bowel Disease in the Managed Care Era Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 13-18. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220.
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Summary: This chapter on managed care issues is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). The clinician is besieged daily by restraints set by managed care organizations (MCO) regarding utilizing diagnostic and therapeutic modalities for the IBD patient. These restraints often require lengthy and often unproductive precertification phone calls, written waivers, or outright rejection of what the physician perceives to be the correct care. The authors review the present vexing problems facing the clinician in this new 'paradigm' of care, that is, the MCO, and attempt to offer some insight into recent legal and legislative inroads with MCO policy. The authors provide the clinician with a user-friendly and hands-on, practical approach to dealing with the problems and obstacles of operating in such a paradigm. Specific strategies are offered in the areas of medical necessity decisions, inappropriate use of clinical guidelines, unionization, what to do when payment is denied, 'late' payment, and for recovery of payments due. The authors conclude that physicians will never be chastised for interceding on behalf of the patient and will win more times than expected. In addition, an organized and sustain response will often achieve success. The chapter concludes with two sample letters to send to MCOs and a summary of the process of dealing with MCO Denial of Services or Care. 8 references. •
Ocular Manifestations of Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 275-277. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on ocular (eye) manifestations of inflammatory bowel disease (IBD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as IBD. Historically, IBD related ocular inflammation could result in blindness, although blindness is less likely today due to better treatments. Ocular inflammation in patients with IBD has a reported range of frequency from as low as 1.9 percent to as high as 13 percent of patients. Ulcerative colitis appears to be less likely to have associated ocular inflammation than does Crohn's disease. Although a large number of inflammatory conditions have been reported with IBD, including uveitis, episcleritis, scleritis, keratitis, conjunctivitis, retinitis, retinal vasculitis, choroiditis, optic neuritis, orbital myositis, and orbital pseudotumor, lesions that appear to be more clearly associated with IBD include anterior uveitis, scleritis, keratitis, and retinal vasculitis and/or posterior uveitis. Of these, anterior uveitis is the most common and the primary focus of this chapter. Most patients with the serious ocular manifestations of IBD will be symptomatic, although the symptoms may need to be elicited. Any ocular symptoms should be evaluated by an ophthalmologist, as there are no symptoms that are specific for IBD related eye disease, and the symptoms of several problems are similar. Acute problems often are manifested by pain, redness, photophobia (sensitivity to light), and sometimes blurred vision, whereas chronic problems may present with blurred vision. Typical treatment involves topical prednisolone acetate 1 percent every hour while awake, and once inflammation is controlled, the frequency of administration is slowly tapered off. 8 references.
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Options in Managing Enteral Fistulae in Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 401-404. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on options in managing enteral fistula is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). Fistulae usually result from penetration of the inflammatory process from a segment of CD into adjacent tissue. Excluding postoperative complications, the most common cause of enteral fistulae in the Western world is CD. Intestinal fistulae are classified as internal, external, or mixed. Internal fistulae (in which an abnormal passageway develops between two segments of the intestinal tract) are relatively uncommon compared with external fistulae, in which a direct communication exists between the intestine and the skin of the abdominal wall or the vagina. Barium contrast radiography is the main diagnostic tool for fistula detection. Fistulae rarely close spontaneously and do not respond to sulfasalazine or steroids. Surgery often is required. Control of the associated inflammatory component by medical therapy (drugs) and bowel rest may allow for a smaller resection and fewer postoperative complications. It also is important to control any underlying infection and to optimize nutrition prior to surgery. However, the role of total parenteral (outside the gastrointestinal system) nutrition (TPN) is controversial. Medical management of fistulae in CD includes the use of antibiotics; immunomodulating agents including azathioprine, 6 mercaptopurine (6 MP), and cyclosporine; and anti tumor necrosis factor (TNF) alpha antibody (Remicade). The authors describe the use of each of these drugs and conclude with a brief discussion of rectovaginal fistulae, gastrocolic and duodenocolic fistulae, and enterovesicular fistulae; for each of the latter, the reader is referred to a separate chapter in the text. 1 table. 12 references.
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Pancreatitis in Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 329-332. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on pancreatitis is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and Ulcerative Colitis (UC), together known as inflammatory bowel disease (IBD). There is a higher incidence and prevalence of pancreatitis in patients with inflammatory bowel disease (IBD) than in the general population. The pancreatitis can be acute or chronic, or subclinical or overt, and has many causes. The most common cause is medications used to treat IBD, especially azathioprine and 6 mercaptopurine. Other causes of pancreatitis include duodenal involvement from Crohn's disease (CD), gallstones (cholelithiasis), and primary sclerosing cholangitis (PSC). Pancreatitis also can be caused by high serum concentrations of triglycerides during total parenteral nutritional (TPN) therapy for CD, and may also be a primary extra-intestinal
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manifestation of IBD. Treatment is different for each cause. For drug-induced pancreatitis, discontinuation of the drug should improvethe pancreatitis. For TPNinduced pancreatitis, oral medium-chain triglycerides should be substituted for the lipid emulsion. For pancreatitis that has developed from gallstones, the usual treatment is laparoscopic cholecystectomy (removal of the gallbladder). Idiopathic (of unknown cause) pancreatitis is often successfully treated by treating the underlying IBD. 1 table. 10 references. •
Pregnancy and Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 613-618. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on pregnancy in inflammatory bowel disease (IBD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as IBD. This chapter focuses on drug therapy and side effects issues in these challenging patients from the point of view of the gastroenterologist; an additional chapter addresses pregnancy in IBD from the perspective of an obstetrician. The author discusses inheritance, fertility, the influence of UC and CD on pregnancy, the activity of disease and the influence on pregnancy, and the assessment of disease activity in pregnant patients. The author then summarizes the use of medications in pregnancy, including nonspecific symptomatic agents, sulfasalazine, mesalamine, antibiotics, steroids, immunomodulatory drugs, methotrexate and cyclosporine, and infliximab. The author stresses the importance of physicians communicating clearly to their female patients desiring to get pregnant that their disease should be in remission before attempting to conceive and that medications that are keeping them in remission should not be discontinued either prior to conception or during the first trimester. 12 references.
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Pseudo-Intractability of Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 77-80. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on pseudointractability of inflammatory bowel disease (IBD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as IBD. Inability to produce or sustain a clinical remission or to prevent frequent relapses should not lead physicians to make too early a presumption that the disease is truly intractable (resistant to treatment). Once the intractability label has been assigned, it connotes a more serious form of IBD, one that will require more time, more attention, more patient-family-physician distress, the likely inclusion of 'big gun' pharmacotherapy (drugs), and even the consideration of surgical intervention. Before embarking on a course of management, whether medical or surgical, for assumed intractability, it is reasonable to consider the alternative: that factors other than the IBD
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itself may account for recurrent, poorly or incompletely responsive, or even intractable symptomatology. It is easy to diagnose active inflammation but not always as easy to attribute the convincing and supportive objective features to a wide range of associated subjective complaints and objective findings. Because of this, pseudo-intractability or pseudo-relapse must always be considered a possible explanation for disagreement between subjective and objective symptoms. Factors possibly responsible for aggravating or mimicking disease activity should be sought, modified, or eliminated whenever possible. The author concludes that initiating, prolonging, or modifying therapies that have the potential for both short-term and long-term complications is serious business and any decision to do so should be considered carefully when managing what is thought to represent intractability or the inability to maintain disease remission. 1 table. 11 references. •
Psychiatric Complications of Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 573-576. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on psychiatric complications is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and UC, together known as inflammatory bowel disease (IBD). About one-half of patients with active Crohn's disease have a diagnosable psychiatric disorder, a proportion that is significantly increased compared with that among patients suffering from other chronic medical illnesses. About one-quarter of patients suffering from ulcerative colitis likewise have a diagnosable psychiatric disorder. However, this proportion is not significantly greater than the proportion of patients with psychiatric disorder with other chronic medical illnesses. The common psychiatric disorders found in association with IBD include delirium, depression, anxiety, and personality disorders. The author discusses each of these disorders, emphasizing current concepts in management. The role of the psychiatrist in IBD is to assist the gastroenterologist in the recognition, diagnosis, and treatment of these conditions. 6 references.
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Remission Maintenance in Ulcerative Colitis Source: in Williams, C.N., et al., eds. Trends in Inflammatory Bowel Disease Therapy 1999. Boston, MA: Kluwer Academic Publishers. 2000. p. 117-127. Contact: Available from Kluwer Academic Publishers. Customer Service Deparment, P.O. Box 358, Accord Station, Hingham, MA 02018-0358. (781) 871-6600. Fax (781) 6819045. E-mail:
[email protected]. Website: www.wkap.nl. PRICE: 145.00 plus shipping and handling. ISBN: 0792387627. Summary: This chapter on remission maintenance in ulcerative colitis (UC) is from a monograph that reprints the presentations given at the Trends in Inflammatory Bowel Disease Therapy Symposium, held in Vancouver, British Columbia, Canada, in August 1999. The general objective of the conference was to provide an update in the etiology, pathogenesis, and treatment of inflammatory bowel disease (IBD), including UC and Crohn's disease (CD). In this chapter, the author reports on a large patient cohort from Copenhagen. From this group, it is known that about 50 percent of all patients with UC
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who are in a continuous supervision program are in remission each year. However, cumulatively, 90 percent of patients have repetitive relapses over time. In this group, 25 percent of patients had undergone colectomy (removal of a portion of the colon) after 10 years; however, more than 90 percent were able to continue to work during this time. These disease characteristics indicate that continuous supervision and remission maintenance contributes to such a generally positive outcome of this disease, with a goal of decreasing the number of relapses and normalization of cancer risk. The newer 5 aminosalicylic acid (5 ASA) releasing drugs have been tested for remission maintenance; they seem to be more or less equally effective (compared to sulphasalazine). For patients who have frequent relapses in spite of drug treatment, or those who can only be brought into remission using azathioprine, this drug has also been used for remission maintenance with a relatively good success rate. The author concludes that currently every patient with a definitive diagnosis of UC in remission should be treated with either sulphasalazine or the newer 5 ASA releasing drugs. The exact duration of such treatment is not yet known; indefinite treatment is normally recommended. Since this will normally not be accepted by the patient, a withdrawal attempt can be made after 3 to 4 years of continuous maintenance treatment. In all patients who are difficut to treat and are having relapses in spite of 5 ASA, azathioprine should be considered. However, it should be kept in mind that surgery can cure the disease, although at a price. 4 figures. 12 tables. 44 references. •
Coexistence of Inflammatory Bowel Disease and Irritable Bowel Syndrome Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 87-90. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on the coexistence of irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as IBD. Irritable bowel syndrome (IBS) is a chronic abdominal symptom complex for which no structural underlying abnormality can be demonstrated. It is a common disorder that affects all age groups with an increased frequency in females. Few if any of the clinical features of IBS can confidently distinguish it from IBD. The multiplicity and chronicity of symptoms and their relationship to altered bowel habit can be helpful hints. A psychoneurotic disposition, evidence of anxiety or depression, and a tendency to somatize symptoms referable not only to the gut but other organ systems are pointers in favor of IBS. However, when IBS occurs in a patient with established IBD, this can be a difficult diagnosis. Since IBS is a very common disorder, it is not unexpected to find patients with both IBS and IBD. The author considers whether there is a special relationship between these two disorders. There is good scientific evidence that inflammation of the gut alters its physiologic performance, and this may persist after resolution of the inflammation. The author concludes that IBS occurs with greater frequency in certain patients in remission from IBD, and this is more easily seen in UC than in CD. Symptoms of IBS in the context of IBD are no different from those typical for that condition. An awareness of this relationship is of key importance in making a confident diagnosis, as is a good knowledge of the patients' history and the characteristic behavior of their IBD. In some complicated IBD patients, extensive
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investigation by colonoscopy with or without small bowel radiography may be required. For most patients, treatment of IBS should follow the usual guidelines with notable exceptions in the case of patients with histories of obstruction. 1 figure. 17 references. •
Consultations and the Patient with Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 23-24. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on the consultative process is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). Effective medical care of the patient with IBD not only requires concern for the patient's medical and psychosocial problems but also necessitates an understanding of the gastroenterologist-referring physician interface. The chronic nature of these disorders should prompt managed care organizations (MCOs) to recognize the importance of promoting a coordinated approach. Most primary care physicians are uncomfortable with assuming significant responsibility for the overall supervision of IBD patients, yet they usually do not wish to be excluded from the decision-making process. The chapter offers some personal views of the IBD consultative process, observations of the generalist-gastroenterologist interface as it relates to IBD, and several clinical suggestions regarding IBD patient management. Topics include parents and the IBD consultation, information seeking, hereditary concerns, communications with the referring physician, multiple visits, and surgical referral. The author concludes that the IBD consultation requires evaluation of the impact of IBD on the patient's ability to function as well as other clinical factors. The referring physician may either wish to delegate ongoing IBD care to the consultant or may intermittently refer the patient for reevaluation. In either case, close attention to letters after each visit and efforts to keep the referring physician involved in the management process are essential. 5 references.
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Diagnosis of Inflammatory Bowel Disease: An Update Source: in Williams, C.N., et al., eds. Trends in Inflammatory Bowel Disease Therapy 1999. Boston, MA: Kluwer Academic Publishers. 2000. p. 73-86. Contact: Available from Kluwer Academic Publishers. Customer Service Deparment, P.O. Box 358, Accord Station, Hingham, MA 02018-0358. (781) 871-6600. Fax (781) 6819045. E-mail:
[email protected]. Website: www.wkap.nl. PRICE: 145.00 plus shipping and handling. ISBN: 0792387627. Summary: This chapter on the diagnosis of inflammatory bowel disease (IBD) is from a monograph that reprints the presentations given at the Trends in Inflammatory Bowel Disease Therapy Symposium, held in Vancouver, British Columbia, Canada, in August 1999. The general objective of the conference was to provide an update in the etiology, pathogenesis, and treatment of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD). In this chapter, the author notes that although the causes of IBD are still unknown, evidence is accumulating for the idea that both UC and CD are syndromes with multiple causes. Diagnosis of IBD has relied largely on patient
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history and physical examination, radiographic and endoscopic findings, and standard laboratory parameters. In general, UC is characterized by diffuse and relatively superficial mucosal inflammation with bloody diarrhea as it predominant symptom. CD involves focal and transmural inflammatory changes, often causing systemic manifestations in addition to pain, tenderness, and diarrhea. Antibody to Saccharomyces cerevisiae (ASCA) has been demonstrated in up to 79 percent of CD patients. Antineutrophil cytoplasmic antibodies (ANCA), autoantibodies directed against intracellular components of neutrophils, are present in the blood of 60 to 80 percent of patients with UC. ANCA antibodies have also been detected in a clinically distinct subpopulation of patients with CD. Analysis of these markers provides evidence of clinical, genetic and immunological heterogeneity, and implies distinct types of mucosal inflammation. As more is understood about the development of IBD, it seems likely that therapy can be refined to interfere at specific points in the disease process, depending on the specific dysregulation identified. Diagnosis and therapy can thus merge. The author notes that there is still some reluctance to use these diagnostic tests, even though there is mounting evidence for their utility. The author calls for additional research usingthese serum immune markers in large groups of new patients with UC and CD. 62 references. •
Sequential and Combination Therapy of Ulcerative Colitis Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 115-118. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on the drug therapy of ulcerative colitis is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). UC is a chronic inflammatory disease of unknown cause and incurable with current medications. For palliation, the clinician must choose from an array of oral, per-rectal, and intravenous treatments with many dosing options. The medications, doses, and routes of delivery for treatment of active disease may be different from those used for maintenance of remission. Initial treatment of every patient with one drug at a single dose and delivery route (sequential therapy) is the traditional and least complicated way for clinicians and patients to judge the effectiveness and tolerability of a treatment. The compliance with using a single drug is likely to be better than with multiple drugs or delivery routes and the cost probably will be less. If the initial treatment is not effective or tolerable, then the dose can be adjusted, with or without starting other drugs. The main drawback to sequential therapy is that the trial and error method of adding medications may prolong the time to response, compared to starting multiple drugs together, so this approach is most attractive for mildly active disease when controlling symptoms quickly is less critical. Starting multiple treatments at once, either with the same drug or by different delivery routes, or using two or more drugs (combination therapy) may give a combined effect with more prompt onset of action and better efficacy than starting with a single drug and adding others later. The approach is most commonly used for moderate or severe disease when there is urgency to get the symptoms controlled promptly. Drawbacks to combination therapy are the lack of data from controlled trials to confirm the benefits, difficulty
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identifying the offending drug if an adverse effect occurs with multiple drug therapy, lower patient compliance, and probably higher cost. 2 tables. 7 references. •
Inflammatory Bowel Disease: Autoimmunity or Chronic Inflammation? Source: in Williams, C.N., et al., eds. Trends in Inflammatory Bowel Disease Therapy 1999. Boston, MA: Kluwer Academic Publishers. 2000. p. 46-53. Contact: Available from Kluwer Academic Publishers. Customer Service Deparment, P.O. Box 358, Accord Station, Hingham, MA 02018-0358. (781) 871-6600. Fax (781) 6819045. E-mail:
[email protected]. Website: www.wkap.nl. PRICE: 145.00 plus shipping and handling. ISBN: 0792387627. Summary: This chapter on the etiology of inflammatory bowel disease (IBD) is from a monograph that reprints the presentations given at the Trends in Inflammatory Bowel Disease Therapy Symposium, held in Vancouver, British Columbia, Canada, in August 1999. The general objective of the conference was to provide an update in the etiology, pathogenesis, and treatment of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD). In this chapter, the author considers the question of whether IBD is an autoimmune disease or simply a condition of chronic inflammation. Many chronic inflammatory diseases have been called autoimmune by virtue of the presence of autoantibodies in the blood. In UC there are well described autoantibodies (pANCA, anti tropomyosin) but there is little evidence that they contribute to the inflammatory process. In CD, there are fewer examples of autoreactivity, especially related to the intestine. There is no evidence of enhanced autoreactive cytotoxic T cell activity (for example, against epithelium). The author considers the alternative hypothesis that both UC and CD may be exaggerated immune responses against non specific antigens (e.g., luminal contents), noting that there is growing evidence for such a concept. The author reviews the animal models supporting this hypothesis. The author concludes that a role for autoimmunity in IBD is less and less apparent. 59 references.
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Management of Ulcerative Colitis in Children Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 153-155. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on the management of ulcerative colitis (UC) in children is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and UC, together known as inflammatory bowel disease (IBD). Inflammatory bowel diseases (IBDs) in children are chronic illnesses with symptoms that wax and wane. Although some children may experience a prolonged remission, many have recurrent exacerbations that require ongoing medical evaluation and therapy. In a recent study, children with UC were diagnosed more rapidly than children with CD; however, in both diseases, a significant time elapsed prior to the start of effective therapy. This delay of over 6 months from the time of onset of symptoms to initiation of treatment indicates that more awareness of these diseases is needed among primary care providers. Quality of life is reduced in children with IBD; pediatric gastroenterologists should be aware of the typical psychological patterns in these patients and integrate psychosocial support into the
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treatment plan. Deciding which medication to use to induce remission in a child with new-onset UC depends on the severity of the disease. Children who have mild disease characterized by bloody diarrhea or abdominal cramps, without fever, anemia, or hypoalbuminemia, usually respond to sulfasalazine, mesalamine, or olsalazine. About 70 percent of children with moderate to severe disease require corticosteroids in the first year of treatment. Characteristics of moderate to severe disease include more than six bloody stools daily, abdominal cramps, awakening at night to defecate, fever, anemia, or hypoalbuminemia (low levels of protein in the blood). The decision to perform a colectomy (removal of part of the colon) in a child with UC should be made by the patient, family, and health care providers all working together to reach consensus. As surgical techniques improve and more is learned about the adaptation of pouches in growing children, patients and providers will be better prepared with information upon which to base a decision. The risks of using potent immunosuppressive agents must be balanced against the potential complications of surgery and the possibility for cure. 1 table. 8 references. •
Therapeutic Expectations: Medical Management of Ulcerative Colitis Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 111-113. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on the medical management of ulcerative colitis is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). The author stresses that therapeutic expectations for UC must take into consideration the chronic, medically incurable nature of inflammatory bowel disease (IBD), the varied mucosal extent, potential severity, and disease or therapy related complications. It is most useful to consider the therapeutic expectations with regard to inducing remission, maintaining remission, treating symptoms, and treating or preventing complications. Ulcerative colitis can be complicated by intestinal or extra-intestinal complications. Intestinal complications, such as bleeding and associated anemia, hypoproteinemia, or electrolyte abnormalities require prompt control with inductive therapies. Thereafter, supplementation with iron and folic acid (with sulfasalazine) should treat and prevent further development of anemia during maintenance therapy. Other intestinal complications, such as toxic megacolon or perforation, can be prevented with aggressive inductive therapies, according to the severity of presentation. Patients should be warned against the use of NSAIDs and to alert their physician when primary care physicians or other specialists prescribe antibiotics or other medications, to be certain they do not induce diarrhea (Clostridium difficile) and are compatible with UC therapy. Controlling colonic inflammation usually prevents extraintestinal complications, such as peripheral arthritis and cutaneous manifestations. In addition, with the advent of pelvic pouch procedures, an additional goal of medical therapy is to treat, and eventually prevent, pouchitis. This chapter serves as an introduction to a section of 12 chapters on UC. 6 references.
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Azthioprine Metabolism in Inflammatory Bowel Disease: Correlation with Efficacy and Toxicity Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 377-381. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on the metabolism of azathioprine in patients with Crohn's disease (CD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with CD and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). In active CD, when combined with corticosteroids, azathioprine (AZA) induces remission faster, more frequently, and with a lower cumulative steroid dose than prednisone alone. Furthermore, AZA and 6MP (6 mercaptopurine, a subcompound of AZA) have been shown to eliminate the need for corticosteroids in about 75 percent of patients, with a median response time of 12 to 16 weeks, and these drugs have proven efficacy in maintaining long-term remission. Several well-controlled clinical trials in patients with CD has affirmed that the clinical response to azathioprine therapy largely is dependent on the duration of therapy. Indeed, patients who were weaned from prednisone before azathioprine could achieve its effect did not have a favorable clinical response to therapy. In most patients, treatment required at least 4 months of combination therapy. However, 30 percent of patients do not respond favorably to the usually administered doses (1 to 2 milligrams per kilogram). Most physicians measure drug efficacy either by an improvement in clinical symptoms and quality of life or by the ability to maintain remission while weaning off corticosteroid therapy. Practitioners tend to rely on their clinical judgment and experience in determining the dose of azathioprine to be used in treating patients with inflammatory bowel disease (IBD). Some start with 50 or 75 milligrams per day regardless of weight and then increase by 25 milligram increments. The wide dose range of azathioprine currently used in clinical practice would suggest that a safe and established therapeutic dose has not yet been established. As a consequence, clinicians must always remain aware of potential adverse effects, including allergic reactions, hepatitis (inflamed liver), pancreatitis, bone marrow suppression, and lymphoma (tumors of the lymphoid tissue), while attempting to achieve a therapeutic response. 1 figure. 18 references.
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Therapeutic Expectations: Surgical Management of Ulcerative Colitis Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 171-173. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on the surgical management of ulcerative colitis (UC) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and UC, together known as inflammatory bowel disease (IBD). This chapter focuses on what patients can expect after surgery for medically refractory (not responsive to drug therapy) UC. Almost all patients will be better off after operation than before operation. The operation is safe.
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Their colitis will be 'cured,' their colitis medications will be discontinued, and their intestinal symptoms will subside. Their physiologic and social functions will generally be preserved or improved, and a feeling of good health and a satisfactory quality of life will return. However, the outcome may not be perfect, and long-term complications can occur. Physicians do their best to achieve an excellent outcome and avoid complications, while providing compassionate, cost-effective, surgical care. Currently, most patients who undergo elective surgery for ulcerative colitis have a proctocolectomy and an ileal pouch-anal canal anastomosis (IPAA). In IPAA, the entire disease colon and rectum are removed, but the anal sphincters are preserved. A new rectum is formed from the terminal ileum (ileal pouch); attaching the pouch to the anal canal restores defecation to the standard transanal route with satisfactory fecal continence. However, proctocolectomy and Brooke ileostomy, proctocolectomy and continent ileostomy (Kock pouch), and colectomy and ileorectostomy still are used, and are also explained to the patient. Indeed, these operations still are the operations of choice for selected patients. 6 references. •
Surgical Treatment of Inflammatory Bowel Disease Source: in Textbook of Gastroenterology. 4th ed. [2-volume set]. Hagerstown, MD: Lippincott Williams and Wilkins. 2003. p. 1760-1790. Contact: Available from Lippincott Williams and Wilkins. P.O. Box 1600, Hagerstown, MD 21741. (800) 638-6423. Fax: (301) 223-2400. Website: www.lww.com. PRICE: $289.00. ISBN: 781728614. Summary: This chapter on the surgical treatment of inflammatory bowel disease (IBD) is from a comprehensive gastroenterology textbook that provides an encyclopedic discussion of virtually all the disease states encountered in a gastroenterology practice. This chapter covers Crohn's disease, ulcerative colitis, and indeterminate colitis. The authors note that although as many of half of the patients who have IBD require at least one surgical procedure during their lifetime, the decision to operate is rarely an easy one. Factors to take into consideration are the age and the general condition of the patient; the extent of the disease; the duration of the disease and the treatment offered to that point; and the specific complication in regard to the available treatment options. The authors consider surgical options and their anticipated results in view of the different indications for surgical treatment of IBD. The authors emphasize new options offered by advances in laparoscopic surgery. The chapter is illustrated with black-andwhite reproductions of imaging studies and drawings. 22 figures. 2 tables. 250 references.
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Computer Database for Patients with Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 29-33. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on the use of a computer database is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). While physicians are seeing more and more patients with IBD, it remains a relatively rare entity, characterized by varied symptoms and
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possibly etiologies (causes). Progress in understanding and treating this heterogeneity will require the creation of large national and international cross-sectional IBD data resources. The goal of such a database would be to characterize a large number of currently followed IBD patients according to validated clinical classification systems. Use of a database system is now indispensable both at the individual (gastroenterologist) and collective (referral centers, national and international organizations) levels. The computer will allow the gastroenterologist to easily retrieve the history of each patient and to monitor other course in the context of other patients. The chapter describes a computer software program that was created on the Microsoft Access(r) DataBase Manager, with the oriented object language V.B.A. (Visual Basic for Application) concept, allowing a great level of interactivity. The two main bodies of the software are data management and data processing. Data management comprises four main parts: Patient identification record, which deals with administrative data; one or more patient evolution records, which describe the patient's history, clinical characteristics, and treatment; synthesis, which are summary files containing selected medical data; and tools to facilitate a patient's record search. The author notes that the data processing portion of the software is not in its final version. Numerous illustrations depict the screens of the software program. The author concludes by briefly describing the possibilities of putting the IBD database on the Internet. 6 figures. 8 references. •
Use of Antibiotics and Other Anti-infectious Agents in Ulcerative Colitis Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 149-151. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on the use of antibiotics and other anti infectious agents in ulcerative colitis (UC) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and UC, together known as inflammatory bowel disease (IBD). Abundant evidence suggests that an imbalance between luminal (in the intestines) bacteria and the host inflammatory and immune response plays a central role in the pathogenesis (development) of inflammatory bowel disease (IBD). Development of UC has been observed after enteric (through the gastrointestinal tract) infection with Salmonella, Shigella, and Yersinia species. While these specific pathogens are not considered etiologic (causative) agents of UC, a transient infection may initiate a cascade of inflammatory events that, in predisposed individuals, can lead to UC. Similarly, although many enteric pathogens have been associated with relapse of UC, there is no evidence that persistence of these infections is a cause of the disease. In recent UC clinical trials, administration of live non-pathogenic Escherichia coli or a mixture of bifidobacteria, lactobacilli, and streptococci was equivalent to mesalamine in maintenance of remission. Taken together, these data suggest that the beneficial effect of antibiotics may not result from a long-term reduction in total bacterial load but rather from a qualitative alteration of the resident bacterial population. The recent human data further suggest a role for probiotics in the maintenance therapy for UC patients. This topic is also discussed in the chapter on the role of bacteria in CD and the chapter on pouchitis. The authors note that the lack of antibiotic benefits in randomized trials should not completely preclude their use in the management of selected UC patients. In clinical practice, these drugs may benefit patients with an acute flare of the disease, toxic
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patients with or without megacolon, and subsets of patients with refractory disease. 11 references. •
Appropriate Use of Corticosteroids in Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 363-366. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on the use of corticosteroids in managing inflammatory bowel disease (IBD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as IBD. Glucocorticoids are a mainstay for the treatment of severe IBD. The efficacy of corticosteroids to induce remission in both CD and Ulcerative Colitis (UC) has been well established in large randomized controlled trials. At times, a focus on adverse events has diminished the recognition of the usefulness of corticosteroids. The authors suggest approaches for the appropriate use of corticosteroids, including corticosteroid-sparing strategies, in patients with IBD. Corticosteroids used in the treatment of IBD are prednisone, prednisolone, methylprednisolone, and budesonide. Prednisone and prednisolone have comparable glucocorticoid potency, whereas methylprednisolone is slightly more potent. In IBD, their use should be restricted to severe, active disease, with the aim of inducing remission. Simple dosing considerations can decrease the possibility of serious side effects. For example, steroids should be given as a single morning dose to coincide with the natural circadian rhythm of endogenous (naturally occurring in the body) corticosteroids. Corticosteroid sparing strategies incorporate the use of nutrition, budesonide, aminosalicylates, antibiotics, azathioprine and 6 mercaptopurine (immunomodulators), methotrexate, cyclosporine, and anti-tumor necrosis factor alpha. 13 references.
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Immunomodulators in Ulcerative Colitis Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 139-142. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on the use of immunomodulators for treating ulcerative colitis is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). The immunomodulators, 6mercaptopurine (6-MP), azathioprine (AZA), and cyclosporin A (CSA), are of value in the management of UC patients who are dependent on, or refractory to, oral steroids. CSA is effective as a short-term intravenous (IV) and oral agent for achieving remission in patients with severe colitis refractory to IV steroids. 6-Mercaptopurine and AZA, but not CSA, also are effective as maintenance agents for patients who have required steroids, 6-MP/AZA, or CSA to achieve remission. The author reviews the indications (patient selection), how to initiate therapy, daily monitoring (including monitoring for
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toxicity), and assessment of the patient for each of these immunomodulating drugs. 9 references. •
Systemic Corticosteroids in Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 127-131. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on the use of systemic corticosteroids in the treatment of ulcerative colitis is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). Any therapy in UC must be considered with respect to its use in acute relapse, maintenance, and with chronic continuous (chronic active colitis) or frequently relapsing colitis. Corticosteroid therapy in UC may be initiated topically or systemically, and systemic treatment may be given orally or parenterally (outside the gastrointestinal tract, e.g., intravenous or intramuscular). Systemic administration may be combined with local therapy; systemic corticosteroids may be combined with 5-ASA preparations, again either topically, orally, or both, and occasionally with immunosuppression. Different systemic corticosteroid preparations are available, with similar anti-inflammatory effects, but with some differences in potency and tendency to cause side effects. Despite the relative homogeneity of patients in UC as a clinical group (at least in comparison with Crohn's disease), there are different scenarios of disease onset, activity, severity, and distribution. With this substantial number of variables, despite a number of clinical trials performed since those that initially established the value of corticosteroids, there remain extensive areas in which there is no firm evidence to guide management. This chapter briefly surveys those corticosteroids available for systemic use before considering practicalities of use in patients with various categories of UC. 10 references.
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Methotrexate in Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 383-386. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on the use of the antiinflammatory drug methotrexate in treating inflammatory bowel disease (IBD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as IBD. The majority of patients who are treated with a course of conventional glucocorticoid therapy become either steroid dependent (36 percent) or steroid resistant (20 percent). Patients who require chronic steroid therapy are appropriate candidates for immunosuppressive drug therapy. The purine antimetabolites, 6-mercaptopurine (6-MP) and azathioprine, are effective in the majority of, but not all, patients both for induction of remission and for maintenance therapy in CD. Approximately 30 percent of patients are unresponsive to low-to-moderate doses of azathioprine. Although these agents are relatively well
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tolerated as chronic therapy, serious toxicity can occur; therefore, alternative medical treatments are desirable. Kozarek and colleagues (1989) pioneered the use of methotrexate for the treatment of IBD. In their studies, two-thirds of patients had improvement in symptoms and a steroid-sparing effect also was documented. Colonoscopic improvement was demonstrated in one-third of the patients with CD but not in the patients with Ulcerative Colitis (UC). Additional studies over the decade since Kozarek's work support the effectiveness of methotrexate both in active disease and for maintenance therapy in previously steroid dependent patients. Methotrexate given intramuscularly at a relatively high dose (25 milligrams per week) in conjunction with prednisone was an effective remission induction therapy. Fifteen milligrams of methotrexate intramuscularly was effective for maintenance therapy. Currently, no reliable data from controlled trials exist to support the use of methotrexate as a therapy for UC. The authors conclude with a brief discussion of the use of methotrexate in combination with other drugs, notably infliximab (a drug used to treat rheumatoid arthritis). 30 references. •
Ulcerative Colitis: A Diverse Disease with Diverse Questions and Diverse Solutions Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 119-121. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on ulcerative colitis is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). The author notes that clinicians think of UC as one disease, but it is, in fact, a blend of several conditions whose final common denominator is diffuse inflammation of the colon associated with distortion of crypts on microscopic examination. Clinicians move from one therapy for colitis to another as if UC is a spectrum. First, 5 ASA is tried for one type of UC; if this therapy fails, corticosteroids, either local or systemic, follow for what unspokenly is another type of UC. 6-Mercaptopurine or azathioprine enters therapy for a third type of UC and, finally, surgery cures all. The author discusses the different types of therapy and also considers the cancer risk in patients with UC; surveillance of inflamed colons by means of periodic colonoscopy is the standard of care to address the latter. The author concludes that UC presents, responds to therapy, and has a natural history that suggests that it is a spectrum. The host, the luminal environment, the mucosal border, and the immune system of the lamina propria and vascular walls participate in molding this spectrum. Clinical trials that approach UC with these distinct participants in mind may yield more success than outcomes obtained in the past two decades. 10 references.
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Coexistent Irritable Bowel Syndrome and Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 91-94. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220.
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Summary: This second chapter on the coexistence of irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as IBD. Irritable bowel syndrome (IBS) is a chronic abdominal symptom complex for which no structural underlying abnormality can be demonstrated. It is a common disorder that affects all age groups with an increased frequency in females. Few if any of the clinical features of IBS can confidently distinguish it from IBD. This chapter focuses on the prevalence of IBS, clinically relevant pathophysiology, and the importance of the patient-physician relationship. The author notes that there are several pathophysiologic alterations found in the small bowel and colon of patients with IBS that could be aggravated or brought to the level of clinical awareness by IBD or its treatment. These alterations include pain or diarrhea after ileo-right colon resection (removal); active proctosigmoiditis; ileal pouch procedures; and an exaggeration of the patient's response to secretagogues, including caffeine and problems with lactose intolerance. The author emphasizes the benefits of explaining to the patient with both IBS and IBD the fact that she or he has two different disorders and that each may cause its own symptoms. Explaining the pathophysiology seems to help the patient adjust medications and understand and accept symptoms caused by meals or by stress. 6 references. •
Inflammatory Bowel Disease Genetics Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 523-526. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: While both genetic and environmental factors have been implicated in the development of inflammatory bowel disease (IBD), within the environment of Western industrial countries, the greatest risk for developing IBD is genetic. This chapter on genetics is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known IBD. Overall, 15 to 20 percent of patients have a family history of IBD. That familial aggregation is primarily genetic rather than from a shared environmental etiology, such as an infectious agent, is suggested by a lack of increased risk to spouses, and the observed aggregation of IBD occurring among relative raised separately. The authors discuss how risk is defined in the offspring of patients with IBD, genetic implications for management, and potential gene markers. The authors note that there are also important nongenetic associations with disease type: younger age of onset is associated with stricturing (narrowing) disease and small bowel disease, and it is inversely associated with inflammatory disease. Jewish ethnicity, smoking, and use of nonsteroidal antiinflammatory drugs (NSAIDs) are important risk factors for fistulizing disease, again including perforating disease. 2 tables. 8 references.
Directories In addition to the references and resources discussed earlier in this chapter, a number of directories relating to ulcerative colitis have been published that consolidate information
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across various sources. The Combined Health Information Database lists the following, which you may wish to consult in your local medical library:12 •
Complete Directory for People with Chronic Illness. 4rd ed Source: Lakeville, CT: Grey House Publishing, Inc. 2000. 1047 p. Contact: Available from Grey House Publishing, Inc. Pocket Knife Square, Lakeville, CT 06039. (860) 435-0868. Fax (860) 435-0867. PRICE: $165.00. ISBN: 0939300931. Summary: This directory provides a comprehensive overview of the support services and information resources available for people with any of 80 specific chronic illnesses. It presents information on various organizations, educational materials, publications, and databases. A chapter is devoted to each chronic illness and includes a brief description of it. The digestive diseases covered include celiac disease, Crohn's disease, gastrointestinal disorders, hepatitis, liver disease, substance abuse, and ulcerative colitis. The description of each disease is followed by subchapters that identify national and State associations and agencies, libraries, research centers, reference books, children's books, magazines, newsletters, pamphlets, videotapes and films, support groups and hotlines, and websites. In addition, the directory includes a chapter on death and bereavement, as well as a chapter on Wish Foundations for terminally and chronically ill children.
12
You will need to limit your search to “Directory” and “ulcerative colitis” using the "Detailed Search" option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find directories, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Select your preferred language and the format option “Directory.” Type “ulcerative colitis” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months.
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CHAPTER 8. MULTIMEDIA ON ULCERATIVE COLITIS Overview In this chapter, we show you how to keep current on multimedia sources of information on ulcerative colitis. We start with sources that have been summarized by federal agencies, and then show you how to find bibliographic information catalogued by the National Library of Medicine.
Video Recordings An excellent source of multimedia information on ulcerative colitis is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “ulcerative colitis” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find video productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Videorecording (videotape, videocassette, etc.).” Type “ulcerative colitis” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on ulcerative colitis: •
Update: Medical and Surgical Intervention in Inflammatory Bowel Disease Source: Secaucus, NJ: Network for Continuing Medical Education (NCME). 1992. Contact: Available from NCME. One Harmon Plaza, Secaucus, NJ 07094. (800) 223-0272 or, in New Jersey, (800) 624-2102, or (201) 867-3550. PRICE: $50 for 2-week rental or $75 for purchase. Available only to NCME subscribers; subscriber fees as of 1995 are $1,920 for VHS subscription, $2,120 for U-matic subscription. Summary: Evolving medical and surgical therapies may delay or eliminate the need for colostomy or ileostomy in patients with conditions such as Crohn's disease or ulcerative colitis. In this continuing education video program, the authors review available diagnostic modalities; explore the new classes of drugs that treat inflammatory bowel disease (IBD); and discuss the advantages and disadvantages of alternative surgical methods for this group of illnesses. The video program confers 2 hours of CME credit. (AA-M).
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Managing Inflammatory Bowel Disease Source: Princton, NJ: Films for the Humanities and Sciences. 2001. (VHS; DVD). Contact: Available from Films for the Humanities and Sciences. PO Box 2053 Princeton, NJ 08543-2053. (800) 257-5126. Fax: (609) 275-3767. Website: www.films.com. PRICE: $129.95 for VHS; $154.95 for DVD; plus shipping and handling. Item number: BVL30009. Summary: For reasons that are not altogether certain, inflammatory bowel disease (IBD) is affecting more and more Americans every year. In this videotape program from The Doctor Is In, Dr. Scott Plevy, formerly of Mount Sinai School of Medicine, and Dr. Susan Edwards, of the Dartmouth-Hitchcock Medical Center, seek to understand the spreading incidence of IBD. The doctors consider both Crohn's disease and colitis, the two primary forms of IBD, while describing pharmaceutical and surgical treatment options. The program includes case studies of two young women with IBD that focus on how they manage their debilitating conditions.
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Inflammatory Bowel Disease: Coping with Crohn's and Colitis Source: Princton, NJ: Films for the Humanities and Sciences. 1998. (VHS; DVD). Contact: Available from Films for the Humanities and Sciences. PO Box 2053 Princeton, NJ 08543-2053. (800) 257-5126. Fax: (609) 275-3767. Website: www.films.com. PRICE: $129.95 for VHS; $154.95 for DVD; plus shipping and handling. Item number: BVL9193. Summary: Inflammatory bowel disease (IBD) accounts for 250,000 doctor visits, 20,000 hospitalizations, and the loss of more than 1 million workdays every year. This videotape program examines the two predominant types of IBD: Crohn's disease and ulcerative colitis. Health professionals and patients discuss various medications being used; surgical options, including the ileal pouch, anal anastomosis, and strictureplasty; and the importance of nutrition, education, and support groups in improving the quality of day to day life for patients and their families. The documentary also includes diagrams, X rays, and endoscopic imaging.
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What You Really Need to Know About Ulcerative Colitis Source: [Toronto, Ontario, Canada]: Videos for Patients. 1993. (videocassette). Contact: Available from Medical Audio Visual Communications, Inc. Suite 240, 2315 Whirlpool Street, Niagara Falls, NY 14305. Or P.O. Box 84548, 2336 Bloor Street West, Toronto, Ontario M6S 1TO, Canada. (800) 757-4868 or (905) 602-1160. Fax (905) 602-8720. PRICE: $99.00 (Canadian); contact producer for current price in American dollars. Order Number VFP001. Summary: This patient education videotape provides information about ulcerative colitis. The videotape begins with a brief sketch featuring comedian John Cleese and narrator Dr. Robert Buckman illustrating the difficulties sometimes experienced by patients during the traditional doctor's explanation. Topics include a definition of ulcerative colitis (UC); how UC develops; symptoms of UC; classification of UC as mild, moderate, or severe; the advantages and disadvantages of various treatment options, including medications; how and when surgical treatment may be indicated; and how to recognize severe attacks of ulcerative colitis. Dr. Buckman presents the medical facts, using models, simple diagrams, and graphics to supplement his explanation, and avoiding medical jargon as much as possible.
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Ulcerative Colitis: The Disease and Enema Therapy Source: Marietta, GA: Solvay Pharmaceuticals, Inc. 1996. (videocassette). Contact: Available from Solvay Pharmaceuticals, Inc. 901 Sawyer Road, Marietta, GA 30062. (800) 354-0026. PRICE: Single copy free. Summary: This videotape program provides information and reassurance for people recently diagnosed with ulcerative colitis (UC). The program notes that UC can have a great impact on a person's life, but that following the prescribed treatment can help relieve symptoms and return a sense of normalcy. The narrator reviews the possible causes of UC, including genetic, infectious, and autoimmune theories, noting that UC is not contagious or caused by stress or food sensitivity. UC is most often found in the developing world, and people are usually diagnosed in their teens or twenties. The program then features brief interviews with six women who describe how they felt when they first received the diagnosis. Reactions ranged from fear and anxiety to relief that they finally had a name for their symptoms. The narrator then lists the common symptoms of UC: diarrhea, rectal bleeding, bloody stool, loss of appetite, anemia, abdominal pain, weight loss, fever, and gas (flatulence). Less common symptoms can include joint pain, skin lesions, and eye inflammation. The program then features a man and two women talking about symptoms, particularly urgency and frequency, and the impact of these symptoms on their lifestyles. The narrator notes that there are rectal agents, oral medications, antibiotics, and combination therapies, but that the video will focus on enema therapy. The program then interviews three patients who use Rowasa (mesalamine in a rectal suspension enema form). The patients talk about enema therapy and the improved quality of life they have found using this form of the drug. The program then uses line drawings to demonstrate how to give oneself an enema. The medication should be given when the patient can stay prone for 30 minutes or, preferably, overnight. The program concludes by encouraging viewers to ask their health care provider to answer any questions they may have. The address and tollfree telephone number (800-343-3637) of the Crohn's and Colitis Foundation of America are also provided.
Bibliography: Multimedia on Ulcerative Colitis The National Library of Medicine is a rich source of information on healthcare-related multimedia productions including slides, computer software, and databases. To access the multimedia database, go to the following Web site: http://locatorplus.gov/. Select “Search LOCATORplus.” Once in the search area, simply type in ulcerative colitis (or synonyms). Then, in the option box provided below the search box, select “Audiovisuals and Computer Files.” From there, you can choose to sort results by publication date, author, or relevance. The following multimedia has been indexed on ulcerative colitis: •
A Color supplement to Histopathologic spectrum of regional enteritis and ulcerative colitis [slide] Source: by N. Karle Mottet; Year: 1971; Format: Slide; Philadelphia: Saunders, 1971
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Alternates to a stoma for ulcerative colitis [sound recording] Source: American College of Surgeons; Year: 1982; Format: Sound recording; [Chicago, Ill.]: The College, [1982]
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Cancer risk in inflammatory bowel disease [videorecording] Source: [presented by] Marshfield Medical Foundation, in cooperation with Marshfield Clinic & St. Joseph's Hospital; Year: 1982; Format: Videorecording; Marshfield, WI: Marshfield Regional Video Network, 1982
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Cancer surveillance in inflammatory bowel disease [slide]. Year: 1985; Format: Slide; Columbus [Ohio]: Center for Continuing Medical Education, the Ohio State University College of Medicine, [1985]
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Granulomatous and ulcerative colitis [motion picture]: diagnosis and differential diagnosis Source: Mayo Clinic; Year: 1968; Format: Motion picture; Rochester, Minn.: The Clinic: [for loan by Mayo Foundation, Audiovisual Center], 1968
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Inflammatory bowel disease [electronic resource] Source: Stefan Schreiber. [et. al.]; Year: 1999; Format: Electronic resource; Berlin: Springer, c1999
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Inflammatory bowel disease [slide] Source: [authors, David B. Sachar. et al.]; Year: 1986; Format: Slide; [Bethesda, Md.]: The Association, c1986
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Inflammatory bowel disease [sound recording] Source: American College of Surgeons; Year: 1978; Format: Sound recording; [Chicago]: The College, [1978]
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Inflammatory bowel disease [videorecording]: medical, nutritional, and surgical management Source: presented by the American Dietetic Association, Division of Continuing Education, the American Medical Association, Division of Continuing Medical Studies, and t; Year: 1979; Format: Videorecording; Chicago, Ill.: American Medical Association, c1979
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Inflammatory bowel disease in children [videorecording] Source: Marshfield Medical Foundation, in cooperation with Marshfield Clinic & St. Joseph's Hospital; Year: 1983; Format: Videorecording; Marshfield, WI: Marshfield Regional Video Network, 1983
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Pediatric surgery [sound recording]: ulcerative colitis and Hirschsprung's disease Source: American College of Surgeons; Year: 1986; Format: Sound recording; [Chicago, Ill.]: The College, [1986]
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Single stage proctocolectomy for ulcerative colitis [motion picture] Source: H. Willian Scott, Walter G. Gobbel; produced by Davis & Geck; Year: 1970; Format: Motion picture; Danbury, Conn.: Davis & Geck; [Atlanta: for loan by National Medical Audiovisual Center], 1970
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Synchronous combined proctocolectomy for mucosal ulcerative colitis [videorecording] Source: Videosurgery; Year: 1977; Format: Videorecording; Don Mills, Ont.: Southam Business Publications, c1977
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The early detection and medical management of ulcerative colitis [motion picture] Source: produced by Sturgis-Grant Productions, Inc.; by Nicholas C. Hightower, Jr., A. Compton Broders, Jr., Henry Laurens, Richard D. Haines; from the Section on Gastroenterology,; Year: 1959; Format: Motion picture; United States: Sturgis-Grant, [1959]
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The Endorectal pull-through for the management of ulcerative colitis [videorecording] Source: MSD, Merck, Sharp & Dohme; Year: 1983; Format: Videorecording; [West Point, Pa.]: Merck & Co, c1983
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Therapy of inflammatory bowel disease [slide]. Year: 1986; Format: Slide; Columbus [Ohio]: Center for Continuing Medical Education, the Ohio State University College of Medicine, [1986]
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Ulcerative colitis & Crohn's disease [videorecording] Source: presented by the Warren Magnuson Clinical Center, National Institutes of Health, Office of Clinical Reports & Inquiries; a production of AVP Inc; Year: 1985; Format: Videorecording; [Los Angeles, Calif.]: Hospital Satellite Network, c1985
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CHAPTER 9. PERIODICALS AND NEWS ON ULCERATIVE COLITIS Overview In this chapter, we suggest a number of news sources and present various periodicals that cover ulcerative colitis.
News Services and Press Releases One of the simplest ways of tracking press releases on ulcerative colitis is to search the news wires. In the following sample of sources, we will briefly describe how to access each service. These services only post recent news intended for public viewing. PR Newswire To access the PR Newswire archive, simply go to http://www.prnewswire.com/. Select your country. Type “ulcerative colitis” (or synonyms) into the search box. You will automatically receive information on relevant news releases posted within the last 30 days. The search results are shown by order of relevance. Reuters Health The Reuters’ Medical News and Health eLine databases can be very useful in exploring news archives relating to ulcerative colitis. While some of the listed articles are free to view, others are available for purchase for a nominal fee. To access this archive, go to http://www.reutershealth.com/en/index.html and search by “ulcerative colitis” (or synonyms). The following was recently listed in this archive for ulcerative colitis: •
5-ASA therapy for inflammatory bowel disease no bar to colon cancer Source: Reuters Industry Breifing Date: January 28, 2004
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Low-dose pegylated interferon alpha offers no benefit for active ulcerative colitis Source: Reuters Industry Breifing Date: January 02, 2004
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Epidermal growth factor enema may reduce disease activity of ulcerative colitis Source: Reuters Industry Breifing Date: July 24, 2003
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Protein Design Labs says early data for ulcerative colitis drug look good Source: Reuters Industry Breifing Date: May 19, 2003
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Isis begins second phase II trial of alicaforsen for ulcerative colitis Source: Reuters Industry Breifing Date: April 08, 2003
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Isis starts new phase II ulcerative colitis trial Source: Reuters Industry Breifing Date: November 21, 2002
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Infliximab therapy can be successful in active ulcerative colitis Source: Reuters Industry Breifing Date: November 11, 2002
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Shire acquires rights to ulcerative colitis drug Source: Reuters Industry Breifing Date: October 15, 2002
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Axcan acquires North American rights to mesalamine gel formulation for ulcerative colitis Source: Reuters Industry Breifing Date: October 10, 2002
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Salix licenses ulcerative colitis drug, restructures leadership Source: Reuters Industry Breifing Date: July 16, 2002
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Shire licenses ulcerative colitis drug Source: Reuters Industry Breifing Date: May 03, 2002
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New compound may ease Crohn's, ulcerative colitis Source: Reuters Health eLine Date: March 28, 2002
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Ulcerative colitis procedure tied to decreased fertility in women Source: Reuters Industry Breifing Date: December 28, 2001
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Self-management training reduces office visits by ulcerative colitis patients Source: Reuters Industry Breifing Date: September 21, 2001
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Measles-containing vaccines do not increase risk of inflammatory bowel disease Source: Reuters Industry Breifing Date: March 14, 2001
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Gene profiling key to inflammatory bowel disease Source: Reuters Health eLine Date: March 14, 2001
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Millennium launches pivotal trial for inflammatory bowel disease therapy Source: Reuters Industry Breifing Date: February 08, 2001
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Incara begins phase II/III trial of ulcerative colitis treatment Source: Reuters Industry Breifing Date: January 30, 2001
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IV azathioprine appears safe for severe ulcerative colitis treatment Source: Reuters Industry Breifing Date: January 26, 2001
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Inflammatory bowel disease, colon cancer link examined Source: Reuters Health eLine Date: January 26, 2001
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Ursodiol may lower risk of colon cancer in ulcerative colitis patients at high risk Source: Reuters Industry Breifing Date: January 15, 2001
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Elan, Incara to partner on ulcerative colitis treatment Source: Reuters Industry Breifing Date: December 22, 2000
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InKine's Colirest shows phase II efficacy in ulcerative colitis Source: Reuters Industry Breifing Date: December 11, 2000
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6-Mercaptopurine favored over azathioprine for inflammatory bowel disease Source: Reuters Industry Breifing Date: October 30, 2000
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Unfractionated heparin alone is not effective for ulcerative colitis Source: Reuters Industry Breifing Date: October 27, 2000
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Engineered bacteria help to treat inflammatory bowel disease Source: Reuters Health eLine Date: August 24, 2000
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FDA grants approval to Salix's ulcerative colitis treatment Colazal Source: Reuters Industry Breifing Date: July 24, 2000
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Early measles infection linked to inflammatory bowel disease Source: Reuters Industry Breifing Date: June 21, 2000
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Diabetes drug may help inflammatory bowel disease Source: Reuters Health eLine Date: August 12, 1999
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Inflammatory bowel disease suppository recalled Source: Reuters Health eLine Date: June 23, 1999
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Anti-clotting drug may help ulcerative colitis Source: Reuters Health eLine Date: May 25, 1999
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Drug cuts cancer risk in ulcerative colitis Source: Reuters Health eLine Date: May 17, 1999
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Genes linked to inflammatory bowel disease Source: Reuters Health eLine Date: June 24, 1998 The NIH
Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine. Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name. Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “ulcerative colitis” (or synonyms) into the search box, and click on “Search News.” As this service is technology oriented, you may wish to use it when searching for press releases covering diagnostic procedures or tests. Search Engines Medical news is also available in the news sections of commercial Internet search engines. See the health news page at Yahoo (http://dir.yahoo.com/Health/News_and_Media/), or you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “ulcerative colitis” (or synonyms). If you know the name of a company that is relevant to ulcerative colitis, you can go to any stock trading Web site (such as http://www.etrade.com/) and search for the company name there. News items across various news sources are reported on indicated hyperlinks. Google offers a similar service at http://news.google.com/.
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BBC Covering news from a more European perspective, the British Broadcasting Corporation (BBC) allows the public free access to their news archive located at http://www.bbc.co.uk/. Search by “ulcerative colitis” (or synonyms).
Newsletters on Ulcerative Colitis Find newsletters on ulcerative colitis using the Combined Health Information Database (CHID). You will need to use the “Detailed Search” option. To access CHID, go to the following hyperlink: http://chid.nih.gov/detail/detail.html. Limit your search to “Newsletter” and “ulcerative colitis.” Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter.” Type “ulcerative colitis” (or synonyms) into the “For these words:” box. The following list was generated using the options described above: •
Evolving Medical Therapies for Inflammatory Bowel Disease Source: Progress in Inflammatory Bowel Disease. 15(2): 1-5. Spring 1994. Contact: Available from Crohn's and Colitis Foundation of America, Inc. 386 Park Avenue South, 17th Floor, New York, NY 10016-8804. (800) 343-3637 or (800) 932-2423 or (212) 685-3440. Summary: This newsletter article reviews advances in medical approaches to treating ulcerative colitis and Crohn's disease (collectively, inflammatory bowel disease or IBD). Topics include the use of aminosalicylates, including 5-ASA, mesalamine, sulfasalazine, administration and dosage considerations, and the use of these agents specifically in Crohn's disease; steroid treatment of IBD, including the use of budesonide; immune modifiers, including azathioprine, 6-mercaptopurine, methotrexate, and cyclosporine; and miscellaneous therapies, including immunoinflammatory mediators, lipoxygenase inhibition, and short-chain fatty acids for ulcerative colitis. 22 references.
Newsletter Articles Use the Combined Health Information Database, and limit your search criteria to “newsletter articles.” Again, you will need to use the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter Article.” Type “ulcerative colitis” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months. The following is a typical result when searching for newsletter articles on ulcerative colitis: •
Inflammatory Bowel Disease: Making Sense of a Mystery Ailment Source: Harvard Health Letter. 22(2): 4-6. December 1996. Contact: Available from Harvard Health Letter. P.O. Box 380, Boston, MA 02117. (617) 432-1485.
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Summary: This article introduces general readers to the symptoms and causes of inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis (UC). The authors discuss the differential diagnosis of IBD, including ruling out irritable bowel syndrome (IBS) and bacterial infections, and the diagnostic tests that are commonly used to confirm IBD. The authors note that IBD appears to run in families, and they report on current genetic research in this area as well as on research into a possible environmental stimulus that can trigger the disease in genetically susceptible people. The choice of therapy is largely determined by which part of the bowel is affected by IBD and whether the problem is Crohn's or UC. People can use topical therapy such as steroid suppositories or enemas to treat the inflammation directly if only the rectum or lower portion of the colon is affected. However, oral medication often becomes necessary. The first choice for drug therapy is sulfasalazine (Azulfidine). The authors conclude with a brief discussion of the surgical options available for people with IBD who don't respond to drug therapy. 1 table. (AA-M). •
Inflammatory Bowel Diseases: Misery Needn't be the Norm Source: Mayo Clinic Health Letter. 19(10): 1-3. October 2001. Contact: Available from Mayo Clinic Health Letter. Subscription Services, P.O. Box 53889, Boulder, CO 80322-3889. (800) 333-9037 or (303) 604-1465. Summary: This health education newsletter article familiarizes readers with inflammatory bowel disease (IBD), which includes Crohn's disease and ulcerative colitis. The author describes the two types of IBD, and their incidence, symptoms, diagnosis, drug therapy, lifestyle treatments, and surgical options. The signs and symptoms of Crohn's disease and ulcerative colitis may develop gradually or suddenly and can be similar: chronic diarrhea, vomiting, abdominal cramping, blood in the stool, weight loss and fatigue, and fever in severe cases. In addition, people with Crohn's disease are more likely to develop open sores (ulcers) in their digestive tract. Blood tests and diagnostic imaging confirm the diagnoses of inflammatory bowel disease. Drug therapy is a key component of treating IBD. Although drugs do not offer a cure for IBD, they often help control the condition. Once the right drug or combination of drugs is determined, symptoms can often be reduced. Drugs can include anti-inflammatory drugs, immune modulators, and antibiotics. Lifestyle treatments include dietary management, adequate fluid intake, stress management (including the use of support groups), and avoidance of nonsteroidal anti-inflammatory drugs (NSAIDs). At least 70 percent of those patients with Crohn's disease will need at least one or more surgeries. One side bar reminds readers of the risk of colon cancer in people with IBD. 1 figure.
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Crohn's Disease and Ulcerative Colitis: Taming Painful Inflammatory Bowel Disease Source: Mayo Clinic Women's Healthsource. 4(6): 4-5. June 2000. Contact: Available from Mayo Foundation for Medical Education and Research. 200 First Street SW, Rochester, MN 55905. Summary: This health newsletter article describes inflammatory bowel disease (IBD), an umbrella term for Crohn's disease and ulcerative colitis (UC). The author notes that the cause of IBD is unclear, but abnormalities of the immune system are associated with these diseases. IBD is an inflammatory disease, and it is this inflammation that results in pain and diarrhea. Symptoms can also include weight loss, fatigue, rectal bleeding, and anemia. The location of the inflammation within the digestive tract is one of the features that differentiates Crohn's disease from ulcerative colitis. Crohn's disease can affect any part of the digestive tract, from the mouth to the anus, although inflammation is usually
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in the small intestine. With UC, inflammation is usually in the large intestine and rectum, and ulcers often form. These disorders may also cause other health complications, including an increased risk for developing colon cancer. The symptoms of Crohn's disease are similar to irritable bowel syndrome (IBS), so diagnostic tests to differentiate the diseases may include blood tests, flexible sigmoidoscopy, colonoscopy, and barium enema. Treatment of IBD depends on the severity of disease and the associated complications. Treatment strategies can include diet, medications, counseling, and surgery. While there is no cure for IBD, some people have long periods of remission when their symptoms are well controlled. One sidebar describes current research efforts on Crohn's disease and ulcerative colitis. 1 figure. •
Ulcerative Colitis: Manageable, With a Brighter Outlook Source: Mayo Clinic Health Letter. 13(12): 1-2. December 1995. Contact: Available from Mayo Clinic Health Letter. Subscription Services, P.O. Box 53889, Boulder, CO 80322-3889. (800) 333-9037. Summary: This newsletter article brings readers up-to-date on the management of ulcerative colitis (UC), a form of inflammatory bowel disease (IBD). The article defines the disease and describes diagnostic tests used to confirm UC. It also includes tips on how to manage flareups of the disease, options for drug therapy, and the role of surgery to treat UC. The article concludes with a brief look at treatments currently in the research stage. 2 figures.
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Inflammatory Bowel Disease. Part II: Treatment Source: Intestinal Fortitude. 10(4): 1-3. 2000. Contact: Available from Intestinal Disease Foundation. 1323 Forbes Avenue, Suite 200, Pittsburgh, PA 15219. (412) 261-5888. Summary: This newsletter article, the second in a two part series on inflammatory bowel disease (IBD), reviews the treatment options for people with the disease. The goals of therapy for IBD include symptom control and remission; good nutrition, for healing and to avoid additional problems relating to nutritional deficiencies; and quality of life, a common goal for all of the therapies used, including medications, coping techniques, and surgeries. For ulcerative colitis (UC) patients, removal of the colon produces a cure. It is major surgery, however, and for that reason needs to be carefully considered. Surgery for Crohn's disease (CD) is usually done to treat obstructions (from strictures), infections (abscesses), or non healing fistulas. There is a 10 percent chance per year of recurrence of the CD following surgery, but use of medications, along with surgery, may help reduce the odds. The author reviews four traditional therapies for IBD: 5 aminosalicylates, antibiotics, corticosteroids, and immunomodulators. The authors also considers a new therapy, infliximab (Remicade), a medication that works on a cellular level to prevent inflammation and was recently approved by the FDA for treatment of CD. The future treatment of UC and CD will involve medications that better target the immune chemicals responsible for inflammation. For now, the treatment of IBD remains a multidisciplinary approach (medical, surgical, and nutritional) aimed at controlling symptoms and maintaining wellness.
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Academic Periodicals covering Ulcerative Colitis Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to ulcerative colitis. In addition to these sources, you can search for articles covering ulcerative colitis that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”
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CHAPTER 10. RESEARCHING MEDICATIONS Overview While a number of hard copy or CD-ROM resources are available for researching medications, a more flexible method is to use Internet-based databases. Broadly speaking, there are two sources of information on approved medications: public sources and private sources. We will emphasize free-to-use public sources.
U.S. Pharmacopeia Because of historical investments by various organizations and the emergence of the Internet, it has become rather simple to learn about the medications recommended for ulcerative colitis. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a non-profit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DI Advice for the Patient can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with ulcerative colitis. If you would like more information on a particular medication, the provided hyperlinks will direct you to ample documentation (e.g. typical dosage, side effects, drug-interaction risks, etc.).
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The following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to ulcerative colitis: Azathioprine •
Systemic - U.S. Brands: Imuran http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202077.html
Balsalazide •
Systemic - U.S. Brands: Colazal http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500233.html
Corticosteroids •
Dental - U.S. Brands: Kenalog in Orabase; Orabase-HCA; Oracort; Oralone http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202010.html
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Inhalation - U.S. Brands: AeroBid; AeroBid-M; Azmacort; Beclovent; Decadron Respihaler; Pulmicort Respules; Pulmicort Turbuhaler; Vanceril; Vanceril 84 mcg Double Strength http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202011.html
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Nasal - U.S. Brands: Beconase; Beconase AQ; Dexacort Turbinaire; Flonase; Nasacort; Nasacort AQ; Nasalide; Nasarel; Nasonex; Rhinocort; Vancenase; Vancenase AQ 84 mcg; Vancenase pockethaler http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202012.html
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Ophthalmic - U.S. Brands: AK-Dex; AK-Pred; AK-Tate; Baldex; Decadron; Dexair; Dexotic; Econopred; Econopred Plus; Eflone; Flarex; Fluor-Op; FML Forte; FML Liquifilm; FML S.O.P.; HMS Liquifilm; Inflamase Forte; Inflamase Mild; I-Pred; Lite Pred; Maxidex; Ocu-Dex; Ocu-Pred; Ocu-Pr http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202013.html
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Otic - U.S. Brands: Decadron http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202014.html
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Rectal - U.S. Brands: Anucort-HC; Anu-Med HC; Anuprep HC; Anusol-HC; Anutone-HC; Anuzone-HC; Cort-Dome; Cortenema; Cortifoam; Hemorrhoidal HC; Hemril-HC Uniserts; Proctocort; Proctosol-HC; Rectosol-HC http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203366.html
Cyclosporine •
Systemic - U.S. Brands: Neoral; Sandimmune; SangCya http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202176.html
Infliximab •
Systemic - U.S. Brands: Remicade http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203667.html
Levamisole •
Systemic http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202176.html
Loperamide •
Oral - U.S. Brands: Imodium http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202332.html
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Mercaptopurine •
Systemic - U.S. Brands: Purinethol http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202350.html
Mesalamine •
Oral - U.S. Brands: Asacol; Pentasa http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202734.html
•
Rectal - U.S. Brands: Canasa; Rowasa http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202351.html
Metronidazole •
Systemic - U.S. Brands: Flagyl; Protostat http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202365.html
•
Vaginal - U.S. Brands: MetroGel-Vaginal http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202704.html
Olsalazine •
Oral - U.S. Brands: Dipentum http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202422.html
Sucralfate •
Oral - U.S. Brands: Carafate http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202533.html
Sulfasalazine •
Systemic - U.S. Brands: Azulfidine http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202537.html
Thiamine (Vitamin B 1 ) •
Systemic - U.S. Brands: Biamine http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202560.html
Commercial Databases In addition to the medications listed in the USP above, a number of commercial sites are available by subscription to physicians and their institutions. Or, you may be able to access these sources from your local medical library.
Mosby’s Drug Consult Mosby’s Drug Consult database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/.
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PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html. Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter, Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee.
Researching Orphan Drugs Although the list of orphan drugs is revised on a daily basis, you can quickly research orphan drugs that might be applicable to ulcerative colitis by using the database managed by the National Organization for Rare Disorders, Inc. (NORD), at http://www.rarediseases.org/. Scroll down the page, and on the left toolbar, click on “Orphan Drug Designation Database.” On this page (http://www.rarediseases.org/search/noddsearch.html), type “ulcerative colitis” (or synonyms) into the search box, and click “Submit Query.” When you receive your results, note that not all of the drugs may be relevant, as some may have been withdrawn from orphan status. Write down or print out the name of each drug and the relevant contact information. From there, visit the Pharmacopeia Web site and type the name of each orphan drug into the search box at http://www.nlm.nih.gov/medlineplus/druginformation.html. You may need to contact the sponsor or NORD for further information. NORD conducts “early access programs for investigational new drugs (IND) under the Food and Drug Administration’s (FDA’s) approval ‘Treatment INDs’ programs which allow for a limited number of individuals to receive investigational drugs before FDA marketing approval.” If the orphan product about which you are seeking information is approved for marketing, information on side effects can be found on the product’s label. If the product is not approved, you may need to contact the sponsor. The following is a list of orphan drugs currently listed in the NORD Orphan Drug Designation Database for ulcerative colitis: •
4-aminosalicylic acid (trade name: Pamisyl (P-D), Rezipas (Squibb)) http://www.rarediseases.org/nord/search/nodd_full?code=499
•
Short chain fatty acid solution http://www.rarediseases.org/nord/search/nodd_full?code=47
If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.
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APPENDICES
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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.
NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute13: •
Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm
•
National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
•
National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
•
National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25
•
National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm
•
National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm
•
National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
•
National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
13
These publications are typically written by one or more of the various NIH Institutes.
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•
National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm
•
National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
•
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
•
National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
•
National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
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National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
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National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
•
National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
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National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm
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National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm
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National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm
•
National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html
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National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm
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Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
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National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/
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National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp
•
Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html
•
Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm
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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.14 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:15 •
Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html
•
HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html
•
NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html
•
Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/
•
Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
•
Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
•
Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/
•
Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
•
Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html
•
Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html
•
MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html
14 Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 15 See http://www.nlm.nih.gov/databases/databases.html.
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•
Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html
•
Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html The Combined Health Information Database
A comprehensive source of information on clinical guidelines written for professionals is the Combined Health Information Database. You will need to limit your search to one of the following: Brochure/Pamphlet, Fact Sheet, or Information Package, and “ulcerative colitis” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For the publication date, select “All Years.” Select your preferred language and the format option “Fact Sheet.” Type “ulcerative colitis” (or synonyms) into the “For these words:” box. The following is a sample result: •
Practical Guide to Topical and Oral 5-ASA Products for the Treatment of Inflammatory Bowel Disease Source: New York, NY: Crohn's and Colitis Foundation of America, Inc. 1993. 14 p. Contact: Available from Crohn's and Colitis Foundation of America, Inc. 386 Park Avenue South, 17th Floor, New York, NY 10016-8804. (800) 343-3637 or (800) 932-2423 or (212) 685-3440. PRICE: Single copy free. Summary: This publication includes highlights from a conference on the use of topical and oral 5-ASA drug therapy to treat inflammatory bowel disease (IBD). Four articles address mechanisms of action and sites of delivery of these drug products; acute and maintenance treatment of left-sided colitis and proctitis; acute and maintenance treatment of Crohn's disease and ulcerative colitis; and the use of steroids and immunosuppressive drugs in conjunction with 5-ASA products for Crohn's disease and ulcerative colitis. The publication also includes four illustrative case examples. After each article and case example, the faculty and audience members' discussion is reprinted. The publication concludes with a description of the Crohn's and Colitis Foundation of America (CCFA) and its research and educational activities. 22 references.
The NLM Gateway16 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.17 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “ulcerative colitis” (or synonyms) into the search box and click “Search.” The results
16 17
Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.
The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH).
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will be presented in a tabular form, indicating the number of references in each database category. Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total
Items Found 20466 246 990 17 65 21784
HSTAT18 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.19 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.20 Simply search by “ulcerative colitis” (or synonyms) at the following Web site: http://text.nlm.nih.gov.
Coffee Break: Tutorials for Biologists21 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.22 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.23 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/. 18
Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html.
19
The HSTAT URL is http://hstat.nlm.nih.gov/.
20
Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations. 21 Adapted from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html. 22 The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 23 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process.
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Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •
CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.
•
Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.
The Genome Project and Ulcerative Colitis In the following section, we will discuss databases and references which relate to the Genome Project and ulcerative colitis. Online Mendelian Inheritance in Man (OMIM) The Online Mendelian Inheritance in Man (OMIM) database is a catalog of human genes and genetic disorders authored and edited by Dr. Victor A. McKusick and his colleagues at Johns Hopkins and elsewhere. OMIM was developed for the World Wide Web by the National Center for Biotechnology Information (NCBI).24 The database contains textual information, pictures, and reference information. It also contains copious links to NCBI’s Entrez database of MEDLINE articles and sequence information. To search the database, go to http://www.ncbi.nlm.nih.gov/Omim/searchomim.html. Type “ulcerative colitis” (or synonyms) into the search box, and click “Submit Search.” If too many results appear, you can narrow the search by adding the word “clinical.” Each report will have additional links to related research and databases. In particular, the option “Database Links” will search across technical databases that offer an abundance of information. The following is an example of the results you can obtain from the OMIM for ulcerative colitis: •
Inflammatory Bowel Disease 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?266600
•
Inflammatory Bowel Disease 2 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?601458
•
Inflammatory Bowel Disease 3 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?604519
•
Inflammatory Bowel Disease 5 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?606348
24
Adapted from http://www.ncbi.nlm.nih.gov/. Established in 1988 as a national resource for molecular biology information, NCBI creates public databases, conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information--all for the better understanding of molecular processes affecting human health and disease.
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Inflammatory Bowel Disease 6 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?606674
•
Inflammatory Bowel Disease 7 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605225
•
Ulcerative Colitis, Susceptibility to Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?191390
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Genes and Disease (NCBI - Map) The Genes and Disease database is produced by the National Center for Biotechnology Information of the National Library of Medicine at the National Institutes of Health. This Web site categorizes each disorder by system of the body. Go to http://www.ncbi.nlm.nih.gov/disease/, and browse the system pages to have a full view of important conditions linked to human genes. Since this site is regularly updated, you may wish to revisit it from time to time. The following systems and associated disorders are addressed: •
Cancer: Uncontrolled cell division. Examples: Breast and ovarian cancer, Burkitt lymphoma, chronic myeloid leukemia, colon cancer, lung cancer, malignant melanoma, multiple endocrine neoplasia, neurofibromatosis, p53 tumor suppressor, pancreatic cancer, prostate cancer, Ras oncogene, RB: retinoblastoma, von Hippel-Lindau syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Cancer.html
•
Immune System: Fights invaders. Examples: Asthma, autoimmune polyglandular syndrome, Crohn’s disease, DiGeorge syndrome, familial Mediterranean fever, immunodeficiency with Hyper-IgM, severe combined immunodeficiency. Web site: http://www.ncbi.nlm.nih.gov/disease/Immune.html
•
Metabolism: Food and energy. Examples: Adreno-leukodystrophy, atherosclerosis, Best disease, Gaucher disease, glucose galactose malabsorption, gyrate atrophy, juvenile-onset diabetes, obesity, paroxysmal nocturnal hemoglobinuria, phenylketonuria, Refsum disease, Tangier disease, Tay-Sachs disease. Web site: http://www.ncbi.nlm.nih.gov/disease/Metabolism.html
•
Muscle and Bone: Movement and growth. Examples: Duchenne muscular dystrophy, Ellis-van Creveld syndrome, Marfan syndrome, myotonic dystrophy, spinal muscular atrophy. Web site: http://www.ncbi.nlm.nih.gov/disease/Muscle.html
•
Nervous System: Mind and body. Examples: Alzheimer disease, amyotrophic lateral sclerosis, Angelman syndrome, Charcot-Marie-Tooth disease, epilepsy, essential tremor, fragile X syndrome, Friedreich’s ataxia, Huntington disease, Niemann-Pick disease, Parkinson disease, Prader-Willi syndrome, Rett syndrome, spinocerebellar atrophy, Williams syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Brain.html
•
Signals: Cellular messages. Examples: Ataxia telangiectasia, Cockayne syndrome, glaucoma, male-patterned baldness, SRY: sex determination, tuberous sclerosis, Waardenburg syndrome, Werner
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syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Signals.html •
Transporters: Pumps and channels. Examples: Cystic fibrosis, deafness, diastrophic dysplasia, Hemophilia A, long-QT syndrome, Menkes syndrome, Pendred syndrome, polycystic kidney disease, sickle cell anemia, Wilson’s disease, Zellweger syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Transporters.html Entrez
Entrez is a search and retrieval system that integrates several linked databases at the National Center for Biotechnology Information (NCBI). These databases include nucleotide sequences, protein sequences, macromolecular structures, whole genomes, and MEDLINE through PubMed. Entrez provides access to the following databases: •
3D Domains: Domains from Entrez Structure, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
•
Books: Online books, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=books
•
Genome: Complete genome assemblies, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Genome
•
NCBI’s Protein Sequence Information Survey Results: Web site: http://www.ncbi.nlm.nih.gov/About/proteinsurvey/
•
Nucleotide Sequence Database (Genbank): Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Nucleotide
•
OMIM: Online Mendelian Inheritance in Man, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=OMIM
•
PopSet: Population study data sets, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Popset
•
ProbeSet: Gene Expression Omnibus (GEO), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
•
Protein Sequence Database: Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Protein
•
PubMed: Biomedical literature (PubMed), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
•
Structure: Three-dimensional macromolecular structures, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Structure
•
Taxonomy: Organisms in GenBank, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Taxonomy
To access the Entrez system at the National Center for Biotechnology Information, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=genome, and then select the database that you would like to search. The databases available are listed in the drop box next to “Search.” Enter “ulcerative colitis” (or synonyms) into the search box and click “Go.”
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Jablonski’s Multiple Congenital Anomaly/Mental Retardation (MCA/MR) Syndromes Database25 This online resource has been developed to facilitate the identification and differentiation of syndromic entities. Special attention is given to the type of information that is usually limited or completely omitted in existing reference sources due to space limitations of the printed form. At http://www.nlm.nih.gov/mesh/jablonski/syndrome_toc/toc_a.html, you can search across syndromes using an alphabetical index. Search by keywords at http://www.nlm.nih.gov/mesh/jablonski/syndrome_db.html. The Genome Database26 Established at Johns Hopkins University in Baltimore, Maryland in 1990, the Genome Database (GDB) is the official central repository for genomic mapping data resulting from the Human Genome Initiative. In the spring of 1999, the Bioinformatics Supercomputing Centre (BiSC) at the Hospital for Sick Children in Toronto, Ontario assumed the management of GDB. The Human Genome Initiative is a worldwide research effort focusing on structural analysis of human DNA to determine the location and sequence of the estimated 100,000 human genes. In support of this project, GDB stores and curates data generated by researchers worldwide who are engaged in the mapping effort of the Human Genome Project (HGP). GDB’s mission is to provide scientists with an encyclopedia of the human genome which is continually revised and updated to reflect the current state of scientific knowledge. Although GDB has historically focused on gene mapping, its focus will broaden as the Genome Project moves from mapping to sequence, and finally, to functional analysis. To access the GDB, simply go to the following hyperlink: http://www.gdb.org/. Search “All Biological Data” by “Keyword.” Type “ulcerative colitis” (or synonyms) into the search box, and review the results. If more than one word is used in the search box, then separate each one with the word “and” or “or” (using “or” might be useful when using synonyms).
25 Adapted from the National Library of Medicine: http://www.nlm.nih.gov/mesh/jablonski/about_syndrome.html. 26 Adapted from the Genome Database: http://gdbwww.gdb.org/gdb/aboutGDB.html - mission.
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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on ulcerative colitis can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internet-based services that post them.
Patient Guideline Sources The remainder of this chapter directs you to sources which either publish or can help you find additional guidelines on topics related to ulcerative colitis. Due to space limitations, these sources are listed in a concise manner. Do not hesitate to consult the following sources by either using the Internet hyperlink provided, or, in cases where the contact information is provided, contacting the publisher or author directly. The National Institutes of Health The NIH gateway to patients is located at http://health.nih.gov/. From this site, you can search across various sources and institutes, a number of which are summarized below. Topic Pages: MEDLINEplus The National Library of Medicine has created a vast and patient-oriented healthcare information portal called MEDLINEplus. Within this Internet-based system are “health topic pages” which list links to available materials relevant to ulcerative colitis. To access this system, log on to http://www.nlm.nih.gov/medlineplus/healthtopics.html. From there you can either search using the alphabetical index or browse by broad topic areas. Recently, MEDLINEplus listed the following when searched for “ulcerative colitis”:
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•
Guides on ulcerative colitis Ulcerative Colitis http://www.nlm.nih.gov/medlineplus/tutorials/ulcerativecolitisloader.html
•
Other guides Colonic Diseases http://www.nlm.nih.gov/medlineplus/colonicdiseases.html Crohn's Disease http://www.nlm.nih.gov/medlineplus/crohnsdisease.html Digestive Diseases http://www.nlm.nih.gov/medlineplus/digestivediseases.html Peptic Ulcer http://www.nlm.nih.gov/medlineplus/pepticulcer.html Ulcerative Colitis http://www.nlm.nih.gov/medlineplus/ulcerativecolitis.html
Within the health topic page dedicated to ulcerative colitis, the following was listed: •
General/Overviews Inflammatory Bowel Disease Source: American Gastroenterological Association http://www.gastro.org/clinicalRes/brochures/ibd.html Introduction to Ulcerative Colitis Source: Crohn's & Colitis Foundation of America http://www.ccfa.org/research/info/aboutuc
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Diagnosis/Symptoms Abdominal Pain, Long-Term Source: American Academy of Family Physicians http://familydoctor.org/528.xml Abdominal Pain, Short-Term Source: American Academy of Family Physicians http://familydoctor.org/527.xml Colonoscopy http://www.nlm.nih.gov/medlineplus/tutorials/colonoscopyloader.html Colonoscopy Source: National Digestive Diseases Information Clearinghouse http://digestive.niddk.nih.gov/ddiseases/pubs/colonoscopy/index.htm C-Reactive Protein (CRP) Source: American Association for Clinical Chemistry http://www.labtestsonline.org/understanding/analytes/crp/test.html
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Flexible Sigmoidoscopy Source: National Digestive Diseases Information Clearinghouse http://digestive.niddk.nih.gov/ddiseases/pubs/sigmoidoscopy/index.htm Radiography-Lower GI Tract (Barium Enema “BE”) Source: American College of Radiology, Radiological Society of North America http://www.radiologyinfo.org/content/lower_gi.htm •
Treatment Colostomy http://www.nlm.nih.gov/medlineplus/tutorials/colostomyloader.html Ileostomy, Colostomy and Ileoanal Reservoir Surgery Source: National Digestive Diseases Information Clearinghouse http://digestive.niddk.nih.gov/ddiseases/pubs/ileostomy/index.htm Laparoscopic Intestinal Surgery: A Guide for Patients Source: Cleveland Clinic Foundation http://www.clevelandclinic.org/health/healthinfo/docs/0900/0962.asp?index=4356 Surgery for Ulcerative Colitis Source: Crohn's & Colitis Foundation of America http://www.ccfa.org/medinfo/medinfo/surgeryuc.html Treatment Options in IBD Source: Crohn's & Colitis Foundation of America http://www.ccfa.org/medinfo/medinfo/treatmentoptions.html Types of Medications for Inflammatory Bowel Disease Source: Crohn's & Colitis Foundation of America http://www.ccfa.org/medinfo/medinfo/medications.html
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Nutrition Diet and Nutrition Source: Crohn's & Colitis Foundation of America http://www.ccfa.org/research/info/diet
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Specific Conditions/Aspects Extraintestinal Complications of IBD: Arthritis Source: Crohn's & Colitis Foundation of America http://www.ccfa.org/medinfo/medinfo/arthritis.html Extraintestinal Complications: Bone Loss Source: Crohn's & Colitis Foundation of America http://www.ccfa.org/medinfo/medinfo/bone.html Extraintestinal Complications: Eye Disorders Source: Crohn's & Colitis Foundation of America http://www.ccfa.org/medinfo/medinfo/eye.html Extraintestinal Complications: Kidney Disorders Source: Crohn's & Colitis Foundation of America http://www.ccfa.org/medinfo/medinfo/kidney.html
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Extraintestinal Complications: Liver Disease Source: Crohn's & Colitis Foundation of America http://www.ccfa.org/medinfo/medinfo/liver.html Extraintestinal Complications: Skin Disorders Source: Crohn's & Colitis Foundation of America http://www.ccfa.org/medinfo/medinfo/skin.html Measles Vaccine and Inflammatory Bowel Disease (IBD) Source: National Immunization Program http://www.cdc.gov/nip/vacsafe/concerns/autism/ibd.htm What Is Primary Sclerosing Cholangitis? Source: American Liver Foundation http://www.liverfoundation.org/cgibin/dbs/articles.cgi?db=articles&uid=default&ID=1015&view_records=1 •
Children Inflammatory Bowel Disease Source: Nemours Foundation http://kidshealth.org/parent/medical/digestive/ibd.html Treating IBD in Children and Adolescents Source: Crohn's & Colitis Foundation of America http://www.ccfa.org/medinfo/medinfo/kidsmeds.html
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Latest News Bowel Diseases, Depression May Be Linked Source: 01/27/2004, United Press International http://www.nlm.nih.gov//www.nlm.nih.gov/medlineplus/news/fullstory_15758 .html
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Men Women's Issues http://www.ccfa.org/frameviewer/?url=/media/pdf/womens.pdf
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Organizations American Gastroenterological Association http://www.gastro.org/ Crohn's & Colitis Foundation of America http://www.ccfa.org/ National Digestive Diseases Information Clearinghouse http://digestive.niddk.nih.gov/ National Institute of Diabetes and Digestive and Kidney Diseases http://www.niddk.nih.gov/
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Pictures/Diagrams Atlas of the Body: The Digestive System Source: American Medical Association http://www.medem.com/MedLb/article_detaillb.cfm?article_ID=ZZZ7C4T46JC&s ub_cat=338
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Research Challenges in IBD Research: Updating the Scientific Agendas 2002 http://www.ccfa.org/medinfo/research/laychallenges.pdf
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Teenagers Inflammatory Bowel Disease Source: Nemours Foundation http://kidshealth.org/teen/diseases_conditions/digestive/ibd.html
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Women Women's Issues http://www.ccfa.org/frameviewer/?url=/media/pdf/womens.pdf
You may also choose to use the search utility provided by MEDLINEplus at the following Web address: http://www.nlm.nih.gov/medlineplus/. Simply type a keyword into the search box and click “Search.” This utility is similar to the NIH search utility, with the exception that it only includes materials that are linked within the MEDLINEplus system (mostly patient-oriented information). It also has the disadvantage of generating unstructured results. We recommend, therefore, that you use this method only if you have a very targeted search. The Combined Health Information Database (CHID) CHID Online is a reference tool that maintains a database directory of thousands of journal articles and patient education guidelines on ulcerative colitis. CHID offers summaries that describe the guidelines available, including contact information and pricing. CHID’s general Web site is http://chid.nih.gov/. To search this database, go to http://chid.nih.gov/detail/detail.html. In particular, you can use the advanced search options to look up pamphlets, reports, brochures, and information kits. The following was recently posted in this archive: •
Q and A. Crohn's Disease and Ulcerative Colitis: Surgery Source: New York, NY: Crohn's and Colitis Foundation of America, Inc. 2002. 12 p. Contact: Available from Crohn's and Colitis Foundation of America, Inc. (CCFA). 386 Park Avenue South, 17th Floor, New York, NY 10016-8804. (800) 343-3637 or (800) 9322423 or (212) 685-3440. Fax (212) 779-4098. Website: www.ccfa.org. E-mail:
[email protected] PRICE: Single copy free. Summary: About two-thirds to three-fourths of people with Crohn's disease, and about 25 to 40 percent of people with ulcerative colitis will need surgery at some time during their lives. This brochure is written in a question-and-answer format and clearly
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separates information about Crohn's disease from information about ulcerative colitis. Topics covered include indications for surgery; the role of nutrition in surgical patients with inflammatory bowel disease (Crohn's disease or ulcerative colitis); common surgical procedures; surgical treatment of abscesses and fistulas; recurrence of Crohn's disease following surgery; and selecting the best surgical option for ulcerative colitis. •
Q and A. Crohn's Disease and Ulcerative Colitis: Women's Issues Source: New York, NY: Crohn's and Colitis Foundation of America. 2002. 6 p. Contact: Available from Crohn's and Colitis Foundation of America (CCFA). 386 Park Avenue South, 17th Floor, New York, NY 10016-8804. (800) 932-2423. E-mail:
[email protected]. Website: www.ccfa.org. PRICE: Single copy free. Summary: Crohn's disease and ulcerative colitis are chronic digestive diseases of the small and large intestines, collectively known as inflammatory bowel disease (IBD). This brochure answers common questions that women with these diseases may have. Symptoms of IBD can include diarrhea, abdominal pain, rectal bleeding, and fever; loss of appetite and weight loss are also common. If medications fail to control the symptoms of the disease, or if certain complications occur, surgery may be required. Yet, in spite of the physical and emotional demands of coping with IBD, most patients are able to lead full, satisfying lives. The brochure covers specific topics including the impact of IBD on menstruation, birth control and conception, dyspareunia (painful sexual intercourse), iron deficiency, pregnancy, drug therapy for IBD during pregnancy and breastfeeding, diagnostic procedures and surgery during pregnancy, pregnancy in women who have had prior bowel surgery, the genetic risks of IBD (passing along the disease to one's child), dietary recommendations for pregnant women with IBD, osteoporosis, and menopause. The brochure includes a brief description of the goals and activities of the Crohn's and Colitis Foundation of American (www.ccfa.org).
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Crohn's Disease or Ulcerative Colitis: How to Choose a Doctor and Hospital for Your Treatment Source: Cleveland, OH: Cleveland Clinic Foundation. 1998. 23 p. Contact: Available from Cleveland Clinic Foundation. Department of Nutrition Services, One Clinic Center, 9500 Euclid Avenue, Cleveland, OH 44195. (216) 444-8950. PRICE: Single copy free. Summary: Selecting a doctor and hospital for treatment of inflammatory bowel disease (IBD, including Crohn's disease and ulcerative colitis) involves making some difficult and important decisions. Patients must carefully consider where to go and what physicians and surgeons are the most qualified to treat IBD. This brochure offers information for patients with IBD, focusing on choosing a doctor and hospital for treatment. The brochure describes the difference between ulcerative colitis and Crohn's disease, how IBD is diagnosed, treatment options (including nonsurgical therapies and surgical procedures), and six points that indicate quality. The six points that patients should consider are credentials, experience, range of services, participation in research and education, patient satisfaction, and outcome indicators. In each area, the brochure offers suggested questions for patients to ask of their health care providers and facilities. Surgical options discussed include pelvic pouch surgery (which allows for nearly normal bowel movements), continent ileostomy (a conversion procedure for old style ileostomy patients to have their external pouch converted to an internal pouch), and strictureplasty (an option for some Crohn's patients, this relieves obstruction but preserves the intestine). The brochure also provides information about the Cleveland
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Clinic, the producer of the brochure and a nationally known clinic in the treatment of urologic, gynecologic, and colorectal disorders (www.ccf.org ). •
Physician's Guide to Pediatric Crohn's Disease and Ulcerative Colitis Source: New York, NY: Crohn's and Colitis Foundation of America. Boston, MA: Boston University School of Medicine. 1992. 43. Contact: Available from Crohn's and Colitis Foundation of America, Inc. 386 Park Avenue South, 17th Floor, New York, NY 10016-8804. (800) 343-3637 or (800) 932-2423 or (212) 685-3440. PRICE: Single copy free. Distribution may be limited to physicians only. Summary: The purpose of this guide is to provide basic information to primary clinicians, pediatricians, and internists, who treat patients with Crohn's disease and ulcerative colitis. As with any chronic disease, there is always a balance between the suppression of disease activity and the consequences of medical and/or surgical therapy. Topics include a review of inflammatory bowel disease (IBD) and how it affects children, clinical aspects of IBD in children, differences between Crohn's disease and ulcerative colitis in adults and children, differential diagnosis in children, medical treatment and management, surgical treatment and management, and quality of life issues. A quiz for continuing medical education credit is included. 16 charts summarize the material presented. 19 figures.
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Facts About Inflammatory Bowel Disease Source: Toronto, Canada: Crohn's and Colitis Foundation of Canada. 1997. 12 p. Contact: Available from Crohn's and Colitis Foundation of Canada. 21 St. Clair Avenue East, Suite 30, Toronto, Ontario, Canada M4T 1L9. (800) 387-1479 or (416) 920-5035. Fax (416) 929-0364. E-mail:
[email protected]. PRICE: Single copy free. Summary: This booklet describes inflammatory bowel disease (IBD), a term used to describe two similar, but distinct conditions: Crohn's disease and ulcerative colitis (UC). These diseases affect the digestive system and cause the intestines to become inflamed, form sores (ulcers), bleed easily, and scar. The booklet outlines the symptoms of IBD, the parts of the body involved, complications, and possible treatments (diet, medication, surgery). Potential complications of IBD include malnutrition and malabsorption. Nutritional therapy, which includes a combination of diet, nutritional supplements, and bowel rest is important in the treatment of IBD-related malnutrition and malabsorption. To control IBD, anti-inflammatory drugs, drugs to prevent or reduce symptoms, and drugs that treat complications are prescribed. People with Crohn's disease may need surgery to treat abscesses and fistulas, to remove an obstruction or blockage of the intestine, or to remove a piece of diseased intestine. Surgery is less common in UC than in Crohn's disease. This booklet also explains diagnostic tests, surgical procedures, and the role of the health care team. 1 figure.
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Nutrition, Diet and Inflammatory Bowel Disease Source: Toronto, Canada: Crohn's and Colitis Foundation of Canada. 1997. 8 p. Contact: Available from Crohn's and Colitis Foundation of Canada. 21 St. Clair Avenue East, Suite 30, Toronto, Ontario, Canada M4T 1L9. (800) 387-1479 or (416) 920-5035. Fax (416) 929-0364. E-mail:
[email protected]. PRICE: Single copy free. Summary: This booklet describes the relationship between nutrition and inflammatory bowel disease (IBD), a term used to describe two similar, yet distinct conditions: Crohn's
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disease and ulcerative colitis (UC). These diseases affect the digestive system and cause the intestines to become inflamed, form sores (ulcers), bleed easily, scar, and lose the normal smoothness of their inner lining. Symptoms of IBD include abdominal pain, cramping, fatigue, and diarrhea. Malabsorption refers to the reduced ability of the digestive tract to absorb nutrients. Malabsorption may happen in IBD when nutrients are lost through bleeding and diarrhea, when medications interact adversely with nutrients, or when part of the intestine is surgically removed, leaving less absorptive tissue to process ingested nutrients. A healthy diet is a key component in the treatment of IBD. The booklet concludes with a nutrition checklist to help readers determine whether they ought to consult a physician or dietitian. 1 figure. 3 tables. •
Medication for Inflammatory Bowel Disease Source: Toronto, Canada: Crohn's and Colitis Foundation of Canada. 1997. 12 p. Contact: Available from Crohn's and Colitis Foundation of Canada. 21 St. Clair Avenue East, Suite 30, Toronto, Ontario, Canada M4T 1L9. (800) 387-1479 or (416) 920-5035. Fax (416) 929-0364. E-mail:
[email protected]. PRICE: Single copy free. Summary: This booklet describes the role of medications in the management of inflammatory bowel disease (IBD), a term used to describe two similar, but distinct conditions: Crohn's disease and ulcerative colitis (UC). These diseases affect the digestive system and cause the intestines to become inflamed, form sores (ulcers), bleed easily, and scar. People with Crohn's disease or UC may take prescription or over-thecounter medications to reduce inflammation in the gastrointestinal tract, to control diarrhea and cramps, and to treat complications. This booklet describes the most commonly prescribed medications: how they work, and common (or especially serious) side effects. The brochure also discusses the role of nicotine in UC and briefly mentions medications used to treat other symptoms and problems, including hemorrhoids and anal fissures, anal itching, vitamins and minerals, and pain killers. 1 figure.
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Sexuality, Fertility, Pregnancy and Inflammatory Bowel Disease Source: Toronto, Canada: Crohn's and Colitis Foundation of Canada. 1997. 8 p. Contact: Available from Crohn's and Colitis Foundation of Canada. 21 St. Clair Avenue East, Suite 30, Toronto, Ontario, Canada M4T 1L9. (800) 387-1479 or (416) 920-5035. Fax (416) 929-0364. E-mail:
[email protected]. PRICE: Single copy free. Summary: This booklet discusses sexuality, fertility, pregnancy and inflammatory bowel disease (IBD), which is a term used to describe two similar, but distinct conditions: Crohn's disease and ulcerative colitis (UC). These diseases affect the digestive system and cause the intestines to become inflamed, form sores (ulcers), bleed easily, and scar. Abdominal cramps and diarrhea, which are common in IBD, may inhibit sexual activity. Malabsorption (which reduces the ability of the digestive tract to absorb the vitamins and minerals in food) may lead to undernourishment, weakness, or loss of energy, all of which may have an impact on the person's sexuality. Medications used to treat IBD do not particularly affect sexual desire or performance, although surgery, a common form of treatment for IBD, and postoperative recovery times do. IBD itself does not affect fertility, although the lack of proper nutrition can affect both men's and women's reproductive abilities. If IBD was controlled at the time of conception, the disease has little or no effect on the outcome of pregnancy. If the disease was active at conception, or becomes active during the pregnancy, there's a slightly increased risk of miscarriage or premature birth. Pregnancy does not increase the chance of recurrence of IBD. Good nutrition, important for all IBD patients, is especially crucial for a pregnant woman with
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IBD. Pregnant women should discuss with their physician the benefits and risks of taking IBD medications during pregnancy. 1 figure. •
Physicians' Guide to Inflammatory Bowel Disease Source: New York, NY: Crohn's and Colitis Foundation of America. 1990. 26 p. Contact: Available from Crohn's and Colitis Foundation of America, Inc. 386 Park Avenue South, 17th Floor, New York, NY 10016-8804. (800) 343-3637 or (800) 932-2423 or (212) 685-3440. PRICE: Single copy free. Summary: This booklet is aimed at increasing awareness of inflammatory bowel disease (IBD) among health care professionals, specialists, generalists, pharmacists, and nurses, by providing practical and specific information on diagnosing, treating, and managing IBD and its complications. Topics include a definition of IBD, diagnostic issues, treating the symptoms, treating the mucosal inflammation, surgical intervention, nutritional management in Crohn's disease, issues in infertility and pregnancy, and complications of IBD. Seven appendixes summarize the material presented. A quiz for continuing medical education credit is included.
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Inflammatory Bowel Diseases: Information for Patients and Their Families Source: Chicago, IL: Gastro-Intestinal Research Foundation. 1996. 17 p. Contact: Available from Gastro-Intestinal Research Foundation. 70 East Lake Street, Suite 1015, Chicago, IL 60601. (312) 332-1350. PRICE: Single copy free. Summary: This booklet was written to answer some of the questions patients often ask about inflammatory bowel diseases (IBD), including Crohn's disease and ulcerative colitis (UC). Topics include the normal digestive system, the nature of IBD, incidence, symptoms, diagnosis, treatment, and prognosis. Ulcerative colitis is an inflammation of the colon (large bowel). The inner lining of the colon is affected most severely, with vascular congestion, tiny ulcerations, and bleeding. Crohn's disease of the small intestine is an inflammation involving the entire thickness of the bowel wall. The most common area of the small intestine affected is the last segment entering the colon, known as the ileum. Diagnosis is aided by a description of the nature of the diarrhea, the type of abdominal pain, and characteristics of the rectal bleeding, in addition to a complete account of the health status and the life situation of the individual patient. The authors focus on the diagnosis of IBD as differentiated from irritable bowel syndrome (IBS). Since the causes of IBD are not known, treatment is directed at relieving the symptoms and improving and maintaining the general health of the patient physically, nutritionally, and emotionally. In most instances, IBD can be controlled and the majority of patients live a normal life, even though they may need to take medication and remain under medical supervision indefinitely. The authors hope that the booklet will reduce patient anxiety, increase understanding among patients and their families, aid in the effective implementation of treatment programs, and encourage interest in the support of the research necessary to identify the causes and subsequently the cures of these disorders. The brochure concludes with a discussion of the present basic research and clinical studies being undertaken in this area. 3 figures. (AA-M).
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Q and A. Crohn's Disease and Ulcerative Colitis: Medications Source: New York, NY: Crohn's and Colitis Foundation of America. 2002. 20 p.
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Contact: Available from Crohn's and Colitis Foundation of America (CCFA). 386 Park Avenue South, 17th Floor, New York, NY 10016-8804. (800) 932-2423. E-mail:
[email protected]. Website: www.ccfa.org. PRICE: Single copy free. Summary: This brochure answers commonly asked questions about the medications used to treat ulcerative colitis and Crohn's disease, two conditions that are collectively called inflammatory bowel disease (IBD). The goals of medical treatment are to suppress the inflammatory response to permit healing of tissue, to improve quality of life, to maintain adequate nutritional status, and to relieve the symptoms of fever, diarrhea, and abdominal pain. Several groups of drugs are used: aminosalicylates, corticosteroids, immune modifiers, and antibiotics. In general, aminosalicylate pills, enemas, and suppositories remain the first line of therapy for people with active IBD, as well as for maintaining remission. Oral aminosalicylates may also prevent Crohn's from recurring after surgery. Oral corticosteroids are usually reserved for individuals who fail to respond to aminosalicylates or who require rapid control of symptoms. Antibiotics may be beneficial in certain clinical situations. Infliximab (a biologic therapy) is appropriate for those with Crohn's disease who fail to respond to conventional medical therapy or who have fistulas. A final section considers the medical treatment for children and adolescents with IBD. All of the medications used for adults are also used for children, and the indications and contraindications are similar. Individualized treatment is required, however, as dosages must be tailored for children, who are of smaller size, and adolescents, who are moving through a period of both physical and psychosocial growth and development. •
Living with Inflammatory Bowel Disease: Your Illness and Its Treatment Source: San Bruno, CA: StayWell Company. 1998. 16 p. Contact: Available from StayWell Company. Order Department, 1100 Grundy Lane, San Bruno, CA 94066-9821. (800) 333-3032. Fax (650) 244-4512. PRICE: $1.60 plus shipping and handling; bulk copies available. Order number 11003. Summary: This brochure describes inflammatory bowel disease (IBD), characterized by inflammation (irritation and swelling) of the digestive tract. IBD has two subtypes: ulcerative colitis (UC) and Crohn's disease (CD). Ulcerative colitis occurs in the rectum and sometimes in the colon; Crohn's disease can occur anywhere from the mouth to the anus, but usually affects the last part of the small intestine. The brochure describes how the digestive tract works, how IBD affects the digestive tract, diagnosing and monitoring IBD, treating IBD with medication, managing daily life, managing nutrition, and surgery for IBD. The symptoms of Crohn's can include abdominal pain and bloating after meals, sores in the anal area, high fever and chills, loss of appetite (possible weight loss), bloody diarrhea, and nausea or vomiting. Diagnostic tests that may be used to confirm Crohn's disease include barium enema, upper GI series, and small bowel series, endoscopy, blood or stool tests, and CT scan. The symptoms of UC can include frequent, loose bowel movements; blood and pus in stools; rectal bleeding; feeling of incomplete bowel movement; urgency; severe straining with bowel movement; joint pain; and rectal pain that comes and goes. Diagnostic tests that may be used to confirm UC include endoscopy, biopsy, blood or stool tests, and xrays of the colon. Drug therapy for IBD can include antiinflammatory agents, corticosteroids, immunosuppressive agents, and antibiotics. Readers are advised to monitor their dietary habits and take note of which foods seem to be problematic. Surgical options described include limited bowel resection, ileoanal pouch, proctocolectomy with permanent ileostomy, continent ileostomy, strictureplasty, and anal fistula surgery; each technique is illustrated with a simple line drawing. The brochure also explains what patients can expect before and
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after surgery for IBD. The brochure encourages readers to work closely with their health care providers and to seek out support groups to talk with others who are dealing with IBD. The toll free telephone numbers of the Crohn's and Colitis Foundation (800-9322423) and the United Ostomy Association (800-826-0826) are provided. The brochure is illustrated with full color drawings. 19 figures. •
Ulcerative Colitis: Understanding This Chronic Illness Source: San Bruno, CA: StayWell Company. 2003. [2 p.]. Contact: StayWell Company: Krames Health and Safety Education. 780 Township Line Road, Yardley, PA 19067. (800) 333-3032. Fax (415) 244-4512. E-mail:
[email protected]. Website: www.staywell.com. PRICE: $ 20.95 for 50 copies; plus shipping and handling; bulk copies available. Order number 9784. Summary: This brochure describes ulcerative colitis (UC), a type of inflammatory bowel disease (IBD). The symptoms of UC can include frequent, loose bowel movements; blood and pus in stools; rectal bleeding; feeling of incomplete bowel movement; urgency; severe straining with bowel movement; joint pain; and rectal pain that comes and goes. Diagnostic tests that may be used to confirm UC include endoscopy, biopsy, blood or stool tests, and xrays of the colon. The brochure reviews treatment options, including medications, dietary strategies, and surgery. One sidebar reviews the anatomy of the digestive tract and how UC can impact the digestive tract. UC is inflammation (irritation and swelling) that occurs in the rectum. It can also affect the colon, but affects only the inside layers of tissue lining the rectum and colon. The brochure concludes by encouraging readers to work closely with their health care providers and to seek out support groups to talk with others who are dealing with IBD. The toll free telephone number of the Crohn's and Colitis Foundation (800-932-2423) is provided. The brochure is illustrated with full color drawings. 6 figures.
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Q and A. About Ulcerative Colitis Source: New York, NY: Crohn's and Colitis Foundation of America, Inc. (CCFA). 2002. 12 p. Contact: Available from Crohn's and Colitis Foundation of America, Inc. (CCFA). 386 Park Avenue South, 17th Floor, New York, NY 10016-8804. (800) 343-3637 or (800) 9322423 or (212) 685-3440. Fax (212) 779-4098. Website: www.ccfa.org. E-mail:
[email protected] PRICE: Single copy free. Summary: This brochure familiarizes readers with ulcerative colitis, an inflammatory disease of the colon that is characterized by inflammation and ulceration of the innermost lining of the colon. Written in a question and answer format, the brochure describes ulcerative colitis (UC) and covers the incidence of UC, the role of genetics, the symptoms of UC, diagnostic tests used to confirm the condition, medications used to treat UC, the role of surgery in treatment, the importance of nutrition, the role of emotional stress as a trigger for attacks of UC, considerations of everyday life with UC, and theories as to the causes of UC. The booklet concludes with a brief description of the activities of the Crohn's and Colitis Foundation of America (CCFA) and a glossary of terms related to IBD. 1 figure.
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Q and A. Crohn's Disease and Ulcerative Colitis: A Teacher's Guide Source: New York, NY: Crohn's and Colitis Foundation of America, Inc. 2002. 8 p.
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Contact: Available from Crohn's and Colitis Foundation of America, Inc. (CCFA). 386 Park Avenue South, 17th Floor, New York, NY 10016-8804. (800) 343-3637 or (800) 9322423 or (212) 685-3440. Fax (212) 779-4098. Website: www.ccfa.org. E-mail:
[email protected] PRICE: Single copy free. Summary: This brochure is designed to help teachers understand the needs of students and young people who have Crohn's disease or ulcerative colitis. It provides a brief description and explanation of these two kinds of inflammatory bowel diseases (IBD's) and covers the problems of coping with them and their treatment. Potential problems and issues for students include isolation and depression; absence from school; frequent and sudden need to leave the classroom for the bathroom; participation in class trips and sports; and taking medication during school hours. The brochure emphasizes the often crucial role that teachers play in identifying exacerbations of IBD's, and recommends direct communication with medical personnel and parents •
ABC's of Pediatric Inflammatory Bowel Disease Source: Newton, MA: Pediatric Crohn's and Colitis Association, Inc. 199x. 8 p. Contact: Available from Pediatric Crohn's and Colitis Association, Inc. Box 188, Newton, MA 02168. (617) 244-6678. PRICE: Single copy free. Summary: This brochure provides information for the parents of children newly diagnosed with inflammatory bowel disease (IBD), either in the form of Crohn's disease or ulcerative colitis. Written in a question-and-answer format, the brochure covers topics including a definition of IBD; the incidence and prevalence of IBD in children; the cause of IBD; medical tests that might be indicated; how the child's growth can be affected by IBD; treatment considerations; the emotional impact of IBD on a child; how IBD may affect the child at school; and how IBD affects family life. One chart summarizes the physical, social, emotional, and family issues that may exist for children with IBD and their families. The brochure concludes with a glossary of terms and a list of the scientific advisory board members of the association.
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Inflammatory Bowel Disease Source: Bethesda, MD: American Gastroenterological Association. 1996. 5 p. Contact: Available from GIDH-AGA Patient Education Center. P.O. Box 1274, West Caldwell, NJ 07007-9562. PRICE: 25 copies free to health care professionals for distribution to patients. Summary: This brochure provides patients with basic information about inflammatory bowel disease (IBD), a term that refers to both ulcerative colitis (UC) and Crohn's disease. Ulcerative colitis causes inflammation of the lining of the large intestine. Crohn's disease causes inflammation of the lining and wall of the large and or small intestine. When inflamed, the lining of the intestinal wall is red and swollen, becomes ulcerated, and bleeds. The brochure describes the normal function of the digestive system, the causes of IBD, the symptoms of UC, diagnostic tests used to confirm UC, the risk of colon cancer in people with UC, the symptoms of Crohn's disease, the complications associated with Crohn's disease (intestinal blockage, fistulas), treatment options for IBD, the role of nutrition and food choices, coping with IBD, and determining when surgery is needed. The goal of nutritional management for people with IBD is to modify the diet to decrease gastrointestinal symptoms while maintaining adequate nutrient intake. The author stresses that, although IBD is a chronic disease that has periods of remission and relapse, most people have a normal life span and a good
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quality of life. The brochure concludes with a glossary of terms. 4 figures. 3 references. (AA-M). •
Crohn's Disease, Ulcerative Colitis, and School Source: Newton, MA: Pediatric Crohn's and Colitis Association, Inc. 199x. 6 p. Contact: Available from Pediatric Crohn's and Colitis Association, Inc. Box 188, Newton, MA 02168-0002. (617) 244-6678. PRICE: Single copy free. Summary: This brochure reviews the school-related problems that a young person with inflammatory bowel disease (IBD) may face. Filled with numerous quotes from children with IBD, the brochure discusses the physical ups and downs of IBD; making-up missed school work; changes in appearance; mood swings; physical activities; diet; meeting needs during class time; and activities outside the classroom. The brochure emphasizes that the support, encouragement, and understanding of teachers, friends, and family can make a significant difference in helping children and teenagers to have a productive and satisfying school experience.
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Inflammatory Bowel Disease: Clinical Features and Comparison to the Functional Bowel Disorders Source: Milwaukee, WI: International Foundation for Functional Gastrointestinal Disorders (IFFGD). 1996. 2 p. Contact: Available from International Foundation for Functional Gastrointestinal Disorders (IFFGD). P.O. Box 170864, Milwaukee, WI 53217. (888) 964-2001 or (414) 9641799. Fax (414) 964-7176. E-mail:
[email protected]. Website: www.iffgd.org. PRICE: Single copy free; bulk copies available. Summary: This fact sheet summarizes the clinical features of inflammatory bowel disease (IBD) and compares IBD to the functional bowel disorders. The inflammatory bowel diseases cause the traditional gastrointestinal symptoms, but may also cause fever, chills, night sweats, weight loss, and inflammation within various organs of the body (oral cavity, eye, skin, liver, joints, ileum, and colon). The author describes the symptoms associated with ulcerative colitis (UC) and Crohn's disease and current treatment options. The fact sheet gives the toll free telephone number of the Crohn's and Colitis Foundation of America (800-932-2423).
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Q and A. Crohn's Disease and Ulcerative Colitis: A Guide for Children and Teenagers Source: New York, NY: Crohn's and Colitis Foundation of America, Inc. 2002. 8 p. Contact: Available from Crohn's and Colitis Foundation of America, Inc. (CCFA). 386 Park Avenue South, 17th Floor, New York, NY 10016-8804. (800) 343-3637 or (800) 9322423 or (212) 685-3440. Fax (212) 779-4098. Website: www.ccfa.org. E-mail:
[email protected] PRICE: Single copy free. Summary: This pamphlet, written for children and teenagers, discusses Crohn's disease and ulcerative colitis (known together as inflammatory bowel disease or IBD's). The brochure explains the possible causes of IBD; how IBD affects the gastrointestinal tract; treatment; types of medicine and their side effects; the role of diet and nutrition in treatment; physical growth and IBD; tests used to diagnose and monitor IBD; and surgery. The authors also discuss attitudes and habits that may help children and teenagers with IBD to feel better.
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•
Q and A. Crohn's Disease and Ulcerative Colitis: A Parent's Guide Source: New York, NY: Crohn's and Colitis Foundation of America. 2002. 20 p. Contact: Available from Crohn's and Colitis Foundation of America, Inc. (CCFA). 386 Park Avenue South, 17th Floor, New York, NY 10016-8804. (800) 343-3637 or (800) 9322423 or (212) 685-3440. Fax (212) 779-4098. Website: www.ccfa.org. E-mail:
[email protected] PRICE: Single copy free. Summary: This pamphlet, written for parents, answers questions about Crohn's disease and ulcerative colitis (together known as inflammatory bowel disease, or IBD) in children. Written in question-and-answer format, the brochure describes the causes, symptoms, and prevalence of IBD; diagnostic tests; inheritance of IBD; the role of surgery; eating habits and nutrition; and special foods and vitamins. The authors point out that children do not grown IBD but that many people enjoy long periods of remission. The common medications used to treat IBD are described in detail. The authors also discuss the emotional and social challenges sometimes presented by IBD's and give parents hints to help their children cope. A glossary of terms is appended.
•
Q and A. Crohn's Disease and Ulcerative Colitis: Emotional Factors Source: New York, NY: Crohn's and Colitis Foundation of America, Inc. 2002. 8 p. Contact: Available from Crohn's and Colitis Foundation of America, Inc. (CCFA). 386 Park Avenue South, 17th Floor, New York, NY 10016-8804. (800) 343-3637 or (800) 9322423 or (212) 685-3440. Fax (212) 779-4098. Website: www.ccfa.org. E-mail:
[email protected] PRICE: Single copy free. Summary: This pamphlet, written in question-and-answer format, answers some of the most commonly asked questions about the role of emotional factors in Crohn's disease and ulcerative colitis (known together as inflammatory bowel disease or IBD's). The authors point out that IBD's are biological disorders of unknown origin and are not caused by tension or anxiety, or more common in people with certain personality types. The brochure clarifies the difference between IBD's and a completely different condition, irritable bowel syndrome, the cause of which does seem to be related to emotional factors. The authors suggest that this brochure be used to explain to friends and family that IBD's are not caused by being 'overly emotional'. Specific topics addressed include the possible role of severe chronic stress in increasing inflammation; emotional difficulties caused by the challenges of living with an IBD; feelings of guilt; ways to cope with fears of relapse, attacks in public places, and travel; medications used to cope with psychological difficulties; psychiatric consultation; the special concerns of young people; the emotional effects of ileostomy surgery; and discussion of attitudes which may help IBD patients to better cope with these diseases.
•
New Surgical Options for the Treatment of Ulcerative Colitis: Questions and Answers Source: Arlington Heights, IL: American Society of Colon and Rectal Surgeons. 1996. [2 p.]. Contact: Available from American Society of Colon and Rectal Surgeons. 85 West Algonquin Road, Suite 550, Arlington Heights, IL 60005. (800) 791-0001 or (847) 2909184. Fax (847) 290-9203. E-mail:
[email protected]. Website: www.fascrs.org. PRICE: Full-text available online at no charge; Single copy free; bulk copies available.
Patient Resources
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Summary: This patient education brochure describes new surgical treatments for ulcerative colitis (UC), an inflammation of the lining of the large bowel (colon). Symptoms of UC include rectal bleeding, diarrhea, abdominal cramps, weight loss, and fever. In addition, patients who have had extensive UC for many years are at an increased risk to develop large bowel cancer. Initial treatment of UC is medical, using antibiotics and antiinflammatory medications. Surgery is indicated for patients who have life threatening complications of inflammatory bowel diseases, such as massive bleeding, perforation, or infection. It may also be necessary for those who have the chronic form of the disease, which fails medical therapy. Historically, the standard operation for UC has been removal of the entire colon, rectum, and anus; this procedure is called a proctocolectomy. This operation requires creation of a Brooke ileostomy and chronic use of an appliance on the abdominal wall to collect waste from the bowel. Another option is the continent ileostomy, in which an internal reservoir is created. The bowel still comes through the abdominal wall, but an external appliance is not required. This option eliminates the risks of cancer and risks of recurrent persistent colitis, but the internal reservoir may begin to leak and require another surgical procedure to revise the reservoir. Some patients may be treated by removal of the colon, with preservation of the rectum and anus. The small bowel can then be reconnected to the rectum and the person retains continence. This avoids the ileostomy, but the risks of ongoing active colitis, increased stool frequency, urgency, and cancer in the retained rectum remain. The brochure then describes the ileoanal procedure, a newer alternative for the management of UC in which all of the colon and rectum are removed, but the anal canal is preserved. The rectum is replaced with a small bowel, which is fashioned to form a small pouch. The pouch acts as a reservoir to help decrease the stool frequency. This maintains a normal route of defecation, but most patients experience 5 to 10 bowel movements per day. The brochure concludes by encouraging readers to educate themselves about these alternatives, so that they can take part in the decisions about their own health care and pursue the highest quality of life. 8 figures. •
Learning to Live with Inflammatory Bowel Disease Source: American Family Physician. 57(1): 71-72. January 1, 1998. Contact: Available from American Academy of Family Physicians. 11400 Tomahawk Creek Parkway, Leawood, KS 66211-2672. (800) 274-2237. Website: www.aafp.org. Also available at http://www.aafp.org/healthinfo. Summary: This patient education fact sheet provides a general overview of managing inflammatory bowel disease (IBD). IBD is a group of disorders that cause the intestines to become inflamed. Symptoms can include abdominal cramping and pain, diarrhea, weight loss, and bleeding from the intestines. The fact sheet describes Crohn's disease and ulcerative colitis, two types of IBD. The fact sheet also describes the causes of IBD, diagnostic considerations, treatment options, and where to obtain more information about IBD. Treatment relieves the inflammation through the use of anti-inflammatory medicines. A healthy diet and adequate rest can also be part of therapy for IBD. For severe symptoms, such as diarrhea, fever, or vomiting, patients may need to be hospitalized to be rehydrated and treated with intravenous medications. Also, because Crohn's disease and ulcerative colitis keep coming back and their symptoms cannot be predicted ahead of time, patients with these illnesses can become depressed. Sometimes antidepressant medications are prescribed. The fact sheet notes the contact information for the Crohn's and Colitis Foundation of America and the National Digestive Diseases Information Clearinghouse. The fact sheet is designed to be copied and distributed to patients by family care providers.
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•
Ulcerative Colitis Source: St. Albans, England: National Association for Colitis and Crohn's Disease (NACC). 1999. 16 p. Contact: Available from National Association for Colitis and Crohn's Disease (NACC). 4 Beaumont House, Sutton Road, St. Albans, Hertfordshire, AL1 5HH. 01727 844296. Email:
[email protected]. Website: www.nacc.org.uk. PRICE: Single copy free to members. Summary: Ulcerative colitis (UC) is a disease of the lining of the large bowel or colon. This booklet, written for people newly diagnosed with UC, offers an overview of the disease and its treatment. The booklet first describes how the colon works within the digestive system, then discusses how UC affects the working of the colon, the symptoms of the disease, how UC is diagnosed, the causes of UC, dietary impact on the disease, treatment options, drug therapy (antiinflammatory agents, antidiarrheals, analgesics, anemia treatments, nutritional aids), and surgical options (proctocolectomy and ileostomy, colectomy with ileostomy and mucous fistula, colectomy and ileorectal anastomosis, and proctocolectomy with ileal reservoir or pouch). Although the symptoms and signs of UC can disappear for many years, and even for a lifetime, without treatment, the more usual course is one of periodic flareups. The condition is normally managed by drugs, but surgery may become necessary under some circumstances. The booklet concludes with a list of commonly asked questions and answers, covering prognosis, the interrelationship between UC and bowel cancer, UC and pregnancy, the epidemiology of UC, and the role of heredity in UC. 5 figures. 2 tables.
The National Guideline Clearinghouse™ The National Guideline Clearinghouse™ offers hundreds of evidence-based clinical practice guidelines published in the United States and other countries. You can search this site located at http://www.guideline.gov/ by using the keyword “ulcerative colitis” (or synonyms). The following was recently posted: •
Management of ulcerative colitis Source: Society for Surgery of the Alimentary Tract, Inc - Medical Specialty Society; 2000 (revised 2001); 4 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2967&nbr=2193&a mp;string=ulcerative+AND+colitis Healthfinder™
Healthfinder™ is sponsored by the U.S. Department of Health and Human Services and offers links to hundreds of other sites that contain healthcare information. This Web site is located at http://www.healthfinder.gov. Again, keyword searches can be used to find guidelines. The following was recently found in this database:
Patient Resources
•
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Ulcerative Colitis Summary: In ulcerative colitis, the inner lining of the large intestine (colon or bowel) and rectum becomes inflamed. Source: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=734 The NIH Search Utility
The NIH search utility allows you to search for documents on over 100 selected Web sites that comprise the NIH-WEB-SPACE. Each of these servers is “crawled” and indexed on an ongoing basis. Your search will produce a list of various documents, all of which will relate in some way to ulcerative colitis. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. PEDBASE Similar to NORD, PEDBASE covers relatively rare disorders, limited mainly to pediatric conditions. PEDBASE was designed by Dr. Alan Gandy. To access the database, which is more oriented to researchers than patients, you can view the current list of health topics covered at the following Web site: http://www.icondata.com/health/pedbase/pedlynx.htm. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
•
Family Village: http://www.familyvillage.wisc.edu/specific.htm
•
Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
•
Med Help International: http://www.medhelp.org/HealthTopics/A.html
•
Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
•
Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
•
WebMDHealth: http://my.webmd.com/health_topics
Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to ulcerative colitis. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with ulcerative colitis.
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The National Health Information Center (NHIC) The National Health Information Center (NHIC) offers a free referral service to help people find organizations that provide information about ulcerative colitis. For more information, see the NHIC’s Web site at http://www.health.gov/NHIC/ or contact an information specialist by calling 1-800-336-4797. Directory of Health Organizations The Directory of Health Organizations, provided by the National Library of Medicine Specialized Information Services, is a comprehensive source of information on associations. The Directory of Health Organizations database can be accessed via the Internet at http://www.sis.nlm.nih.gov/Dir/DirMain.html. It is composed of two parts: DIRLINE and Health Hotlines. The DIRLINE database comprises some 10,000 records of organizations, research centers, and government institutes and associations that primarily focus on health and biomedicine. To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/. Simply type in “ulcerative colitis” (or a synonym), and you will receive information on all relevant organizations listed in the database. Health Hotlines directs you to toll-free numbers to over 300 organizations. You can access this database directly at http://www.sis.nlm.nih.gov/hotlines/. On this page, you are given the option to search by keyword or by browsing the subject list. When you have received your search results, click on the name of the organization for its description and contact information. The Combined Health Information Database Another comprehensive source of information on healthcare associations is the Combined Health Information Database. Using the “Detailed Search” option, you will need to limit your search to “Organizations” and “ulcerative colitis”. Type the following hyperlink into your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “ulcerative colitis” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months. The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “ulcerative colitis” (or a synonym) into the search box, and click “Submit Query.”
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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.
Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.27
Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.
Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of
27
Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.
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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)28: •
Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/
•
Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)
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Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm
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California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html
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California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html
•
California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html
•
California: Gateway Health Library (Sutter Gould Medical Foundation)
•
California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
•
California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
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California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
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California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
•
California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
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California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
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California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
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California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
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Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
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Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/
•
Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/
28
Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
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•
Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
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Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm
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Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html
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Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm
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Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp
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Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/
•
Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm
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Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html
•
Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/
•
Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm
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Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/
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Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/
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Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/
•
Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm
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Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html
•
Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm
•
Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/
•
Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/
•
Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10
•
Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/
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•
Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html
•
Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp
•
Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp
•
Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/
•
Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html
•
Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm
•
Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp
•
Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/
•
Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html
•
Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/
•
Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm
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Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/
•
Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html
•
Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm
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Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330
•
Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)
•
National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html
•
National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/
•
National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/
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•
Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
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New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
•
New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
•
New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
•
New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
•
New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
•
New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/
•
New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html
•
New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/
•
Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm
•
Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp
•
Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/
•
Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/
•
Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml
•
Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html
•
Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html
•
Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml
•
Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp
•
Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm
•
Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/
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•
South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp
•
Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/
•
Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/
•
Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72
365
ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •
ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html
•
MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
•
Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
•
Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html
•
On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
•
Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp
•
Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm
Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a). The NIH suggests the following Web sites in the ADAM Medical Encyclopedia when searching for information on ulcerative colitis: •
Basic Guidelines for Ulcerative Colitis Chlamydia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001345.htm Neoplasm Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001310.htm TB Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000077.htm Ulcerative colitis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000250.htm
•
Signs & Symptoms for Ulcerative Colitis Abdominal distention Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003122.htm
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Abdominal pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003120.htm Abdominal sounds Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003137.htm Diarrhea Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003126.htm Erythema Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003220.htm Fever Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003090.htm Gastrointestinal bleeding Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003133.htm Hepatomegaly Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003275.htm Joint pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003261.htm Nausea and vomiting Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003117.htm Nausea and vomiting Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003117.htm Stools - foul smelling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003132.htm Stress Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003211.htm Tenesmus Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003131.htm Ulcers Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003228.htm Vomiting Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003117.htm Weight loss Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003107.htm •
Diagnostics and Tests for Ulcerative Colitis Albumin Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003480.htm
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Barium enema Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003817.htm Biopsy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003416.htm Colonoscopy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003886.htm Liver function tests Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003436.htm Radiography Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003337.htm Sedimentation rate Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003638.htm Sigmoidoscopy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003885.htm •
Surgery and Procedures for Ulcerative Colitis Colectomy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002941.htm
•
Background Topics for Ulcerative Colitis Acute Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002215.htm Chronic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002312.htm Incidence Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002387.htm Respiratory Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002290.htm
Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •
Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical
•
MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html
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•
Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/
•
Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine
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ULCERATIVE COLITIS DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 6-Mercaptopurine: An antimetabolite antineoplastic agent with immunosuppressant properties. It interferes with nucleic acid synthesis by inhibiting purine metabolism and is used, usually in combination with other drugs, in the treatment of or in remission maintenance programs for leukemia. [NIH] Abdomen: That portion of the body that lies between the thorax and the pelvis. [NIH] Abdominal: Having to do with the abdomen, which is the part of the body between the chest and the hips that contains the pancreas, stomach, intestines, liver, gallbladder, and other organs. [NIH] Abdominal Cramps: Abdominal pain due to spasmodic contractions of the bowel. [NIH] Abdominal Pain: Sensation of discomfort, distress, or agony in the abdominal region. [NIH] Aberrant: Wandering or deviating from the usual or normal course. [EU] Abscess: Accumulation of purulent material in tissues, organs, or circumscribed spaces, usually associated with signs of infection. [NIH] Acatalasia: A rare autosomal recessive disorder resulting from the absence of catalase activity. Though usually asymptomatic, a syndrome of oral ulcerations and gangrene may be present. [NIH] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] Accommodation: Adjustment, especially that of the eye for various distances. [EU] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acute Disease: Disease having a short and relatively severe course. [NIH] Acute lymphoblastic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow. Also called acute lymphocytic leukemia. [NIH] Acute lymphocytic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow. Also called acute lymphoblastic leukemia. [NIH] Acute renal: A condition in which the kidneys suddenly stop working. In most cases, kidneys can recover from almost complete loss of function. [NIH] Acute-Phase Proteins: Proteins that are secreted into the blood in increased or decreased quantities by hepatocytes in response to trauma, inflammation, or disease. These proteins can serve as inhibitors or mediators of the inflammatory processes. Certain acute-phase proteins have been used to diagnose and follow the course of diseases or as tumor markers. [NIH]
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Acyl: Chemical signal used by bacteria to communicate. [NIH] Adaptation: 1. The adjustment of an organism to its environment, or the process by which it enhances such fitness. 2. The normal ability of the eye to adjust itself to variations in the intensity of light; the adjustment to such variations. 3. The decline in the frequency of firing of a neuron, particularly of a receptor, under conditions of constant stimulation. 4. In dentistry, (a) the proper fitting of a denture, (b) the degree of proximity and interlocking of restorative material to a tooth preparation, (c) the exact adjustment of bands to teeth. 5. In microbiology, the adjustment of bacterial physiology to a new environment. [EU] Adenine: A purine base and a fundamental unit of adenine nucleotides. [NIH] Adenocarcinoma: A malignant epithelial tumor with a glandular organization. [NIH] Adenoma: A benign epithelial tumor with a glandular organization. [NIH] Adenomatous Polyposis Coli: An autosomal dominant polyposis syndrome in which the colon contains few to thousands of adenomatous polyps, often occurring by age 15 to 25. [NIH]
Adenosine: A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. [NIH] Adenovirus: A group of viruses that cause respiratory tract and eye infections. Adenoviruses used in gene therapy are altered to carry a specific tumor-fighting gene. [NIH] Adenylate Cyclase: An enzyme of the lyase class that catalyzes the formation of cyclic AMP and pyrophosphate from ATP. EC 4.6.1.1. [NIH] Adherens Junctions: Anchoring points where the cytoskeleton of neighboring cells are connected to each other. They are composed of specialized areas of the plasma membrane where bundles of microfilaments attach to the membrane through the transmembrane linkers, cadherins, which in turn attach through their extracellular domains to cadherins in the neighboring cell membranes. In sheets of cells, they form into adhesion belts (zonula adherens) that go all the way around a cell. [NIH] Adipocytes: Fat-storing cells found mostly in the abdominal cavity and subcutaneous tissue. Fat is usually stored in the form of tryglycerides. [NIH] Adipose Tissue: Connective tissue composed of fat cells lodged in the meshes of areolar tissue. [NIH] Adjunctive Therapy: Another treatment used together with the primary treatment. Its purpose is to assist the primary treatment. [NIH] Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [NIH] Adjuvant: A substance which aids another, such as an auxiliary remedy; in immunology, nonspecific stimulator (e.g., BCG vaccine) of the immune response. [EU] Adjuvant Therapy: Treatment given after the primary treatment to increase the chances of a cure. Adjuvant therapy may include chemotherapy, radiation therapy, or hormone therapy. [NIH]
Adolescence: The period of life beginning with the appearance of secondary sex characteristics and terminating with the cessation of somatic growth. The years usually referred to as adolescence lie between 13 and 18 years of age. [NIH] Adoptive Transfer: Form of passive immunization where previously sensitized immunologic agents (cells or serum) are transferred to non-immune recipients. When transfer of cells is used as a therapy for the treatment of neoplasms, it is called adoptive
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immunotherapy (immunotherapy, adoptive). [NIH] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [NIH] Adrenal Glands: Paired glands situated in the retroperitoneal tissues at the superior pole of each kidney. [NIH] Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Adrenergic Uptake Inhibitors: Drugs that block the transport of adrenergic transmitters into axon terminals or into storage vesicles within terminals. The tricyclic antidepressants (antidepressive agents, tricyclic) and amphetamines are among the therapeutically important drugs that may act via inhibition of adrenergic transport. Many of these drugs also block transport of serotonin. [NIH] Adsorption: The condensation of gases, liquids, or dissolved substances on the surfaces of solids. It includes adsorptive phenomena of bacteria and viruses as well as of tissues treated with exogenous drugs and chemicals. [NIH] Adsorptive: It captures volatile compounds by binding them to agents such as activated carbon or adsorptive resins. [NIH] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [NIH] Aerosol: A solution of a drug which can be atomized into a fine mist for inhalation therapy. [EU]
Aetiology: Study of the causes of disease. [EU] Afferent: Concerned with the transmission of neural impulse toward the central part of the nervous system. [NIH] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the complex. 5. In immunology, a thermodynamic expression of the strength of interaction between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]
Age Groups: Persons classified by age from birth (infant, newborn) to octogenarians and older (aged, 80 and over). [NIH] Age of Onset: The age or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual. [NIH] Age-Adjusted: Summary measures of rates of morbidity or mortality in a population using
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statistical procedures to remove the effect of age differences in populations that are being compared. Age is probably the most important and the most common variable in determining the risk of morbidity and mortality. [NIH] Aged, 80 and Over: A person 80 years of age and older. [NIH] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] Agoraphobia: Obsessive, persistent, intense fear of open places. [NIH] Agranulocytosis: A decrease in the number of granulocytes (basophils, eosinophils, and neutrophils). [NIH] Airway: A device for securing unobstructed passage of air into and out of the lungs during general anesthesia. [NIH] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Alertness: A state of readiness to detect and respond to certain specified small changes occurring at random intervals in the environment. [NIH] Alexia: The inability to recognize or comprehend written or printed words. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU] Alkaline: Having the reactions of an alkali. [EU] Alkaline Phosphatase: An enzyme that catalyzes the conversion of an orthophosphoric monoester and water to an alcohol and orthophosphate. EC 3.1.3.1. [NIH] Alkalinization: The process by which a substance becomes an alkali. An alkali is the opposite of an acid. [NIH] Alkaloid: A member of a large group of chemicals that are made by plants and have nitrogen in them. Some alkaloids have been shown to work against cancer. [NIH] Alkylating Agents: Highly reactive chemicals that introduce alkyl radicals into biologically active molecules and thereby prevent their proper functioning. Many are used as antineoplastic agents, but most are very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. They have also been used as components in poison gases. [NIH]
Allantois: An embryonic diverticulum of the hindgut of reptiles, birds, and mammals; in man its blood vessels give rise to those of the umbilical cord. [NIH] Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] Allergen: An antigenic substance capable of producing immediate-type hypersensitivity (allergy). [EU] Allergic Rhinitis: Inflammation of the nasal mucous membrane associated with hay fever;
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fits may be provoked by substances in the working environment. [NIH] Allogeneic: Taken from different individuals of the same species. [NIH] Allograft: An organ or tissue transplant between two humans. [NIH] Allylamine: Possesses an unusual and selective cytotoxicity for vascular smooth muscle cells in dogs and rats. Useful for experiments dealing with arterial injury, myocardial fibrosis or cardiac decompensation. [NIH] Alopecia: Absence of hair from areas where it is normally present. [NIH] Alpha Particles: Positively charged particles composed of two protons and two neutrons, i.e., helium nuclei, emitted during disintegration of very heavy isotopes; a beam of alpha particles or an alpha ray has very strong ionizing power, but weak penetrability. [NIH] Alpha-1: A protein with the property of inactivating proteolytic enzymes such as leucocyte collagenase and elastase. [NIH] Alternative medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Aluminum: A metallic element that has the atomic number 13, atomic symbol Al, and atomic weight 26.98. [NIH] Alveoli: Tiny air sacs at the end of the bronchioles in the lungs. [NIH] Amebiasis: Infection with any of various amebae. It is an asymptomatic carrier state in most individuals, but diseases ranging from chronic, mild diarrhea to fulminant dysentery may occur. [NIH] Ameliorating: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Amine: An organic compound containing nitrogen; any member of a group of chemical compounds formed from ammonia by replacement of one or more of the hydrogen atoms by organic (hydrocarbon) radicals. The amines are distinguished as primary, secondary, and tertiary, according to whether one, two, or three hydrogen atoms are replaced. The amines include allylamine, amylamine, ethylamine, methylamine, phenylamine, propylamine, and many other compounds. [EU] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Amino Acid Substitution: The naturally occurring or experimentally induced replacement of one or more amino acids in a protein with another. If a functionally equivalent amino acid is substituted, the protein may retain wild-type activity. Substitution may also diminish or eliminate protein function. Experimentally induced substitution is often used to study enzyme activities and binding site properties. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Aminosalicylic Acids: A group of 2-hydroxybenzoic acids that can be substituted by amino
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groups at any of the 3-, 4-, 5-, or 6-positions. [NIH] Amino-terminal: The end of a protein or polypeptide chain that contains a free amino group (-NH2). [NIH] Ammonia: A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. [NIH] Amnion: The extraembryonic membrane which contains the embryo and amniotic fluid. [NIH]
Amphetamines: Analogs or derivatives of amphetamine. Many are sympathomimetics and central nervous system stimulators causing excitation, vasopression, bronchodilation, and to varying degrees, anorexia, analepsis, nasal decongestion, and some smooth muscle relaxation. [NIH] Amplification: The production of additional copies of a chromosomal DNA sequence, found as either intrachromosomal or extrachromosomal DNA. [NIH] Ampulla: A sac-like enlargement of a canal or duct. [NIH] Amyloid: A general term for a variety of different proteins that accumulate as extracellular fibrils of 7-10 nm and have common structural features, including a beta-pleated sheet conformation and the ability to bind such dyes as Congo red and thioflavine (Kandel, Schwartz, and Jessel, Principles of Neural Science, 3rd ed). [NIH] Amyloidosis: A group of diseases in which protein is deposited in specific organs (localized amyloidosis) or throughout the body (systemic amyloidosis). Amyloidosis may be either primary (with no known cause) or secondary (caused by another disease, including some types of cancer). Generally, primary amyloidosis affects the nerves, skin, tongue, joints, heart, and liver; secondary amyloidosis often affects the spleen, kidneys, liver, and adrenal glands. [NIH] Anaerobic: 1. Lacking molecular oxygen. 2. Growing, living, or occurring in the absence of molecular oxygen; pertaining to an anaerobe. [EU] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Anal: Having to do with the anus, which is the posterior opening of the large bowel. [NIH] Anal Fissure: A small tear in the anus that may cause itching, pain, or bleeding. [NIH] Anal Fistula: A channel that develops between the anus and the skin. Most fistulas are the result of an abscess (infection) that spreads to the skin. [NIH] Analgesic: An agent that alleviates pain without causing loss of consciousness. [EU] Analog: In chemistry, a substance that is similar, but not identical, to another. [NIH] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] Analytes: A component of a test sample the presence of which has to be demonstrated. The term "analyte" includes where appropriate formed from the analyte during the analyses. [NIH]
Anaphylactic: Pertaining to anaphylaxis. [EU] Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but
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shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anaphylaxis: An acute hypersensitivity reaction due to exposure to a previously encountered antigen. The reaction may include rapidly progressing urticaria, respiratory distress, vascular collapse, systemic shock, and death. [NIH] Anaplasia: Loss of structural differentiation and useful function of neoplastic cells. [NIH] Anastomosis: A procedure to connect healthy sections of tubular structures in the body after the diseased portion has been surgically removed. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Androgens: A class of sex hormones associated with the development and maintenance of the secondary male sex characteristics, sperm induction, and sexual differentiation. In addition to increasing virility and libido, they also increase nitrogen and water retention and stimulate skeletal growth. [NIH] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Anergy: Absence of immune response to particular substances. [NIH] Anesthesia: A state characterized by loss of feeling or sensation. This depression of nerve function is usually the result of pharmacologic action and is induced to allow performance of surgery or other painful procedures. [NIH] Anesthetics: Agents that are capable of inducing a total or partial loss of sensation, especially tactile sensation and pain. They may act to induce general anesthesia, in which an unconscious state is achieved, or may act locally to induce numbness or lack of sensation at a targeted site. [NIH] Aneuploidy: The chromosomal constitution of cells which deviate from the normal by the addition or subtraction of chromosomes or chromosome pairs. In a normally diploid cell the loss of a chromosome pair is termed nullisomy (symbol: 2N-2), the loss of a single chromosome is monosomy (symbol: 2N-1), the addition of a chromosome pair is tetrasomy (symbol: 2N+2), the addition of a single chromosome is trisomy (symbol: 2N+1). [NIH] Angiogenesis: Blood vessel formation. Tumor angiogenesis is the growth of blood vessels from surrounding tissue to a solid tumor. This is caused by the release of chemicals by the tumor. [NIH] Angioplasty: Endovascular reconstruction of an artery, which may include the removal of atheromatous plaque and/or the endothelial lining as well as simple dilatation. These are procedures performed by catheterization. When reconstruction of an artery is performed surgically, it is called endarterectomy. [NIH] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Annealing: The spontaneous alignment of two single DNA strands to form a double helix. [NIH]
Anode: Electrode held at a positive potential with respect to a cathode. [NIH] Anomalies: Birth defects; abnormalities. [NIH] Anorectal: Pertaining to the anus and rectum or to the junction region between the two. [EU] Anorexia: Lack or loss of appetite for food. Appetite is psychologic, dependent on memory
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and associations. Anorexia can be brought about by unattractive food, surroundings, or company. [NIH] Antagonism: Interference with, or inhibition of, the growth of a living organism by another living organism, due either to creation of unfavorable conditions (e. g. exhaustion of food supplies) or to production of a specific antibiotic substance (e. g. penicillin). [NIH] Antiallergic: Counteracting allergy or allergic conditions. [EU] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]
Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Antibody therapy: Treatment with an antibody, a substance that can directly kill specific tumor cells or stimulate the immune system to kill tumor cells. [NIH] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Anticonvulsants: Drugs used to prevent seizures or reduce their severity. [NIH] Antidepressant: A drug used to treat depression. [NIH] Antidiarrheals: Miscellaneous agents found useful in the symptomatic treatment of diarrhea. They have no effect on the agent(s) that cause diarrhea, but merely alleviate the condition. [NIH] Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Antigen-presenting cell: APC. A cell that shows antigen on its surface to other cells of the immune system. This is an important part of an immune response. [NIH] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Antimetabolite: A chemical that is very similar to one required in a normal biochemical reaction in cells. Antimetabolites can stop or slow down the reaction. [NIH] Antimicrobial: Killing microorganisms, or suppressing their multiplication or growth. [EU]
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Antimycotic: Suppressing the growth of fungi. [EU] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antiproliferative: Counteracting a process of proliferation. [EU] Antipyretic: An agent that relieves or reduces fever. Called also antifebrile, antithermic and febrifuge. [EU] Antiviral: Destroying viruses or suppressing their replication. [EU] Anus: The opening of the rectum to the outside of the body. [NIH] Anxiety: Persistent feeling of dread, apprehension, and impending disaster. [NIH] Anxiety Disorders: Disorders in which anxiety (persistent feelings of apprehension, tension, or uneasiness) is the predominant disturbance. [NIH] Aphakia: Absence of crystalline lens totally or partially from field of vision, from any cause except after cataract extraction. Aphakia is mainly congenital or as result of lens dislocation and subluxation. [NIH] Apheresis: Components plateletpheresis. [NIH]
being
separated
out,
as
leukapheresis,
plasmapheresis,
Aplasia: Lack of development of an organ or tissue, or of the cellular products from an organ or tissue. [EU] Aplastic anemia: A condition in which the bone marrow is unable to produce blood cells. [NIH]
Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Appendectomy: An operation to remove the appendix. [NIH] Appendicitis: Acute inflammation of the vermiform appendix. [NIH] Aqueous: Having to do with water. [NIH] Arachidonate 12-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 12-hydroperoxyarachidonate (12-HPETE) which is itself rapidly converted by a peroxidase to 12-hydroxy-5,8,10,14-eicosatetraenoate (12-HETE). The 12-hydroperoxides are preferentially formed in platelets. EC 1.13.11.31. [NIH] Arachidonate 15-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 15-hydroperoxyarachidonate (15-HPETE) which is rapidly converted to 15-hydroxy5,8,11,13-eicosatetraenoate (15-HETE). The 15-hydroperoxides are preferentially formed in neutrophils and lymphocytes. EC 1.13.11.33. [NIH] Arachidonate Lipoxygenases: Enzymes catalyzing the oxidation of arachidonic acid to hydroperoxyarachidonates (HPETES). These products are then rapidly converted by a peroxidase to hydroxyeicosatetraenoic acids (HETES). The positional specificity of the enzyme reaction varies from tissue to tissue. The final lipoxygenase pathway leads to the
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leukotrienes. EC 1.13.11.- . [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Aromatic: Having a spicy odour. [EU] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arteriolar: Pertaining to or resembling arterioles. [EU] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Arteriolosclerosis: Sclerosis and thickening of the walls of the smaller arteries (arterioles). Hyaline arteriolosclerosis, in which there is homogeneous pink hyaline thickening of the arteriolar walls, is associated with benign nephrosclerosis. Hyperplastic arteriolosclerosis, in which there is a concentric thickening with progressive narrowing of the lumina may be associated with malignant hypertension, nephrosclerosis, and scleroderma. [EU] Arteriosclerosis: Thickening and loss of elasticity of arterial walls. Atherosclerosis is the most common form of arteriosclerosis and involves lipid deposition and thickening of the intimal cell layers within arteries. Additional forms of arteriosclerosis involve calcification of the media of muscular arteries (Monkeberg medial calcific sclerosis) and thickening of the walls of small arteries or arterioles due to cell proliferation or hyaline deposition (arteriolosclerosis). [NIH] Arteritis: Inflammation of an artery. [NIH] Articular: Of or pertaining to a joint. [EU] Ascending Colon: The part of the colon on the right side of the abdomen. [NIH] Aseptic: Free from infection or septic material; sterile. [EU] Aspartic: The naturally occurring substance is L-aspartic acid. One of the acidic-amino-acids is obtained by the hydrolysis of proteins. [NIH] Aspartic Endopeptidases: A sub-subclass of endopeptidases that depend on an aspartic acid residue for their activity. EC 3.4.23. [NIH] Aspirin: A drug that reduces pain, fever, inflammation, and blood clotting. Aspirin belongs to the family of drugs called nonsteroidal anti-inflammatory agents. It is also being studied in cancer prevention. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Astrocytes: The largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the blood brain barrier. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with microglia) respond to injury. Astrocytes have high- affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitter, but their role in signaling (as in many other functions) is not well understood. [NIH] Astrocytoma: A tumor that begins in the brain or spinal cord in small, star-shaped cells called astrocytes. [NIH]
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Asymptomatic: Having no signs or symptoms of disease. [NIH] Ataxia: Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharnyx, larnyx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or peripheral nerve diseases. Motor ataxia may be associated with cerebellar diseases; cerebral cortex diseases; thalamic diseases; basal ganglia diseases; injury to the red nucleus; and other conditions. [NIH] Atmospheric Pressure: The pressure at any point in an atmosphere due solely to the weight of the atmospheric gases above the point concerned. [NIH] Atopic: Pertaining to an atopen or to atopy; allergic. [EU] Atopic Eczema: Generic term for acute or chronic inflammatory conditions of the skin, typically erythematous, edematous, papular, vesicular, and crusting; often accompanied by sensations of itching and burning. [NIH] Atresia: Lack of a normal opening from the esophagus, intestines, or anus. [NIH] Atrial: Pertaining to an atrium. [EU] Atrioventricular: Pertaining to an atrium of the heart and to a ventricle. [EU] Atrium: A chamber; used in anatomical nomenclature to designate a chamber affording entrance to another structure or organ. Usually used alone to designate an atrium of the heart. [EU] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Attenuated: Strain with weakened or reduced virulence. [NIH] Atypical: Irregular; not conformable to the type; in microbiology, applied specifically to strains of unusual type. [EU] Autacoids: A chemically diverse group of substances produced by various tissues in the body that cause slow contraction of smooth muscle; they have other intense but varied pharmacologic activities. [NIH] Autoantibodies: Antibodies that react with self-antigens (autoantigens) of the organism that produced them. [NIH] Autoantigens: Endogenous tissue constituents that have the ability to interact with autoantibodies and cause an immune response. [NIH] Autodigestion: Autolysis; a condition found in disease of the stomach: the stomach wall is digested by the gastric juice. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autoimmune Hepatitis: A liver disease caused when the body's immune system destroys liver cells for no known reason. [NIH] Autoimmunity: Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by autoimmune diseases. [NIH] Autologous: Taken from an individual's own tissues, cells, or DNA. [NIH] Autologous bone marrow transplantation: A procedure in which bone marrow is removed from a person, stored, and then given back to the person after intensive treatment. [NIH] Autolysis: The spontaneous disintegration of tissues or cells by the action of their own autogenous enzymes. [NIH]
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Autonomic: Self-controlling; functionally independent. [EU] Autopsy: Postmortem examination of the body. [NIH] Avian: A plasmodial infection in birds. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] Bacterial Infections: Infections by bacteria, general or unspecified. [NIH] Bacterial Physiology: Physiological processes and activities of bacteria. [NIH] Bactericidal: Substance lethal to bacteria; substance capable of killing bacteria. [NIH] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Barbiturate: A drug with sedative and hypnotic effects. Barbiturates have been used as sedatives and anesthetics, and they have been used to treat the convulsions associated with epilepsy. [NIH] Barium: An element of the alkaline earth group of metals. It has an atomic symbol Ba, atomic number 56, and atomic weight 138. All of its acid-soluble salts are poisonous. [NIH] Barium enema: A procedure in which a liquid with barium in it is put into the rectum and colon by way of the anus. Barium is a silver-white metallic compound that helps to show the image of the lower gastrointestinal tract on an x-ray. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Basal Ganglia Diseases: Diseases of the basal ganglia including the putamen; globus pallidus; claustrum; amygdala; and caudate nucleus. Dyskinesias (most notably involuntary movements and alterations of the rate of movement) represent the primary clinical manifestations of these disorders. Common etiologies include cerebrovascular disease; neurodegenerative diseases; and craniocerebral trauma. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Base Sequence: The sequence of purines and pyrimidines in nucleic acids and polynucleotides. It is also called nucleotide or nucleoside sequence. [NIH] Basement Membrane: Ubiquitous supportive tissue adjacent to epithelium and around smooth and striated muscle cells. This tissue contains intrinsic macromolecular components such as collagen, laminin, and sulfated proteoglycans. As seen by light microscopy one of its subdivisions is the basal (basement) lamina. [NIH] Basophils: Granular leukocytes characterized by a relatively pale-staining, lobate nucleus and cytoplasm containing coarse dark-staining granules of variable size and stainable by basic dyes. [NIH] Beclomethasone: An anti-inflammatory, synthetic glucocorticoid. It is used topically as an anti-inflammatory agent and in aerosol form for the treatment of asthma. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body.
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[NIH]
Benzene: Toxic, volatile, flammable liquid hydrocarbon biproduct of coal distillation. It is used as an industrial solvent in paints, varnishes, lacquer thinners, gasoline, etc. Benzene causes central nervous system damage acutely and bone marrow damage chronically and is carcinogenic. It was formerly used as parasiticide. [NIH] Benzodiazepines: A two-ring heterocyclic compound consisting of a benzene ring fused to a diazepine ring. Permitted is any degree of hydrogenation, any substituents and any Hisomer. [NIH] Benzoic Acid: A fungistatic compound that is widely used as a food preservative. It is conjugated to glycine in the liver and excreted as hippuric acid. [NIH] Bereavement: Refers to the whole process of grieving and mourning and is associated with a deep sense of loss and sadness. [NIH] Beta-Defensins: Defensins found mainly in epithelial cells. [NIH] Beta-pleated: Particular three-dimensional pattern of amyloidoses. [NIH] Beta-Thromboglobulin: A platelet-specific protein which is released when platelets aggregate. Elevated plasma levels have been reported after deep venous thrombosis, preeclampsia, myocardial infarction with mural thrombosis, and myeloproliferative disorders. Measurement of beta-thromboglobulin in biological fluids by radioimmunoassay is used for the diagnosis and assessment of progress of thromboembolic disorders. [NIH] Bewilderment: Impairment or loss of will power. [NIH] Bilateral: Affecting both the right and left side of body. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile Acids: Acids made by the liver that work with bile to break down fats. [NIH] Bile Acids and Salts: Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones. [NIH] Bile Ducts: Tubes that carry bile from the liver to the gallbladder for storage and to the small intestine for use in digestion. [NIH] Bile Pigments: Pigments that give a characteristic color to bile including: bilirubin, biliverdine, and bilicyanin. [NIH] Biliary: Having to do with the liver, bile ducts, and/or gallbladder. [NIH] Biliary Tract: The gallbladder and its ducts. [NIH] Bilirubin: A bile pigment that is a degradation product of heme. [NIH] Binding Sites: The reactive parts of a macromolecule that directly participate in its specific combination with another molecule. [NIH] Bioavailability: The degree to which a drug or other substance becomes available to the target tissue after administration. [EU] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biological response modifier: BRM. A substance that stimulates the body's response to infection and disease. [NIH]
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Biological therapy: Treatment to stimulate or restore the ability of the immune system to fight infection and disease. Also used to lessen side effects that may be caused by some cancer treatments. Also known as immunotherapy, biotherapy, or biological response modifier (BRM) therapy. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH] Biopsy specimen: Tissue removed from the body and examined under a microscope to determine whether disease is present. [NIH] Biosynthesis: The building up of a chemical compound in the physiologic processes of a living organism. [EU] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Biotransformation: The chemical alteration of an exogenous substance by or in a biological system. The alteration may inactivate the compound or it may result in the production of an active metabolite of an inactive parent compound. The alteration may be either nonsynthetic (oxidation-reduction, hydrolysis) or synthetic (glucuronide formation, sulfate conjugation, acetylation, methylation). This also includes metabolic detoxication and clearance. [NIH] Bipolar Disorder: A major affective disorder marked by severe mood swings (manic or major depressive episodes) and a tendency to remission and recurrence. [NIH] Bismuth: A metallic element that has the atomic symbol Bi, atomic number 83 and atomic weight 208.98. [NIH] Bismuth Subsalicylate: A nonprescription medicine such as Pepto-Bismol. Used to treat diarrhea, heartburn, indigestion, and nausea. It is also part of the treatment for ulcers caused by the bacterium Helicobacter pylori (HELL-uh-koh-BAK-tur py-LOH-ree). [NIH] Bladder: The organ that stores urine. [NIH] Blast phase: The phase of chronic myelogenous leukemia in which the number of immature, abnormal white blood cells in the bone marrow and blood is extremely high. Also called blast crisis. [NIH] Blastocyst: The mammalian embryo in the post-morula stage in which a fluid-filled cavity, enclosed primarily by trophoblast, contains an inner cell mass which becomes the embryonic disc. [NIH] Bloating: Fullness or swelling in the abdomen that often occurs after meals. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Glucose: Glucose in blood. [NIH] Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH]
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Blood transfusion: The administration of blood or blood products into a blood vessel. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blot: To transfer DNA, RNA, or proteins to an immobilizing matrix such as nitrocellulose. [NIH]
Blotting, Western: Identification of proteins or peptides that have been electrophoretically separated by blotting and transferred to strips of nitrocellulose paper. The blots are then detected by radiolabeled antibody probes. [NIH] Body Composition: The relative amounts of various components in the body, such as percent body fat. [NIH] Body Fluids: Liquid components of living organisms. [NIH] Body Image: Individuals' personal concept of their bodies as objects in and bound by space, independently and apart from all other objects. [NIH] Bone Density: The amount of mineral per square centimeter of bone. This is the definition used in clinical practice. Actual bone density would be expressed in grams per milliliter. It is most frequently measured by photon absorptiometry or x-ray computed tomography. [NIH] Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bone Marrow Transplantation: The transference of bone marrow from one human or animal to another. [NIH] Bone Resorption: Bone loss due to osteoclastic activity. [NIH] Bone scan: A technique to create images of bones on a computer screen or on film. A small amount of radioactive material is injected into a blood vessel and travels through the bloodstream; it collects in the bones and is detected by a scanner. [NIH] Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Bowel Movement: Body wastes passed through the rectum and anus. [NIH] Bradykinin: A nonapeptide messenger that is enzymatically produced from kallidin in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from mast cells during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter. [NIH] Branch: Most commonly used for branches of nerves, but applied also to other structures. [NIH]
Breakdown: A physical, metal, or nervous collapse. [NIH] Bromelain: An enzyme found in pineapples that breaks down other proteins, such as collagen and muscle fiber, and has anti-inflammatory properties. It is used as a meat tenderizer in the food industry. [NIH] Bronchi: The larger air passages of the lungs arising from the terminal bifurcation of the trachea. [NIH] Bronchial: Pertaining to one or more bronchi. [EU] Bronchioles: The tiny branches of air tubes in the lungs. [NIH]
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Bronchitis: Inflammation (swelling and reddening) of the bronchi. [NIH] Bronchoconstriction: Diminution of the caliber of a bronchus physiologically or as a result of pharmacological intervention. [NIH] Bronchus: A large air passage that leads from the trachea (windpipe) to the lung. [NIH] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [EU] Budesonide: A glucocorticoid used in the management of asthma, the treatment of various skin disorders, and allergic rhinitis. [NIH] Bulimia: Episodic binge eating. The episodes may be associated with the fear of not being able to stop eating, depressed mood, or self-deprecating thoughts (binge-eating disorder) and may frequently be terminated by self-induced vomiting (bulimia nervosa). [NIH] Bullous: Pertaining to or characterized by bullae. [EU] Butyric Acid: A four carbon acid, CH3CH2CH2COOH, with an unpleasant odor that occurs in butter and animal fat as the glycerol ester. [NIH] Cachexia: General ill health, malnutrition, and weight loss, usually associated with chronic disease. [NIH] Cadherins: A group of functionally related glycoproteins responsible for the calciumdependent cell-to-cell adhesion mechanism. They are divided into subclasses E-, P-, and Ncadherins, which are distinct in immunological specificity and tissue distribution. They promote cell adhesion via a homophilic mechanism. These compounds play a role in the construction of tissues and of the whole animal body. [NIH] Caffeine: A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes smooth muscle, stimulates cardiac muscle, stimulates diuresis, and appears to be useful in the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide phosphodiesterases, antagonism of adenosine receptors, and modulation of intracellular calcium handling. [NIH] Calcification: Deposits of calcium in the tissues of the breast. Calcification in the breast can be seen on a mammogram, but cannot be detected by touch. There are two types of breast calcification, macrocalcification and microcalcification. Macrocalcifications are large deposits and are usually not related to cancer. Microcalcifications are specks of calcium that may be found in an area of rapidly dividing cells. Many microcalcifications clustered together may be a sign of cancer. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Calculi: An abnormal concretion occurring mostly in the urinary and biliary tracts, usually composed of mineral salts. Also called stones. [NIH] Capillary: Any one of the minute vessels that connect the arterioles and venules, forming a network in nearly all parts of the body. Their walls act as semipermeable membranes for the interchange of various substances, including fluids, between the blood and tissue fluid; called also vas capillare. [EU]
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Capillary Permeability: Property of blood capillary walls that allows for the selective exchange of substances. Small lipid-soluble molecules such as carbon dioxide and oxygen move freely by diffusion. Water and water-soluble molecules cannot pass through the endothelial walls and are dependent on microscopic pores. These pores show narrow areas (tight junctions) which may limit large molecule movement. [NIH] Capsules: Hard or soft soluble containers used for the oral administration of medicine. [NIH] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, polyand heterosaccharides. [EU] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carboxy: Cannabinoid. [NIH] Carboxy-terminal: The end of any polypeptide or protein that bears a free carboxyl group. [NIH]
Carcinogen: Any substance that causes cancer. [NIH] Carcinogenesis: The process by which normal cells are transformed into cancer cells. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs. [NIH]
Cardiac: Having to do with the heart. [NIH] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Carotene: The general name for a group of pigments found in green, yellow, and leafy vegetables, and yellow fruits. The pigments are fat-soluble, unsaturated aliphatic hydrocarbons functioning as provitamins and are converted to vitamin A through enzymatic processes in the intestinal wall. [NIH] Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes. [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Case series: A group or series of case reports involving patients who were given similar treatment. Reports of case series usually contain detailed information about the individual patients. This includes demographic information (for example, age, gender, ethnic origin) and information on diagnosis, treatment, response to treatment, and follow-up after treatment. [NIH] Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group. [NIH] Catalase: An oxidoreductase that catalyzes the conversion of hydrogen peroxide to water and oxygen. It is present in many animal cells. A deficiency of this enzyme results in acatalasia. EC 1.11.1.6. [NIH] Cataract: An opacity, partial or complete, of one or both eyes, on or in the lens or capsule, especially an opacity impairing vision or causing blindness. The many kinds of cataract are
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classified by their morphology (size, shape, location) or etiology (cause and time of occurrence). [EU] Catecholamine: A group of chemical substances manufactured by the adrenal medulla and secreted during physiological stress. [NIH] Cathepsins: A group of lysosomal proteinases or endopeptidases found in aqueous extracts of a variety of animal tissue. They function optimally within an acidic pH range. [NIH] Catheterization: Use or insertion of a tubular device into a duct, blood vessel, hollow organ, or body cavity for injecting or withdrawing fluids for diagnostic or therapeutic purposes. It differs from intubation in that the tube here is used to restore or maintain patency in obstructions. [NIH] Cathode: An electrode, usually an incandescent filament of tungsten, which emits electrons in an X-ray tube. [NIH] Caudal: Denoting a position more toward the cauda, or tail, than some specified point of reference; same as inferior, in human anatomy. [EU] Causal: Pertaining to a cause; directed against a cause. [EU] Cecum: The beginning of the large intestine. The cecum is connected to the lower part of the small intestine, called the ileum. [NIH] Celiac Disease: A disease characterized by intestinal malabsorption and precipitated by gluten-containing foods. The intestinal mucosa shows loss of villous structure. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Adhesion: Adherence of cells to surfaces or to other cells. [NIH] Cell Adhesion Molecules: Surface ligands, usually glycoproteins, that mediate cell-to-cell adhesion. Their functions include the assembly and interconnection of various vertebrate systems, as well as maintenance of tissue integration, wound healing, morphogenic movements, cellular migrations, and metastasis. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH] Cell Division: The fission of a cell. [NIH] Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell. [NIH] Cell Size: The physical dimensions of a cell. It refers mainly to changes in dimensions correlated with physiological or pathological changes in cells. [NIH] Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability. [NIH]
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Cellulose: A polysaccharide with glucose units linked as in cellobiose. It is the chief constituent of plant fibers, cotton being the purest natural form of the substance. As a raw material, it forms the basis for many derivatives used in chromatography, ion exchange materials, explosives manufacturing, and pharmaceutical preparations. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Central Nervous System Infections: Pathogenic infections of the brain, spinal cord, and meninges. DNA virus infections; RNA virus infections; bacterial infections; mycoplasma infections; Spirochaetales infections; fungal infections; protozoan infections; helminthiasis; and prion diseases may involve the central nervous system as a primary or secondary process. [NIH] Centrifugation: A method of separating organelles or large molecules that relies upon differential sedimentation through a preformed density gradient under the influence of a gravitational field generated in a centrifuge. [NIH] Cerebellar: Pertaining to the cerebellum. [EU] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral hemispheres: The two halves of the cerebrum, the part of the brain that controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. The right hemisphere controls muscle movement on the left side of the body, and the left hemisphere controls muscle movement on the right side of the body. [NIH] Cerebral Palsy: Refers to a motor disability caused by a brain dysfunction. [NIH] Cerebrospinal: Pertaining to the brain and spinal cord. [EU] Cerebrospinal fluid: CSF. The fluid flowing around the brain and spinal cord. Cerebrospinal fluid is produced in the ventricles in the brain. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] Cesarean Section: Extraction of the fetus by means of abdominal hysterotomy. [NIH] Character: In current usage, approximately equivalent to personality. The sum of the relatively fixed personality traits and habitual modes of response of an individual. [NIH] Chemokines: Class of pro-inflammatory cytokines that have the ability to attract and activate leukocytes. They can be divided into at least three structural branches: C (chemokines, C), CC (chemokines, CC), and CXC (chemokines, CXC), according to variations in a shared cysteine motif. [NIH] Chemokines, C: Group of chemokines without adjacent cysteines that are chemoattractants for lymphocytes only. [NIH] Chemopreventive: Natural or synthetic compound used to intervene in the early precancerous stages of carcinogenesis. [NIH] Chemoprotective: A quality of some drugs used in cancer treatment. Chemoprotective agents protect healthy tissue from the toxic effects of anticancer drugs. [NIH] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chemotaxis: The movement of cells or organisms toward or away from a substance in
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response to its concentration gradient. [NIH] Chemotherapy: Treatment with anticancer drugs. [NIH] Chenodeoxycholic Acid: A bile acid, usually conjugated with either glycine or taurine. It acts as a detergent to solubilize fats for intestinal absorption and is reabsorbed by the small intestine. It is used as cholagogue, a choleretic laxative, and to prevent or dissolve gallstones. [NIH] Chest Pain: Pressure, burning, or numbness in the chest. [NIH] Chest wall: The ribs and muscles, bones, and joints that make up the area of the body between the neck and the abdomen. [NIH] Chimeras: Organism that contains a mixture of genetically different cells. [NIH] Chlorambucil: An anticancer drug that belongs to the family of drugs called alkylating agents. [NIH] Chlorophyll: Porphyrin derivatives containing magnesium that act to convert light energy in photosynthetic organisms. [NIH] Cholangitis: Inflammation of a bile duct. [NIH] Cholecystectomy: Surgical removal of the gallbladder. [NIH] Cholecystostomy: Establishment of an opening into the gallbladder either for drainage or surgical communication with another part of the digestive tract, usually the duodenum or jejunum. [NIH] Cholelithiasis: Presence or formation of gallstones. [NIH] Cholera: An acute diarrheal disease endemic in India and Southeast Asia whose causative agent is vibrio cholerae. This condition can lead to severe dehydration in a matter of hours unless quickly treated. [NIH] Cholera Toxin: The enterotoxin from Vibrio cholerae. It is a protein that consists of two major components, the heavy (H) or A peptide and the light (L) or B peptide or choleragenoid. The B peptide anchors the protein to intestinal epithelial cells, while the A peptide, enters the cytoplasm, and activates adenylate cyclase, and production of cAMP. Increased levels of cAMP are thought to modulate release of fluid and electrolytes from intestinal crypt cells. [NIH] Choleretic: A choleretic agent. [EU] Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] Chorea: Involuntary, forcible, rapid, jerky movements that may be subtle or become confluent, markedly altering normal patterns of movement. Hypotonia and pendular reflexes are often associated. Conditions which feature recurrent or persistent episodes of chorea as a primary manifestation of disease are referred to as choreatic disorders. Chorea is also a frequent manifestation of basal ganglia diseases. [NIH] Choreatic Disorders: Acquired and hereditary conditions which feature chorea as a primary manifestation of the disease process. [NIH] Chorion: The outermost extraembryonic membrane. [NIH] Chorioretinitis: Inflammation of the choroid in which the sensory retina becomes edematous and opaque. The inflammatory cells and exudate may burst through the sensory retina to cloud the vitreous body. [NIH]
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Choroid: The thin, highly vascular membrane covering most of the posterior of the eye between the retina and sclera. [NIH] Choroiditis: Inflammation of the choroid. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] Chronic lymphocytic leukemia: A slowly progressing disease in which too many white blood cells (called lymphocytes) are found in the body. [NIH] Chronic myelogenous leukemia: CML. A slowly progressing disease in which too many white blood cells are made in the bone marrow. Also called chronic myeloid leukemia or chronic granulocytic leukemia. [NIH] Chronic Obstructive Pulmonary Disease: Collective term for chronic bronchitis and emphysema. [NIH] Chronic phase: Refers to the early stages of chronic myelogenous leukemia or chronic lymphocytic leukemia. The number of mature and immature abnormal white blood cells in the bone marrow and blood is higher than normal, but lower than in the accelerated or blast phase. [NIH] Chronic renal: Slow and progressive loss of kidney function over several years, often resulting in end-stage renal disease. People with end-stage renal disease need dialysis or transplantation to replace the work of the kidneys. [NIH] Ciliary: Inflammation or infection of the glands of the margins of the eyelids. [NIH] Ciliary Body: A ring of tissue extending from the scleral spur to the ora serrata of the retina. It consists of the uveal portion and the epithelial portion. The ciliary muscle is in the uveal portion and the ciliary processes are in the epithelial portion. [NIH] Ciprofloxacin: A carboxyfluoroquinoline antimicrobial agent that is effective against a wide range of microorganisms. It has been successfully and safely used in the treatment of resistant respiratory, skin, bone, joint, gastrointestinal, urinary, and genital infections. [NIH] Circadian: Repeated more or less daily, i. e. on a 23- to 25-hour cycle. [NIH] Circadian Rhythm: The regular recurrence, in cycles of about 24 hours, of biological processes or activities, such as sensitivity to drugs and stimuli, hormone secretion, sleeping, feeding, etc. This rhythm seems to be set by a 'biological clock' which seems to be set by recurring daylight and darkness. [NIH] Circulatory system: The system that contains the heart and the blood vessels and moves blood throughout the body. This system helps tissues get enough oxygen and nutrients, and it helps them get rid of waste products. The lymph system, which connects with the blood system, is often considered part of the circulatory system. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner, and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Citrus: Any tree or shrub of the Rue family or the fruit of these plants. [NIH]
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Clamp: A u-shaped steel rod used with a pin or wire for skeletal traction in the treatment of certain fractures. [NIH] Clarithromycin: A semisynthetic macrolide antibiotic derived from erythromycin that is active against a variety of microorganisms. It can inhibit protein synthesis in bacteria by reversibly binding to the 50S ribosomal subunits. This inhibits the translocation of aminoacyl transfer-RNA and prevents peptide chain elongation. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient. [NIH]
Clinical study: A research study in which patients receive treatment in a clinic or other medical facility. Reports of clinical studies can contain results for single patients (case reports) or many patients (case series or clinical trials). [NIH] Clinical trial: A research study that tests how well new medical treatments or other interventions work in people. Each study is designed to test new methods of screening, prevention, diagnosis, or treatment of a disease. [NIH] Clone: The term "clone" has acquired a new meaning. It is applied specifically to the bits of inserted foreign DNA in the hybrid molecules of the population. Each inserted segment originally resided in the DNA of a complex genome amid millions of other DNA segment. [NIH]
Cloning: The production of a number of genetically identical individuals; in genetic engineering, a process for the efficient replication of a great number of identical DNA molecules. [NIH] Clostridium: A genus of motile or nonmotile gram-positive bacteria of the family Bacillaceae. Many species have been identified with some being pathogenic. They occur in water, soil, and in the intestinal tract of humans and lower animals. [NIH] Clostridium difficile: A common inhabitant of the colon flora in human infants and sometimes in adults. It produces a toxin that causes pseudomembranous enterocolitis in patients receiving antibiotic therapy. [NIH] Clotrimazole: An imidazole derivative with a broad spectrum of antimycotic activity. It inhibits biosynthesis of the sterol ergostol, an important component of fungal cell membranes. Its action leads to increased membrane permeability and apparent disruption of enzyme systems bound to the membrane. [NIH] Coagulation: 1. The process of clot formation. 2. In colloid chemistry, the solidification of a sol into a gelatinous mass; an alteration of a disperse phase or of a dissolved solid which causes the separation of the system into a liquid phase and an insoluble mass called the clot or curd. Coagulation is usually irreversible. 3. In surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation and photocoagulation. [EU] Coca: Any of several South American shrubs of the Erythroxylon genus (and family) that yield cocaine; the leaves are chewed with alum for CNS stimulation. [NIH] Cocaine: An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake. [NIH] Cochlea: The part of the internal ear that is concerned with hearing. It forms the anterior part of the labyrinth, is conical, and is placed almost horizontally anterior to the vestibule. [NIH]
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Cod Liver Oil: Oil obtained from fresh livers of the cod family, Gadidae. It is a source of vitamins A and D. [NIH] Codons: Any triplet of nucleotides (coding unit) in DNA or RNA (if RNA is the carrier of primary genetic information as in some viruses) that codes for particular amino acid or signals the beginning or end of the message. [NIH] Coenzyme: An organic nonprotein molecule, frequently a phosphorylated derivative of a water-soluble vitamin, that binds with the protein molecule (apoenzyme) to form the active enzyme (holoenzyme). [EU] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Cognitive restructuring: A method of identifying and replacing fear-promoting, irrational beliefs with more realistic and functional ones. [NIH] Cohort Studies: Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics. [NIH] Colectomy: An operation to remove the colon. An open colectomy is the removal of the colon through a surgical incision made in the wall of the abdomen. Laparoscopic-assisted colectomy uses a thin, lighted tube attached to a video camera. It allows the surgeon to remove the colon without a large incision. [NIH] Colitis: Inflammation of the colon. [NIH] Colitis, Ulcerative: Inflammatory disease of unknown cause which involves the mucosa of the colon. Onset may be acute and fulminant, and its course often continues chronically in an intermittent or continuous form. Diarrhea is a common symptom and bleeding an almost constant concomitant symptom. [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] Collagen disease: A term previously used to describe chronic diseases of the connective tissue (e.g., rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis), but now is thought to be more appropriate for diseases associated with defects in collagen, which is a component of the connective tissue. [NIH] Collagenases: Enzymes that catalyze the degradation of collagen by acting on the peptide bonds. EC 3.4.24.-. [NIH] Collagenous Colitis: A type of colitis. Caused by an abnormal band of collagen, a threadlike protein. [NIH] Collapse: 1. A state of extreme prostration and depression, with failure of circulation. 2. Abnormal falling in of the walls of any part of organ. [EU] Colloidal: Of the nature of a colloid. [EU] Colonoscope: A thin, lighted tube used to examine the inside of the colon. [NIH] Colonoscopy: Endoscopic examination, therapy or surgery of the luminal surface of the
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colon. [NIH] Colony-Stimulating Factors: Glycoproteins found in a subfraction of normal mammalian plasma and urine. They stimulate the proliferation of bone marrow cells in agar cultures and the formation of colonies of granulocytes and/or macrophages. The factors include interleukin-3 (IL-3), granulocyte colony-stimulating factor (G-CSF), macrophage colonystimulating factor (M-CSF), and granulocyte-macrophage colony-stimulating factor (GMCSF). [NIH] Colorectal: Having to do with the colon or the rectum. [NIH] Colorectal Cancer: Cancer that occurs in the colon (large intestine) or the rectum (the end of the large intestine). A number of digestive diseases may increase a person's risk of colorectal cancer, including polyposis and Zollinger-Ellison Syndrome. [NIH] Colorectal Surgery: A surgical specialty concerned with the diagnosis and treatment of disorders and abnormalities of the colon, rectum, and anal canal. [NIH] Colostomy: An opening into the colon from the outside of the body. A colostomy provides a new path for waste material to leave the body after part of the colon has been removed. [NIH] Combination Therapy: Association of 3 drugs to treat AIDS (AZT + DDC or DDI + protease inhibitor). [NIH] Commensal: 1. Living on or within another organism, and deriving benefit without injuring or benefiting the other individual. 2. An organism living on or within another, but not causing injury to the host. [EU] Compassionate: A process for providing experimental drugs to very sick patients who have no treatment options. [NIH] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy,
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spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complete remission: The disappearance of all signs of cancer. Also called a complete response. [NIH] Compulsive Behavior: The behavior of performing an act persistently and repetitively without it leading to reward or pleasure. The act is usually a small, circumscribed behavior, almost ritualistic, yet not pathologically disturbing. Examples of compulsive behavior include twirling of hair, checking something constantly, not wanting pennies in change, straightening tilted pictures, etc. [NIH] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Computed tomography: CT scan. A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized tomography and computerized axial tomography (CAT) scan. [NIH] Computerized axial tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called CAT scan, computed tomography (CT scan), or computerized tomography. [NIH] Conception: The onset of pregnancy, marked by implantation of the blastocyst; the formation of a viable zygote. [EU] Concomitant: Accompanying; accessory; joined with another. [EU] Cone: One of the special retinal receptor elements which are presumed to be primarily concerned with perception of light and color stimuli when the eye is adapted to light. [NIH] Confusion: A mental state characterized by bewilderment, emotional disturbance, lack of clear thinking, and perceptual disorientation. [NIH] Congestion: Excessive or abnormal accumulation of blood in a part. [EU] Congestive heart failure: Weakness of the heart muscle that leads to a buildup of fluid in body tissues. [NIH] Conjugated: Acting or operating as if joined; simultaneous. [EU] Conjugation: 1. The act of joining together or the state of being conjugated. 2. A sexual process seen in bacteria, ciliate protozoa, and certain fungi in which nuclear material is exchanged during the temporary fusion of two cells (conjugants). In bacterial genetics a form of sexual reproduction in which a donor bacterium (male) contributes some, or all, of its DNA (in the form of a replicated set) to a recipient (female) which then incorporates differing genetic information into its own chromosome by recombination and passes the recombined set on to its progeny by replication. In ciliate protozoa, two conjugants of separate mating types exchange micronuclear material and then separate, each now being a fertilized cell. In certain fungi, the process involves fusion of two gametes, resulting in union of their nuclei and formation of a zygote. 3. In chemistry, the joining together of two
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compounds to produce another compound, such as the combination of a toxic product with some substance in the body to form a detoxified product, which is then eliminated. [EU] Conjunctiva: The mucous membrane that lines the inner surface of the eyelids and the anterior part of the sclera. [NIH] Conjunctivitis: Inflammation of the conjunctiva, generally consisting of conjunctival hyperaemia associated with a discharge. [EU] Conjunctivitis, Allergic: Conjunctivitis due to hypersensitivity to various allergens. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue Cells: A group of cells that includes fibroblasts, cartilage cells, adipocytes, smooth muscle cells, and bone cells. [NIH] Connexins: A group of homologous proteins which form the intermembrane channels of gap junctions. The connexins are the products of an identified gene family which has both highly conserved and highly divergent regions. The variety contributes to the wide range of functional properties of gap junctions. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Constipation: Infrequent or difficult evacuation of feces. [NIH] Constitutional: 1. Affecting the whole constitution of the body; not local. 2. Pertaining to the constitution. [EU] Constriction: The act of constricting. [NIH] Constriction, Pathologic: The condition of an anatomical structure's being constricted beyond normal dimensions. [NIH] Consultation: A deliberation between two or more physicians concerning the diagnosis and the proper method of treatment in a case. [NIH] Consumption: Pulmonary tuberculosis. [NIH] Contact dermatitis: Inflammation of the skin with varying degrees of erythema, edema and vesinculation resulting from cutaneous contact with a foreign substance or other exposure. [NIH]
Contamination: The soiling or pollution by inferior material, as by the introduction of organisms into a wound, or sewage into a stream. [EU] Continence: The ability to hold in a bowel movement or urine. [NIH] Continent Ileostomy: An operation to create a pouch from part of the small intestine. Stool that collects in the pouch is removed by inserting a small tube through an opening made in the abdomen. [NIH] Contraceptive: An agent that diminishes the likelihood of or prevents conception. [EU] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Contrast Sensitivity: The ability to detect sharp boundaries (stimuli) and to detect slight changes in luminance at regions without distinct contours. Psychophysical measurements of this visual function are used to evaluate visual acuity and to detect eye disease. [NIH] Control group: In a clinical trial, the group that does not receive the new treatment being studied. This group is compared to the group that receives the new treatment, to see if the new treatment works. [NIH]
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Controlled clinical trial: A clinical study that includes a comparison (control) group. The comparison group receives a placebo, another treatment, or no treatment at all. [NIH] Controlled study: An experiment or clinical trial that includes a comparison (control) group. [NIH]
Conventional therapy: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional treatment. [NIH] Conventional treatment: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional therapy. [NIH] Convulsions: A general term referring to sudden and often violent motor activity of cerebral or brainstem origin. Convulsions may also occur in the absence of an electrical cerebral discharge (e.g., in response to hypotension). [NIH] Coordination: Muscular or motor regulation or the harmonious cooperation of muscles or groups of muscles, in a complex action or series of actions. [NIH] Cor: The muscular organ that maintains the circulation of the blood. c. adiposum a heart that has undergone fatty degeneration or that has an accumulation of fat around it; called also fat or fatty, heart. c. arteriosum the left side of the heart, so called because it contains oxygenated (arterial) blood. c. biloculare a congenital anomaly characterized by failure of formation of the atrial and ventricular septums, the heart having only two chambers, a single atrium and a single ventricle, and a common atrioventricular valve. c. bovinum (L. 'ox heart') a greatly enlarged heart due to a hypertrophied left ventricle; called also c. taurinum and bucardia. c. dextrum (L. 'right heart') the right atrium and ventricle. c. hirsutum, c. villosum. c. mobile (obs.) an abnormally movable heart. c. pendulum a heart so movable that it seems to be hanging by the great blood vessels. c. pseudotriloculare biatriatum a congenital cardiac anomaly in which the heart functions as a three-chambered heart because of tricuspid atresia, the right ventricle being extremely small or rudimentary and the right atrium greatly dilated. Blood passes from the right to the left atrium and thence disease due to pulmonary hypertension secondary to disease of the lung, or its blood vessels, with hypertrophy of the right ventricle. [EU] Cornea: The transparent part of the eye that covers the iris and the pupil and allows light to enter the inside. [NIH] Corneal Ulcer: Loss of epithelial tissue from the surface of the cornea due to progressive erosion and necrosis of the tissue; usually caused by bacterial, fungal, or viral infection. [NIH] Corneum: The superficial layer of the epidermis containing keratinized cells. [NIH] Coronary: Encircling in the manner of a crown; a term applied to vessels; nerves, ligaments, etc. The term usually denotes the arteries that supply the heart muscle and, by extension, a pathologic involvement of them. [EU] Coronary Arteriosclerosis: Thickening and loss of elasticity of the coronary arteries. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Corpus: The body of the uterus. [NIH] Corpus Luteum: The yellow glandular mass formed in the ovary by an ovarian follicle that has ruptured and discharged its ovum. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Corticosteroid: Any of the steroids elaborated by the adrenal cortex (excluding the sex hormones of adrenal origin) in response to the release of corticotrophin (adrenocorticotropic hormone) by the pituitary gland, to any of the synthetic equivalents of these steroids, or to
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angiotensin II. They are divided, according to their predominant biological activity, into three major groups: glucocorticoids, chiefly influencing carbohydrate, fat, and protein metabolism; mineralocorticoids, affecting the regulation of electrolyte and water balance; and C19 androgens. Some corticosteroids exhibit both types of activity in varying degrees, and others exert only one type of effect. The corticosteroids are used clinically for hormonal replacement therapy, for suppression of ACTH secretion by the anterior pituitary, as antineoplastic, antiallergic, and anti-inflammatory agents, and to suppress the immune response. Called also adrenocortical hormone and corticoid. [EU] Cortisol: A steroid hormone secreted by the adrenal cortex as part of the body's response to stress. [NIH] Cortisone: A natural steroid hormone produced in the adrenal gland. It can also be made in the laboratory. Cortisone reduces swelling and can suppress immune responses. [NIH] Counterimmunoelectrophoresis: Immunoelectrophoresis in which immunoprecipitation occurs when antigen at the cathode is caused to migrate in an electric field through a suitable medium of diffusion against a stream of antibody migrating from the anode as a result of endosmotic flow. [NIH] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Craniocerebral Trauma: Traumatic injuries involving the cranium and intracranial structures (i.e., brain; cranial nerves; meninges; and other structures). Injuries may be classified by whether or not the skull is penetrated (i.e., penetrating vs. nonpenetrating) or whether there is an associated hemorrhage. [NIH] Cross-Sectional Studies: Studies in which the presence or absence of disease or other health-related variables are determined in each member of the study population or in a representative sample at one particular time. This contrasts with longitudinal studies which are followed over a period of time. [NIH] Crowding: Behavior with respect to an excessive number of individuals, human or animal, in relation to available space. [NIH] Culture Media: Any liquid or solid preparation made specifically for the growth, storage, or transport of microorganisms or other types of cells. The variety of media that exist allow for the culturing of specific microorganisms and cell types, such as differential media, selective media, test media, and defined media. Solid media consist of liquid media that have been solidified with an agent such as agar or gelatin. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Cutaneous: Having to do with the skin. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cyclophosphamide: Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the liver to form the active aldophosphamide. It is used in the treatment of lymphomas, leukemias, etc. Its side effect, alopecia, has been made use of in defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer. [NIH] Cyclosporine: A drug used to help reduce the risk of rejection of organ and bone marrow transplants by the body. It is also used in clinical trials to make cancer cells more sensitive to anticancer drugs. [NIH] Cysteine: A thiol-containing non-essential amino acid that is oxidized to form cystine. [NIH] Cysteine Endopeptidases: Endopeptidases which have a cysteine involved in the catalytic
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process. This group of enzymes is inactivated by sulfhydryl reagents. EC 3.4.22. [NIH] Cystine: A covalently linked dimeric nonessential amino acid formed by the oxidation of cysteine. Two molecules of cysteine are joined together by a disulfide bridge to form cystine. [NIH]
Cystitis: Inflammation of the urinary bladder. [EU] Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, . New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU] Cytochrome b: Cytochromes (electron-transporting proteins) with protoheme or a related heme as the prosthetic group. The prosthetic group is not covalently bound to the protein moiety. [NIH] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytomegalovirus: A genus of the family Herpesviridae, subfamily Betaherpesvirinae, infecting the salivary glands, liver, spleen, lungs, eyes, and other organs, in which they produce characteristically enlarged cells with intranuclear inclusions. Infection with Cytomegalovirus is also seen as an opportunistic infection in AIDS. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytoprotection: The process by which chemical compounds provide protection to cells against harmful agents. [NIH] Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Cytotoxic: Cell-killing. [NIH] Cytotoxicity: Quality of being capable of producing a specific toxic action upon cells of special organs. [NIH] Cytotoxins: Substances elaborated by microorganisms, plants or animals that are specifically toxic to individual cells; they may be involved in immunity or may be contained in venoms. [NIH]
Databases, Bibliographic: Extensive collections, reputedly complete, of references and citations to books, articles, publications, etc., generally on a single subject or specialized subject area. Databases can operate through automated files, libraries, or computer disks. The concept should be differentiated from factual databases which is used for collections of data and facts apart from bibliographic references to them. [NIH] Decidua: The epithelial lining of the endometrium that is formed before the fertilized ovum reaches the uterus. The fertilized ovum embeds in the decidua. If the ovum is not fertilized, the decidua is shed during menstruation. [NIH] Decision Making: The process of making a selective intellectual judgment when presented
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with several complex alternatives consisting of several variables, and usually defining a course of action or an idea. [NIH] Decompression: Decompression external to the body, most often the slow lessening of external pressure on the whole body (especially in caisson workers, deep sea divers, and persons who ascend to great heights) to prevent decompression sickness. It includes also sudden accidental decompression, but not surgical (local) decompression or decompression applied through body openings. [NIH] Decompression Sickness: A condition occurring as a result of exposure to a rapid fall in ambient pressure. Gases, nitrogen in particular, come out of solution and form bubbles in body fluid and blood. These gas bubbles accumulate in joint spaces and the peripheral circulation impairing tissue oxygenation causing disorientation, severe pain, and potentially death. [NIH] Defecation: The normal process of elimination of fecal material from the rectum. [NIH] Defense Mechanisms: Unconscious process used by an individual or a group of individuals in order to cope with impulses, feelings or ideas which are not acceptable at their conscious level; various types include reaction formation, projection and self reversal. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Dehydration: The condition that results from excessive loss of body water. [NIH] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Delirium: (DSM III-R) an acute, reversible organic mental disorder characterized by reduced ability to maintain attention to external stimuli and disorganized thinking as manifested by rambling, irrelevant, or incoherent speech; there are also a reduced level of consciousness, sensory misperceptions, disturbance of the sleep-wakefulness cycle and level of psychomotor activity, disorientation to time, place, or person, and memory impairment. Delirium may be caused by a large number of conditions resulting in derangement of cerebral metabolism, including systemic infection, poisoning, drug intoxication or withdrawal, seizures or head trauma, and metabolic disturbances such as hypoxia, hypoglycaemia, fluid, electrolyte, or acid-base imbalances, or hepatic or renal failure. Called also acute confusional state and acute brain syndrome. [EU] Delusions: A false belief regarding the self or persons or objects outside the self that persists despite the facts, and is not considered tenable by one's associates. [NIH] Dementia: An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness. [NIH] Demyelinating Diseases: Diseases characterized by loss or dysfunction of myelin in the central or peripheral nervous system. [NIH] Denaturation: Rupture of the hydrogen bonds by heating a DNA solution and then cooling it rapidly causes the two complementary strands to separate. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Dendritic: 1. Branched like a tree. 2. Pertaining to or possessing dendrites. [EU] Dendritic cell: A special type of antigen-presenting cell (APC) that activates T lymphocytes. [NIH]
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Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Deoxycytidine: A drug that protects healthy tissues from the toxic effects of anticancer drugs. [NIH] Deoxyguanosine: A nucleoside consisting of the base guanine and the sugar deoxyribose. [NIH]
Depersonalization: Alteration in the perception of the self so that the usual sense of one's own reality is lost, manifested in a sense of unreality or self-estrangement, in changes of body image, or in a feeling that one does not control his own actions and speech; seen in depersonalization disorder, schizophrenic disorders, and schizotypal personality disorder. Some do not draw a distinction between depersonalization and derealization, using depersonalization to include both. [EU] Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] Derealization: Is characterized by the loss of the sense of reality concerning one's surroundings. [NIH] Dermal: Pertaining to or coming from the skin. [NIH] Dermatitis: Any inflammation of the skin. [NIH] Dermatosis: Any skin disease, especially one not characterized by inflammation. [EU] Desensitization: The prevention or reduction of immediate hypersensitivity reactions by administration of graded doses of allergen; called also hyposensitization and immunotherapy. [EU] Detergents: Purifying or cleansing agents, usually salts of long-chain aliphatic bases or acids, that exert cleansing (oil-dissolving) and antimicrobial effects through a surface action that depends on possessing both hydrophilic and hydrophobic properties. [NIH] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Developed Countries: Countries that have reached a level of economic achievement through an increase of production, per capita income and consumption, and utilization of natural and human resources. [NIH] Dextran Sulfate: Long-chain polymer of glucose containing 17-20% sulfur. It has been used as an anticoagulant and also has been shown to inhibit the binding of HIV-1 to CD4+ Tlymphocytes. It is commonly used as both an experimental and clinical laboratory reagent and has been investigated for use as an antiviral agent, in the treatment of hypolipidemia, and for the prevention of free radical damage, among other applications. [NIH] DHEA: Dehydroepiandrosterone. A substance that is being studied as a cancer prevention drug. It belongs to the family of drugs called steroids. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diabetic Retinopathy: Retinopathy associated with diabetes mellitus, which may be of the background type, progressively characterized by microaneurysms, interretinal punctuate macular edema, or of the proliferative type, characterized by neovascularization of the retina and optic disk, which may project into the vitreous, proliferation of fibrous tissue, vitreous hemorrhage, and retinal detachment. [NIH] Diagnostic Imaging: Any visual display of structural or functional patterns of organs or tissues for diagnostic evaluation. It includes measuring physiologic and metabolic responses
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to physical and chemical stimuli, as well as ultramicroscopy. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Diarrhea: Passage of excessively liquid or excessively frequent stools. [NIH] Diarrhoea: Abnormal frequency and liquidity of faecal discharges. [EU] Diastolic: Of or pertaining to the diastole. [EU] Diencephalon: The paired caudal parts of the prosencephalon from which the thalamus, hypothalamus, epithalamus, and subthalamus are derived. [NIH] Dietary Fiber: The remnants of plant cell walls that are resistant to digestion by the alimentary enzymes of man. It comprises various polysaccharides and lignins. [NIH] Dietitian: An expert in nutrition who helps people plan what and how much food to eat. [NIH]
Diffusion: The tendency of a gas or solute to pass from a point of higher pressure or concentration to a point of lower pressure or concentration and to distribute itself throughout the available space; a major mechanism of biological transport. [NIH] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digestive system: The organs that take in food and turn it into products that the body can use to stay healthy. Waste products the body cannot use leave the body through bowel movements. The digestive system includes the salivary glands, mouth, esophagus, stomach, liver, pancreas, gallbladder, small and large intestines, and rectum. [NIH] Digestive tract: The organs through which food passes when food is eaten. These organs are the mouth, esophagus, stomach, small and large intestines, and rectum. [NIH] Dihydroxy: AMPA/Kainate antagonist. [NIH] Dilatation: The act of dilating. [NIH] Dilation: A process by which the pupil is temporarily enlarged with special eye drops (mydriatic); allows the eye care specialist to better view the inside of the eye. [NIH] Diploid: Having two sets of chromosomes. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Disease Progression: The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis. [NIH] Disease Susceptibility: A constitution or condition of the body which makes the tissues react in special ways to certain extrinsic stimuli and thus tends to make the individual more than usually susceptible to certain diseases. [NIH] Disinfectant: An agent that disinfects; applied particularly to agents used on inanimate objects. [EU] Disorientation: The loss of proper bearings, or a state of mental confusion as to time, place, or identity. [EU] Disposition: A tendency either physical or mental toward certain diseases. [EU] Dissection: Cutting up of an organism for study. [NIH] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's
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mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Distention: The state of being distended or enlarged; the act of distending. [EU] Diuresis: Increased excretion of urine. [EU] Diuretic: A drug that increases the production of urine. [NIH] Dizziness: An imprecise term which may refer to a sense of spatial disorientation, motion of the environment, or lightheadedness. [NIH] Dominance: In genetics, the full phenotypic expression of a gene in both heterozygotes and homozygotes. [EU] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] Dorsal: 1. Pertaining to the back or to any dorsum. 2. Denoting a position more toward the back surface than some other object of reference; same as posterior in human anatomy; superior in the anatomy of quadrupeds. [EU] Dosage Forms: Completed forms of the pharmaceutical preparation in which prescribed doses of medication are included. They are designed to resist action by gastric fluids, prevent vomiting and nausea, reduce or alleviate the undesirable taste and smells associated with oral administration, achieve a high concentration of drug at target site, or produce a delayed or long-acting drug effect. They include capsules, liniments, ointments, pharmaceutical solutions, powders, tablets, etc. [NIH] Drive: A state of internal activity of an organism that is a necessary condition before a given stimulus will elicit a class of responses; e.g., a certain level of hunger (drive) must be present before food will elicit an eating response. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated dose and no-observed-adverse-effect level. [NIH] Drug Toxicity: Manifestations of the adverse effects of drugs administered therapeutically or in the course of diagnostic techniques. It does not include accidental or intentional poisoning for which specific headings are available. [NIH] Duct: A tube through which body fluids pass. [NIH] Duodenal Ulcer: An ulcer in the lining of the first part of the small intestine (duodenum). [NIH]
Duodenitis: An irritation of the first part of the small intestine (duodenum). [NIH]
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Duodenum: The first part of the small intestine. [NIH] Dura mater: The outermost, toughest, and most fibrous of the three membranes (meninges) covering the brain and spinal cord; called also pachymeninx. [EU] Dyes: Chemical substances that are used to stain and color other materials. The coloring may or may not be permanent. Dyes can also be used as therapeutic agents and test reagents in medicine and scientific research. [NIH] Dyskinesia: Impairment of the power of voluntary movement, resulting in fragmentary or incomplete movements. [EU] Dyslexia: Partial alexia in which letters but not words may be read, or in which words may be read but not understood. [NIH] Dyspareunia: Painful sexual intercourse. [NIH] Dyspepsia: Impaired digestion, especially after eating. [NIH] Dysplasia: Cells that look abnormal under a microscope but are not cancer. [NIH] Dyspnea: Difficult or labored breathing. [NIH] Dystonia: Disordered tonicity of muscle. [EU] Dystrophy: Any disorder arising from defective or faulty nutrition, especially the muscular dystrophies. [EU] Eclampsia: Onset of convulsions or coma in a previously diagnosed pre-eclamptic patient. [NIH]
Ectopic: Pertaining to or characterized by ectopia. [EU] Eczema: A pruritic papulovesicular dermatitis occurring as a reaction to many endogenous and exogenous agents (Dorland, 27th ed). [NIH] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH] Educational Status: Educational attainment or level of education of individuals. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Effector cell: A cell that performs a specific function in response to a stimulus; usually used to describe cells in the immune system. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Effusion: The escape of fluid into a part or tissue, as an exudation or a transudation. [EU] Eicosanoids: A class of oxygenated, endogenous, unsaturated fatty acids derived from arachidonic acid. They include prostaglandins, leukotrienes, thromboxanes, and hydroxyeicosatetraenoic acid compounds (HETE). They are hormone-like substances that act near the site of synthesis without altering functions throughout the body. [NIH] Elasticity: Resistance and recovery from distortion of shape. [NIH] Elastin: The protein that gives flexibility to tissues. [NIH] Elective: Subject to the choice or decision of the patient or physician; applied to procedures that are advantageous to the patient but not urgent. [EU] Electroacupuncture: A form of acupuncture using low frequency electrically stimulated needles to produce analgesia and anesthesia and to treat disease. [NIH] Electrocardiogram: Measurement of electrical activity during heartbeats. [NIH]
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Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electrons: Stable elementary particles having the smallest known negative charge, present in all elements; also called negatrons. Positively charged electrons are called positrons. The numbers, energies and arrangement of electrons around atomic nuclei determine the chemical identities of elements. Beams of electrons are called cathode rays or beta rays, the latter being a high-energy biproduct of nuclear decay. [NIH] Electrophoresis: An electrochemical process in which macromolecules or colloidal particles with a net electric charge migrate in a solution under the influence of an electric current. [NIH]
Electroplating: Coating with a metal or alloy by electrolysis. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Emetic: An agent that causes vomiting. [EU] Emphysema: A pathological accumulation of air in tissues or organs. [NIH] Emulsion: A preparation of one liquid distributed in small globules throughout the body of a second liquid. The dispersed liquid is the discontinuous phase, and the dispersion medium is the continuous phase. When oil is the dispersed liquid and an aqueous solution is the continuous phase, it is known as an oil-in-water emulsion, whereas when water or aqueous solution is the dispersed phase and oil or oleaginous substance is the continuous phase, it is known as a water-in-oil emulsion. Pharmaceutical emulsions for which official standards have been promulgated include cod liver oil emulsion, cod liver oil emulsion with malt, liquid petrolatum emulsion, and phenolphthalein in liquid petrolatum emulsion. [EU] Encapsulated: Confined to a specific, localized area and surrounded by a thin layer of tissue. [NIH]
Encephalitis: Inflammation of the brain due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see encephalitis, viral) are a relatively frequent cause of this condition. [NIH] Encephalomyelitis: A general term indicating inflammation of the brain and spinal cord, often used to indicate an infectious process, but also applicable to a variety of autoimmune and toxic-metabolic conditions. There is significant overlap regarding the usage of this term and encephalitis in the literature. [NIH] Endarterectomy: Surgical excision, performed under general anesthesia, of the atheromatous tunica intima of an artery. When reconstruction of an artery is performed as an endovascular procedure through a catheter, it is called atherectomy. [NIH] Endemic: Present or usually prevalent in a population or geographical area at all times; said of a disease or agent. Called also endemial. [EU] Endocytosis: Cellular uptake of extracellular materials within membrane-limited vacuoles or microvesicles. Endosomes play a central role in endocytosis. [NIH] Endometrium: The layer of tissue that lines the uterus. [NIH] Endopeptidases: A subclass of peptide hydrolases. They are classified primarily by their catalytic mechanism. Specificity is used only for identification of individual enzymes. They comprise the serine endopeptidases, EC 3.4.21; cysteine endopeptidases, EC 3.4.22; aspartic endopeptidases, EC 3.4.23, metalloendopeptidases, EC 3.4.24; and a group of enzymes yet to be assigned to any of the above sub-classes, EC 3.4.99. EC 3.4.-. [NIH] Endoscope: A thin, lighted tube used to look at tissues inside the body. [NIH] Endoscopic: A technique where a lateral-view endoscope is passed orally to the duodenum
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for visualization of the ampulla of Vater. [NIH] Endoscopy: Endoscopic examination, therapy or surgery performed on interior parts of the body. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium, Lymphatic: Unbroken cellular lining (intima) of the lymph vessels (e.g., the high endothelial lymphatic venules). It is more permeable than vascular endothelium, lacking selective absorption and functioning mainly to remove plasma proteins that have filtered through the capillaries into the tissue spaces. [NIH] Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components from interstitium to lumen; this function has been most intensively studied in the blood capillaries. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxemia: A condition characterized by the presence of endotoxins in the blood. If endotoxemia is the result of gram-negative rod-shaped bacteria, shock may occur. [NIH] Endotoxic: Of, relating to, or acting as an endotoxin (= a heat-stable toxin, associated with the outer membranes of certain gram-negative bacteria. Endotoxins are not secreted and are released only when the cells are disrupted). [EU] Endotoxin: Toxin from cell walls of bacteria. [NIH] End-stage renal: Total chronic kidney failure. When the kidneys fail, the body retains fluid and harmful wastes build up. A person with ESRD needs treatment to replace the work of the failed kidneys. [NIH] Enema: The injection of a liquid through the anus into the large bowel. [NIH] Energy balance: Energy is the capacity of a body or a physical system for doing work. Energy balance is the state in which the total energy intake equals total energy needs. [NIH] Enhancer: Transcriptional element in the virus genome. [NIH] Enteral Nutrition: Nutritional support given via the alimentary canal or any route connected to the gastrointestinal system (i.e., the enteral route). This includes oral feeding, sip feeding, and tube feeding using nasogastric, gastrostomy, and jejunostomy tubes. [NIH] Enteric bacteria: Single-celled microorganisms that lack chlorophyll. Some bacteria are capable of causing human, animal, or plant diseases; others are essential in pollution control because they break down organic matter in the air and in the water. [NIH] Enteric-coated: A term designating a special coating applied to tablets or capsules which prevents release and absorption of their contents until they reach the intestines. [EU] Enteritis: Inflammation of the intestine, applied chiefly to inflammation of the small intestine; see also enterocolitis. [EU] Enterocolitis: Inflammation of the intestinal mucosa of the small and large bowel. [NIH] Enterocytes: Terminally differentiated cells comprising the majority of the external surface of the intestinal epithelium (see intestinal mucosa). Unlike goblet cells, they do not produce or secrete mucins, nor do they secrete cryptdins as do the paneth cells. [NIH] Environmental Exposure: The exposure to potentially harmful chemical, physical, or
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biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]
Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. [NIH] Eosinophil: A polymorphonuclear leucocyte with large eosinophilic granules in its cytoplasm, which plays a role in hypersensitivity reactions. [NIH] Eosinophilia: Abnormal increase in eosinophils in the blood, tissues or organs. [NIH] Eosinophilic: A condition found primarily in grinding workers caused by a reaction of the pulmonary tissue, in particular the eosinophilic cells, to dust that has entered the lung. [NIH] Eosinophilic Gastroenteritis: Infection and swelling of the lining of the stomach, small intestine, or large intestine. The infection is caused by white blood cells (eosinophils). [NIH] Epidemic: Occurring suddenly in numbers clearly in excess of normal expectancy; said especially of infectious diseases but applied also to any disease, injury, or other healthrelated event occurring in such outbreaks. [EU] Epidemiologic Studies: Studies designed to examine associations, commonly, hypothesized causal relations. They are usually concerned with identifying or measuring the effects of risk factors or exposures. The common types of analytic study are case-control studies, cohort studies, and cross-sectional studies. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermal: Pertaining to or resembling epidermis. Called also epidermic or epidermoid. [EU] Epidermal Growth Factor: A 6 kD polypeptide growth factor initially discovered in mouse submaxillary glands. Human epidermal growth factor was originally isolated from urine based on its ability to inhibit gastric secretion and called urogastrone. epidermal growth factor exerts a wide variety of biological effects including the promotion of proliferation and differentiation of mesenchymal and epithelial cells. [NIH] Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] Epigastric: Having to do with the upper middle area of the abdomen. [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Episcleritis: Inflammation of the episclera and/or the outer layers of the sclera itself. [NIH] Episiotomy: An incision of the posterior vaginal wall and a portion of the pudenda which enlarges the vaginal introitus to facilitate delivery and prevent lacerations. [NIH] Epistasis: The degree of dominance exerted by one gene on the expression of a non-allelic gene. [NIH]
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Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Epitope: A molecule or portion of a molecule capable of binding to the combining site of an antibody. For every given antigenic determinant, the body can construct a variety of antibody-combining sites, some of which fit almost perfectly, and others which barely fit. [NIH]
Erythema: Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes. [NIH] Erythema Nodosum: An erythematous eruption commonly associated with drug reactions or infection and characterized by inflammatory nodules that are usually tender, multiple, and bilateral. These nodules are located predominantly on the shins with less common occurrence on the thighs and forearms. They undergo characteristic color changes ending in temporary bruise-like areas. This condition usually subsides in 3-6 weeks without scarring or atrophy. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Erythromycin: A bacteriostatic antibiotic substance produced by Streptomyces erythreus. Erythromycin A is considered its major active component. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins. [NIH] Erythropoiesis: The production of erythrocytes. [EU] Erythropoietin: Glycoprotein hormone, secreted chiefly by the kidney in the adult and the liver in the fetus, that acts on erythroid stem cells of the bone marrow to stimulate proliferation and differentiation. [NIH] Escalation: Progressive use of more harmful drugs. [NIH] Esophageal: Having to do with the esophagus, the muscular tube through which food passes from the throat to the stomach. [NIH] Esophagitis: Inflammation, acute or chronic, of the esophagus caused by bacteria, chemicals, or trauma. [NIH] Esophagitis, Peptic: Inflammation of the esophagus caused by reflux of gastric juice and/or stomach and duodenal contents. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]
Essential Tremor: A rhythmic, involuntary, purposeless, oscillating movement resulting from the alternate contraction and relaxation of opposing groups of muscles. [NIH] Estrogen: One of the two female sex hormones. [NIH] Estrogen receptor: ER. Protein found on some cancer cells to which estrogen will attach. [NIH]
Ethanol: A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. [NIH] Ethnic Groups: A group of people with a common cultural heritage that sets them apart
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from others in a variety of social relationships. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Evacuation: An emptying, as of the bowels. [EU] Evoke: The electric response recorded from the cerebral cortex after stimulation of a peripheral sense organ. [NIH] Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] Exocrine: Secreting outwardly, via a duct. [EU] Exocytosis: Cellular release of material within membrane-limited vesicles by fusion of the vesicles with the cell membrane. [NIH] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Exon: The part of the DNA that encodes the information for the actual amino acid sequence of the protein. In many eucaryotic genes, the coding sequences consist of a series of exons alternating with intron sequences. [NIH] Expert Systems: Computer programs based on knowledge developed from consultation with experts on a problem, and the processing and/or formalizing of this knowledge using these programs in such a manner that the problems may be solved. [NIH] Extender: Any of several colloidal substances of high molecular weight, used as a blood or plasma substitute in transfusion for increasing the volume of the circulating blood. [NIH] Extensor: A muscle whose contraction tends to straighten a limb; the antagonist of a flexor. [NIH]
Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extracellular Matrix Proteins: Macromolecular organic compounds that contain carbon, hydrogen, oxygen, nitrogen, and usually, sulfur. These macromolecules (proteins) form an intricate meshwork in which cells are embedded to construct tissues. Variations in the relative types of macromolecules and their organization determine the type of extracellular matrix, each adapted to the functional requirements of the tissue. The two main classes of macromolecules that form the extracellular matrix are: glycosaminoglycans, usually linked to proteins (proteoglycans), and fibrous proteins (e.g., collagen, elastin, fibronectins and laminin). [NIH] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extraction: The process or act of pulling or drawing out. [EU] Eye Infections: Infection, moderate to severe, caused by bacteria, fungi, or viruses, which occurs either on the external surface of the eye or intraocularly with probable inflammation, visual impairment, or blindness. [NIH] Faecal: Pertaining to or of the nature of feces. [EU] Fallopian Tubes: Two long muscular tubes that transport ova from the ovaries to the uterus. They extend from the horn of the uterus to the ovaries and consist of an ampulla, an infundibulum, an isthmus, two ostia, and a pars uterina. The walls of the tubes are composed of three layers: mucosal, muscular, and serosal. [NIH]
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Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fasciitis: Inflammation of the fascia. There are three major types: 1) Eosinophilic fasciitis, an inflammatory reaction with eosinophilia, producing hard thickened skin with an orangepeel configuration suggestive of scleroderma and considered by some a variant of scleroderma; 2) Necrotizing fasciitis, a serious fulminating infection (usually by a beta hemolytic Streptococcus) causing extensive necrosis of superficial fascia; 3) Nodular/Pseudosarcomatous/Proliferative fasciitis, characterized by a rapid growth of fibroblasts with mononuclear inflammatory cells and proliferating capillaries in soft tissue, often the forearm; it is not malignant but is sometimes mistaken for fibrosarcoma. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]
Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] Febrile: Pertaining to or characterized by fever. [EU] Fecal Incontinence: Failure of voluntary control of the anal sphincters, with involuntary passage of feces and flatus. [NIH] Feces: The excrement discharged from the intestines, consisting of bacteria, cells exfoliated from the intestines, secretions, chiefly of the liver, and a small amount of food residue. [EU] Femoral: Pertaining to the femur, or to the thigh. [EU] Femur: The longest and largest bone of the skeleton, it is situated between the hip and the knee. [NIH] Ferritin: An iron-containing protein complex that is formed by a combination of ferric iron with the protein apoferritin. [NIH] Fertilizers: Substances or mixtures that are added to the soil to supply nutrients or to make available nutrients already present in the soil, in order to increase plant growth and productivity. [NIH] Fetal Growth Retardation: The failure of a fetus to attain its expected growth potential at any gestational stage. [NIH] Fetal Membranes: Thin layers of tissue which surround the embryo or fetus and provide for its nutrition, respiration, excretion and protection; they are the yolk sac, allantois, amnion, and chorion. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three nonidentical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products. [NIH] Fibroblast Growth Factor: Peptide isolated from the pituitary gland and from the brain. It is a potent mitogen which stimulates growth of a variety of mesodermal cells including chondrocytes, granulosa, and endothelial cells. The peptide may be active in wound healing and animal limb regeneration. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH]
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Fibronectin: An adhesive glycoprotein. One form circulates in plasma, acting as an opsonin; another is a cell-surface protein which mediates cellular adhesive interactions. [NIH] Fibrosarcoma: A type of soft tissue sarcoma that begins in fibrous tissue, which holds bones, muscles, and other organs in place. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Fish Oils: Oils high in unsaturated fats extracted from the bodies of fish or fish parts, especially the livers. Those from the liver are usually high in vitamin A. The oils are used as dietary supplements, in soaps and detergents, as protective coatings, and as a base for other food products such as vegetable shortenings. [NIH] Fistula: Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body. [NIH] Flatulence: Production or presence of gas in the gastrointestinal tract which may be expelled through the anus. [NIH] Flatus: Gas passed through the rectum. [NIH] Flexor: Muscles which flex a joint. [NIH] Flow Cytometry: Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake. [NIH] Fluid Therapy: Therapy whose basic objective is to restore the volume and composition of the body fluids to normal with respect to water-electrolyte balance. Fluids may be administered intravenously, orally, by intermittent gavage, or by hypodermoclysis. [NIH] Fluorescence: The property of emitting radiation while being irradiated. The radiation emitted is usually of longer wavelength than that incident or absorbed, e.g., a substance can be irradiated with invisible radiation and emit visible light. X-ray fluorescence is used in diagnosis. [NIH] Fluorescent Dyes: Dyes that emit light when exposed to light. The wave length of the emitted light is usually longer than that of the incident light. Fluorochromes are substances that cause fluorescence in other substances, i.e., dyes used to mark or label other compounds with fluorescent tags. They are used as markers in biochemistry and immunology. [NIH] Folate: A B-complex vitamin that is being studied as a cancer prevention agent. Also called folic acid. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Folic Acid: N-(4-(((2-Amino-1,4-dihydro-4-oxo-6-pteridinyl)methyl)amino)benzoyl)-Lglutamic acid. A member of the vitamin B family that stimulates the hematopoietic system. It is present in the liver and kidney and is found in mushrooms, spinach, yeast, green leaves, and grasses. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. [NIH] Foramen: A natural hole of perforation, especially one in a bone. [NIH] Forearm: The part between the elbow and the wrist. [NIH]
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Frameshift: A type of mutation which causes out-of-phase transcription of the base sequence; such mutations arise from the addition or delection of nucleotide(s) in numbers other than 3 or multiples of 3. [NIH] Frameshift Mutation: A type of mutation in which a number of nucleotides not divisible by three is deleted from or inserted into a coding sequence, thereby causing an alteration in the reading frame of the entire sequence downstream of the mutation. These mutations may be induced by certain types of mutagens or may occur spontaneously. [NIH] Free Association: Spontaneous verbalization of whatever comes to mind. [NIH] Free Radical Scavengers: Substances that influence the course of a chemical reaction by ready combination with free radicals. Among other effects, this combining activity protects pancreatic islets against damage by cytokines and prevents myocardial and pulmonary perfusion injuries. [NIH] Fungi: A kingdom of eukaryotic, heterotrophic organisms that live as saprobes or parasites, including mushrooms, yeasts, smuts, molds, etc. They reproduce either sexually or asexually, and have life cycles that range from simple to complex. Filamentous fungi refer to those that grow as multicelluar colonies (mushrooms and molds). [NIH] Fungistatic: Inhibiting the growth of fungi. [EU] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gallstones: The solid masses or stones made of cholesterol or bilirubin that form in the gallbladder or bile ducts. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Gap Junctions: Connections between cells which allow passage of small molecules and electric current. Gap junctions were first described anatomically as regions of close apposition between cells with a narrow (1-2 nm) gap between cell membranes. The variety in the properties of gap junctions is reflected in the number of connexins, the family of proteins which form the junctions. [NIH] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gastric: Having to do with the stomach. [NIH] Gastric Acid: Hydrochloric acid present in gastric juice. [NIH] Gastric Emptying: The evacuation of food from the stomach into the duodenum. [NIH] Gastric Juices: Liquids produced in the stomach to help break down food and kill bacteria. [NIH]
Gastric Mucosa: Surface epithelium in the stomach that invaginates into the lamina propria, forming gastric pits. Tubular glands, characteristic of each region of the stomach (cardiac, gastric, and pyloric), empty into the gastric pits. The gastric mucosa is made up of several different kinds of cells. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]
Gastritis: Inflammation of the stomach. [EU] Gastroduodenal: Pertaining to or communicating with the stomach and duodenum, as a gastroduodenal fistula. [EU] Gastroenteritis: An acute inflammation of the lining of the stomach and intestines, characterized by anorexia, nausea, diarrhoea, abdominal pain, and weakness, which has
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various causes, including food poisoning due to infection with such organisms as Escherichia coli, Staphylococcus aureus, and Salmonella species; consumption of irritating food or drink; or psychological factors such as anger, stress, and fear. Called also enterogastritis. [EU] Gastroenterologist: A doctor who specializes in diagnosing and treating disorders of the digestive system. [NIH] Gastroenterology: A subspecialty of internal medicine concerned with the study of the physiology and diseases of the digestive system and related structures (esophagus, liver, gallbladder, and pancreas). [NIH] Gastroesophageal Reflux: Reflux of gastric juice and/or duodenal contents (bile acids, pancreatic juice) into the distal esophagus, commonly due to incompetence of the lower esophageal sphincter. Gastric regurgitation is an extension of this process with entry of fluid into the pharynx or mouth. [NIH] Gastroesophageal Reflux Disease: Flow of the stomach's contents back up into the esophagus. Happens when the muscle between the esophagus and the stomach (the lower esophageal sphincter) is weak or relaxes when it shouldn't. May cause esophagitis. Also called esophageal reflux or reflux esophagitis. [NIH] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gastrointestinal Transit: Passage of food (sometimes in the form of a test meal) through the gastrointestinal tract as measured in minutes or hours. The rate of passage through the intestine is an indicator of small bowel function. [NIH] Gastroscopy: Endoscopic examination, therapy, or surgery of the interior of the stomach. [NIH]
Gastrostomy: Creation of an artificial external opening into the stomach for nutritional support or gastrointestinal compression. [NIH] Gelatin: A product formed from skin, white connective tissue, or bone collagen. It is used as a protein food adjuvant, plasma substitute, hemostatic, suspending agent in pharmaceutical preparations, and in the manufacturing of capsules and suppositories. [NIH] Gelatinases: A class of enzymes that catalyzes the degradation of gelatin by acting on the peptide bonds. EC 3.4.24.-. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]
Gene Amplification: A selective increase in the number of copies of a gene coding for a specific protein without a proportional increase in other genes. It occurs naturally via the excision of a copy of the repeating sequence from the chromosome and its extrachromosomal replication in a plasmid, or via the production of an RNA transcript of the entire repeating sequence of ribosomal RNA followed by the reverse transcription of the molecule to produce an additional copy of the original DNA sequence. Laboratory techniques have been introduced for inducing disproportional replication by unequal crossing over, uptake of DNA from lysed cells, or generation of extrachromosomal sequences from rolling circle replication. [NIH] Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Rearrangement: The ordered rearrangement of gene regions by DNA recombination such as that which occurs normally during development. [NIH]
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General practitioner: A medical practitioner who does not specialize in a particular branch of medicine or limit his practice to a specific class of diseases. [NIH] Genes, mos: Retrovirus-associated DNA sequences (mos) originally isolated from the Moloney murine sarcoma virus (Mo-MSV). The proto-oncogene mos (c-mos) codes for a protein which is a member of the serine kinase family. There is no evidence as yet that human c-mos can become transformed or has a role in human cancer. However, in mice, activation can occur when the retrovirus-like intracisternal A-particle inserts itself near the c-mos sequence. The human c-mos gene is located at 8q22 on the long arm of chromosome 8. [NIH]
Genetic Code: The specifications for how information, stored in nucleic acid sequence (base sequence), is translated into protein sequence (amino acid sequence). The start, stop, and order of amino acids of a protein is specified by consecutive triplets of nucleotides called codons (codon). [NIH] Genetic Counseling: Advising families of the risks involved pertaining to birth defects, in order that they may make an informed decision on current or future pregnancies. [NIH] Genetic Engineering: Directed modification of the gene complement of a living organism by such techniques as altering the DNA, substituting genetic material by means of a virus, transplanting whole nuclei, transplanting cell hybrids, etc. [NIH] Genetic Markers: A phenotypically recognizable genetic trait which can be used to identify a genetic locus, a linkage group, or a recombination event. [NIH] Genetic testing: Analyzing DNA to look for a genetic alteration that may indicate an increased risk for developing a specific disease or disorder. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genital: Pertaining to the genitalia. [EU] Genitourinary: Pertaining to the genital and urinary organs; urogenital; urinosexual. [EU] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Germ Cells: The reproductive cells in multicellular organisms. [NIH] Germ-free: Free of bacteria, disease-causing viruses, and other organisms that can cause infection. [NIH] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] Gestational: Psychosis attributable to or occurring during pregnancy. [NIH] Giant Cells: Multinucleated masses produced by the fusion of many cells; often associated with viral infections. In AIDS, they are induced when the envelope glycoprotein of the HIV virus binds to the CD4 antigen of uninfected neighboring T4 cells. The resulting syncytium leads to cell death and thus may account for the cytopathic effect of the virus. [NIH] Giardiasis: An infection of the small intestine caused by the flagellated protozoan Giardia lamblia. It is spread via contaminated food and water and by direct person-to-person contact. [NIH] Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Glioblastoma: A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres,
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basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures. [NIH] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]
Glomeruli: Plural of glomerulus. [NIH] Glomerulonephritis: Glomerular disease characterized by an inflammatory reaction, with leukocyte infiltration and cellular proliferation of the glomeruli, or that appears to be the result of immune glomerular injury. [NIH] Glomerulus: A tiny set of looping blood vessels in the nephron where blood is filtered in the kidney. [NIH] Glucocorticoid: A compound that belongs to the family of compounds called corticosteroids (steroids). Glucocorticoids affect metabolism and have anti-inflammatory and immunosuppressive effects. They may be naturally produced (hormones) or synthetic (drugs). [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glucose Intolerance: A pathological state in which the fasting plasma glucose level is less than 140 mg per deciliter and the 30-, 60-, or 90-minute plasma glucose concentration following a glucose tolerance test exceeds 200 mg per deciliter. This condition is seen frequently in diabetes mellitus but also occurs with other diseases. [NIH] Glucuronic Acid: Derivatives of uronic acid found throughout the plant and animal kingdoms. They detoxify drugs and toxins by conjugating with them to form glucuronides in the liver which are more water-soluble metabolites that can be easily eliminated from the body. [NIH] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH]
Glutamine: A non-essential amino acid present abundantly throught the body and is involved in many metabolic processes. It is synthesized from glutamic acid and ammonia. It is the principal carrier of nitrogen in the body and is an important energy source for many cells. [NIH] Gluten: The protein of wheat and other grains which gives to the dough its tough elastic character. [EU] Glycerol: A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent. [NIH]
Glycerophospholipids: Derivatives of phosphatidic acid in which the hydrophobic regions are composed of two fatty acids and a polar alcohol is joined to the C-3 position of glycerol through a phosphodiester bond. They are named according to their polar head groups, such as phosphatidylcholine and phosphatidylethanolamine. [NIH] Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycogen: A sugar stored in the liver and muscles. It releases glucose into the blood when cells need it for energy. Glycogen is the chief source of stored fuel in the body. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Goblet Cells: Cells of the epithelial lining that produce and secrete mucins. [NIH]
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Gonadal: Pertaining to a gonad. [EU] Gout: Hereditary metabolic disorder characterized by recurrent acute arthritis, hyperuricemia and deposition of sodium urate in and around the joints, sometimes with formation of uric acid calculi. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Grade: The grade of a tumor depends on how abnormal the cancer cells look under a microscope and how quickly the tumor is likely to grow and spread. Grading systems are different for each type of cancer. [NIH] Grading: A system for classifying cancer cells in terms of how abnormal they appear when examined under a microscope. The objective of a grading system is to provide information about the probable growth rate of the tumor and its tendency to spread. The systems used to grade tumors vary with each type of cancer. Grading plays a role in treatment decisions. [NIH]
Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] Graft Rejection: An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the recipient. [NIH] Grafting: The operation of transfer of tissue from one site to another. [NIH] Gram-negative: Losing the stain or decolorized by alcohol in Gram's method of staining, a primary characteristic of bacteria having a cell wall composed of a thin layer of peptidoglycan covered by an outer membrane of lipoprotein and lipopolysaccharide. [EU] Gram-Negative Bacteria: Bacteria which lose crystal violet stain but are stained pink when treated by Gram's method. [NIH] Gram-positive: Retaining the stain or resisting decolorization by alcohol in Gram's method of staining, a primary characteristic of bacteria whose cell wall is composed of a thick layer of peptidologlycan with attached teichoic acids. [EU] Gram-Positive Bacteria: Bacteria which retain the crystal violet stain when treated by Gram's method. [NIH] Granule: A small pill made from sucrose. [EU] Granulocyte Colony-Stimulating Factor: A glycoprotein of MW 25 kDa containing internal disulfide bonds. It induces the survival, proliferation, and differentiation of neutrophilic granulocyte precursor cells and functionally activates mature blood neutrophils. Among the family of colony-stimulating factors, G-CSF is the most potent inducer of terminal differentiation to granulocytes and macrophages of leukemic myeloid cell lines. [NIH] Granulocyte-Macrophage Colony-Stimulating Factor: An acidic glycoprotein of MW 23 kDa with internal disulfide bonds. The protein is produced in response to a number of inflammatory mediators by mesenchymal cells present in the hemopoietic environment and at peripheral sites of inflammation. GM-CSF is able to stimulate the production of neutrophilic granulocytes, macrophages, and mixed granulocyte-macrophage colonies from bone marrow cells and can stimulate the formation of eosinophil colonies from fetal liver progenitor cells. GM-CSF can also stimulate some functional activities in mature granulocytes and macrophages. [NIH] Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [NIH] Granuloma: A relatively small nodular inflammatory lesion containing grouped
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mononuclear phagocytes, caused by infectious and noninfectious agents. [NIH] Granulomatous Colitis: Another name for Crohn's disease of the colon. [NIH] Granulomatous Disease, Chronic: A recessive X-linked defect of leukocyte function in which phagocytic cells ingest but fail to digest bacteria, resulting in recurring bacterial infections with granuloma formation. [NIH] Grasses: A large family, Gramineae, of narrow-leaved herbaceous monocots. Many grasses produce highly allergenic pollens and are hosts to cattle parasites and toxic fungi. [NIH] Growth: The progressive development of a living being or part of an organism from its earliest stage to maturity. [NIH] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH] Guanylate Cyclase: An enzyme that catalyzes the conversion of GTP to 3',5'-cyclic GMP and pyrophosphate. It also acts on ITP and dGTP. (From Enzyme Nomenclature, 1992) EC 4.6.1.2. [NIH] Habitat: An area considered in terms of its environment, particularly as this determines the type and quality of the vegetation the area can carry. [NIH] Hamartoma: A focal malformation resembling a neoplasm, composed of an overgrowth of mature cells and tissues that normally occur in the affected area. [NIH] Haploid: An organism with one basic chromosome set, symbolized by n; the normal condition of gametes in diploids. [NIH] Haplotypes: The genetic constitution of individuals with respect to one member of a pair of allelic genes, or sets of genes that are closely linked and tend to be inherited together such as those of the major histocompatibility complex. [NIH] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or as a manifestation of a wide variety of conditions including subarachnoid hemorrhage; craniocerebral trauma; central nervous system infections; intracranial hypertension; and other disorders. In general, recurrent headaches that are not associated with a primary disease process are referred to as headache disorders (e.g., migraine). [NIH] Headache Disorders: Common conditions characterized by persistent or recurrent headaches. Headache syndrome classification systems may be based on etiology (e.g., vascular headache, post-traumatic headaches, etc.), temporal pattern (e.g., cluster headache, paroxysmal hemicrania, etc.), and precipitating factors (e.g., cough headache). [NIH] Health Education: Education that increases the awareness and favorably influences the attitudes and knowledge relating to the improvement of health on a personal or community basis. [NIH] Health Promotion: Encouraging consumer behaviors most likely to optimize health potentials (physical and psychosocial) through health information, preventive programs, and access to medical care. [NIH] Health Services: Services for the diagnosis and treatment of disease and the maintenance of health. [NIH] Health Status: The level of health of the individual, group, or population as subjectively assessed by the individual or by more objective measures. [NIH]
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Heart failure: Loss of pumping ability by the heart, often accompanied by fatigue, breathlessness, and excess fluid accumulation in body tissues. [NIH] Heartbeat: One complete contraction of the heart. [NIH] Heartburn: Substernal pain or burning sensation, usually associated with regurgitation of gastric juice into the esophagus. [NIH] Hematogenous: Originating in the blood or spread through the bloodstream. [NIH] Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated hemoglobin is formed when linkages of glucose and related monosaccharides bind to hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level may be 3 to 4 times the normal conentration. Generally, complications are substantially lower among patients with Hb levels of 7 percent or less than in patients with HbA1c levels of 9 percent or more. [NIH] Hemoglobinuria: The presence of free hemoglobin in the urine. [NIH] Hemolytic: A disease that affects the blood and blood vessels. It destroys red blood cells, cells that cause the blood to clot, and the lining of blood vessels. HUS is often caused by the Escherichia coli bacterium in contaminated food. People with HUS may develop acute renal failure. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hemorrhoids: Varicosities of the hemorrhoidal venous plexuses. [NIH] Hemostasis: The process which spontaneously arrests the flow of blood from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements, and the process of blood or plasma coagulation. [NIH]
Heparin: Heparinic acid. A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts. [NIH] Hepatic: Refers to the liver. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatitis A: Hepatitis caused by hepatovirus. It can be transmitted through fecal contamination of food or water. [NIH] Hepatobiliary: Pertaining to the liver and the bile or the biliary ducts. [EU] Hepatocellular: Pertaining to or affecting liver cells. [EU] Hepatocellular carcinoma: A type of adenocarcinoma, the most common type of liver tumor. [NIH] Hepatocytes: The main structural component of the liver. They are specialized epithelial cells that are organized into interconnected plates called lobules. [NIH] Hepatovirus: A genus of Picornaviridae causing infectious hepatitis naturally in humans and experimentally in other primates. It is transmitted through fecal contamination of food or water. [NIH] Hereditary: Of, relating to, or denoting factors that can be transmitted genetically from one
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generation to another. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Heterodimers: Zippered pair of nonidentical proteins. [NIH] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]
Heterogenic: Derived from a different source or species. Also called heterogenous. [NIH] Heterogenous: Derived from a different source or species. Also called heterogenic. [NIH] Heterotrophic: Pertaining to organisms that are consumers and dependent on other organisms for their source of energy (food). [NIH] Histamine: 1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. [NIH] Histidine: An essential amino acid important in a number of metabolic processes. It is required for the production of histamine. [NIH] Histology: The study of tissues and cells under a microscope. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homogeneous: Consisting of or composed of similar elements or ingredients; of a uniform quality throughout. [EU] Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] Hormone therapy: Treatment of cancer by removing, blocking, or adding hormones. Also called endocrine therapy. [NIH] Host: Any animal that receives a transplanted graft. [NIH] Human growth hormone: A protein hormone, secreted by the anterior lobe of the pituitary, which promotes growth of the whole body by stimulating protein synthesis. The human gene has already been cloned and successfully expressed in bacteria. [NIH] Humoral: Of, relating to, proceeding from, or involving a bodily humour - now often used of endocrine factors as opposed to neural or somatic. [EU] Humour: 1. A normal functioning fluid or semifluid of the body (as the blood, lymph or bile) especially of vertebrates. 2. A secretion that is itself an excitant of activity (as certain hormones). [EU] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hybridization: The genetic process of crossbreeding to produce a hybrid. Hybrid nucleic acids can be formed by nucleic acid hybridization of DNA and RNA molecules. Protein hybridization allows for hybrid proteins to be formed from polypeptide chains. [NIH] Hybridoma: A hybrid cell resulting from the fusion of a specific antibody-producing spleen cell with a myeloma cell. [NIH]
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Hydrocephalus: Excessive accumulation of cerebrospinal fluid within the cranium which may be associated with dilation of cerebral ventricles, intracranial hypertension; headache; lethargy; urinary incontinence; and ataxia (and in infants macrocephaly). This condition may be caused by obstruction of cerebrospinal fluid pathways due to neurologic abnormalities, intracranial hemorrhages; central nervous system infections; brain neoplasms; craniocerebral trauma; and other conditions. Impaired resorption of cerebrospinal fluid from the arachnoid villi results in a communicating form of hydrocephalus. Hydrocephalus ex-vacuo refers to ventricular dilation that occurs as a result of brain substance loss from cerebral infarction and other conditions. [NIH] Hydrocortisone: The main glucocorticoid secreted by the adrenal cortex. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrogen Bonding: A low-energy attractive force between hydrogen and another element. It plays a major role in determining the properties of water, proteins, and other compounds. [NIH]
Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxamic Acids: A class of weak acids with the general formula R-conhoh. [NIH] Hydroxybenzoic Acids: Benzoic acid substituted by one or more hydroxy groups in any position on the benzene ring. [NIH] Hydroxylysine: A hydroxylated derivative of the amino acid lysine that is present in certain collagens. [NIH] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hyperaemia: An excess of blood in a part; engorgement. [EU] Hyperbaric: Characterized by greater than normal pressure or weight; applied to gases under greater than atmospheric pressure, as hyperbaric oxygen, or to a solution of greater specific gravity than another taken as a standard of reference. [EU] Hyperbaric oxygen: Oxygen that is at an atmospheric pressure higher than the pressure at sea level. Breathing hyperbaric oxygen to enhance the effectiveness of radiation therapy is being studied. [NIH] Hyperbilirubinemia: Pathologic process consisting of an abnormal increase in the amount of bilirubin in the circulating blood, which may result in jaundice. [NIH] Hyperkinesia: Abnormally increased motor function or activity; hyperactivity. [EU] Hyperplasia: An increase in the number of cells in a tissue or organ, not due to tumor formation. It differs from hypertrophy, which is an increase in bulk without an increase in
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the number of cells. [NIH] Hypersecretion: Excessive secretion. [EU] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hypertrophy: General increase in bulk of a part or organ, not due to tumor formation, nor to an increase in the number of cells. [NIH] Hyperuricemia: A buildup of uric acid (a byproduct of metabolism) in the blood; a side effect of some anticancer drugs. [NIH] Hypnotic: A drug that acts to induce sleep. [EU] Hypoglycaemia: An abnormally diminished concentration of glucose in the blood, which may lead to tremulousness, cold sweat, piloerection, hypothermia, and headache, accompanied by irritability, confusion, hallucinations, bizarre behaviour, and ultimately, convulsions and coma. [EU] Hypotension: Abnormally low blood pressure. [NIH] Hypotensive: Characterized by or causing diminished tension or pressure, as abnormally low blood pressure. [EU] Hypothalamic: Of or involving the hypothalamus. [EU] Hypothalamus: Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle. [NIH] Hypoxia: Reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the tissue by blood. [EU] Hysterotomy: An incision in the uterus, performed through either the abdomen or the vagina. [NIH] Ibuprofen: A nonsteroidal anti-inflammatory agent with analgesic properties used in the therapy of rheumatism and arthritis. [NIH] Ichthyosis: Any of several generalized skin disorders characterized by dryness, roughness, and scaliness, due to hypertrophy of the stratum corneum epidermis. Most are genetic, but some are acquired, developing in association with other systemic disease or genetic syndrome. [NIH] Id: The part of the personality structure which harbors the unconscious instinctive desires and strivings of the individual. [NIH] Idiopathic: Describes a disease of unknown cause. [NIH] Ileal: Related to the ileum, the lowest end of the small intestine. [NIH] Ileitis: Inflammation of the ileum. [EU] Ileoanal Pull-Through: An operation to remove the colon and inner lining of the rectum. The outer muscle of the rectum is not touched. The bottom end of the small intestine (ileum) is pulled through the remaining rectum and joined to the anus. Stool can be passed normally. Also called ileoanal anastomosis. [NIH] Ileoanal Reservoir: An operation to remove the colon, upper rectum, and part of the lower rectum. An internal pouch is created from the remaining intestine to hold stool. The operation may be done in two stages. The pouch may also be called a J-pouch or W-pouch. [NIH]
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Ileostomy: Surgical creation of an external opening into the ileum for fecal diversion or drainage. Loop or tube procedures are most often employed. [NIH] Ileum: The lower end of the small intestine. [NIH] Image Cytometry: A technique encompassing morphometry, densitometry, neural networks, and expert systems that has numerous clinical and research applications and is particularly useful in anatomic pathology for the study of malignant lesions. The most common current application of image cytometry is for DNA analysis, followed by quantitation of immunohistochemical staining. [NIH] Imidazole: C3H4N2. The ring is present in polybenzimidazoles. [NIH] Imipramine: The prototypical tricyclic antidepressant. It has been used in major depression, dysthymia, bipolar depression, attention-deficit disorders, agoraphobia, and panic disorders. It has less sedative effect than some other members of this therapeutic group. [NIH]
Immune adjuvant: A drug that stimulates the immune system to respond to disease. [NIH] Immune Complex Diseases: Group of diseases mediated by the deposition of large soluble complexes of antigen and antibody with resultant damage to tissue. Besides serum sickness and the arthus reaction, evidence supports a pathogenic role for immune complexes in many other systemic immunologic diseases including glomerulonephritis, systemic lupus erythematosus and polyarteritis nodosa. [NIH] Immune function: Production and action of cells that fight disease or infection. [NIH] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]
Immune Sera: Serum that contains antibodies. It is obtained from an animal that has been immunized either by antigen injection or infection with microorganisms containing the antigen. [NIH] Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immunity: Nonsusceptibility to the invasive or pathogenic microorganisms or to the toxic effect of antigenic substances. [NIH]
effects
of
foreign
Immunization: Deliberate stimulation of the host's immune response. Active immunization involves administration of antigens or immunologic adjuvants. Passive immunization involves administration of immune sera or lymphocytes or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow). [NIH] Immunoassay: Immunochemical assay or detection of a substance by serologic or immunologic methods. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance. [NIH] Immunoblotting: Immunologic methods for isolating and quantitatively measuring immunoreactive substances. When used with immune reagents such as monoclonal antibodies, the process is known generically as western blot analysis (blotting, western). [NIH]
Immunocompromised: Having a weakened immune system caused by certain diseases or treatments. [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunofluorescence: A technique for identifying molecules present on the surfaces of cells or in tissues using a highly fluorescent substance coupled to a specific antibody. [NIH]
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Immunogenic: Producing immunity; evoking an immune response. [EU] Immunoglobulin: A protein that acts as an antibody. [NIH] Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents. [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunology: The study of the body's immune system. [NIH] Immunosuppressant: An agent capable of suppressing immune responses. [EU] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Immunosuppressive Agents: Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of suppressor T-cell populations or by inhibiting the activation of helper cells. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of interleukins and other cytokines are emerging. [NIH] Immunosuppressive therapy: Therapy used to decrease the body's immune response, such as drugs given to prevent transplant rejection. [NIH] Immunotherapy: Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to prevent graft rejection. [NIH] Immunotoxins: Semisynthetic conjugates of various toxic molecules, including radioactive isotopes and bacterial or plant toxins, with specific immune substances such as immunoglobulins, monoclonal antibodies, and antigens. The antitumor or antiviral immune substance carries the toxin to the tumor or infected cell where the toxin exerts its poisonous effect. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Implantation: The insertion or grafting into the body of biological, living, inert, or radioactive material. [EU] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] In Situ Hybridization: A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes. [NIH] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Incision: A cut made in the body during surgery. [NIH] Incompetence: Physical or mental inadequacy or insufficiency. [EU] Indicative: That indicates; that points out more or less exactly; that reveals fairly clearly. [EU] Indigestion: Poor digestion. Symptoms include heartburn, nausea, bloating, and gas. Also called dyspepsia. [NIH] Indomethacin: A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes. [NIH]
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Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] Induction therapy: Treatment designed to be used as a first step toward shrinking the cancer and in evaluating response to drugs and other agents. Induction therapy is followed by additional therapy to eliminate whatever cancer remains. [NIH] Infancy: The period of complete dependency prior to the acquisition of competence in walking, talking, and self-feeding. [NIH] Infant, Newborn: An infant during the first month after birth. [NIH] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]
Infectious Diarrhea: Diarrhea caused by infection from bacteria, viruses, or parasites. [NIH] Infertility: The diminished or absent ability to conceive or produce an offspring while sterility is the complete inability to conceive or produce an offspring. [NIH] Infiltration: The diffusion or accumulation in a tissue or cells of substances not normal to it or in amounts of the normal. Also, the material so accumulated. [EU] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Inflammatory bowel disease: A general term that refers to the inflammation of the colon and rectum. Inflammatory bowel disease includes ulcerative colitis and Crohn's disease. [NIH]
Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [NIH] Ingestion: Taking into the body by mouth [NIH] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Initiator: A chemically reactive substance which may cause cell changes if ingested, inhaled or absorbed into the body; the substance may thus initiate a carcinogenic process. [NIH] Inner ear: The labyrinth, comprising the vestibule, cochlea, and semicircular canals. [NIH] Inositol: An isomer of glucose that has traditionally been considered to be a B vitamin although it has an uncertain status as a vitamin and a deficiency syndrome has not been identified in man. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1379) Inositol phospholipids are important in signal transduction. [NIH] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH]
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Instillation: . [EU] Insulator: Material covering the metal conductor of the lead. It is usually polyurethane or silicone. [NIH] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role in the regulation of glucose metabolism, generally promoting the cellular utilization of glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] Insulin-like: Muscular growth factor. [NIH] Insurance Pools: An organization of insurers or reinsurers through which particular types of risk are shared or pooled. The risk of high loss by a particular insurance company is transferred to the group as a whole (the insurance pool) with premiums, losses, and expenses shared in agreed amounts. [NIH] Integrins: A family of transmembrane glycoproteins consisting of noncovalent heterodimers. They interact with a wide variety of ligands including extracellular matrix glycoproteins, complement, and other cells, while their intracellular domains interact with the cytoskeleton. The integrins consist of at least three identified families: the cytoadhesin receptors, the leukocyte adhesion receptors, and the very-late-antigen receptors. Each family contains a common beta-subunit combined with one or more distinct alpha-subunits. These receptors participate in cell-matrix and cell-cell adhesion in many physiologically important processes, including embryological development, hemostasis, thrombosis, wound healing, immune and nonimmune defense mechanisms, and oncogenic transformation. [NIH] Intercellular Junctions: Strictly, and so far as it can be distinguished, the amorphous isotropic layer between adjacent primary walls of cells. [NIH] Interferon: A biological response modifier (a substance that can improve the body's natural response to disease). Interferons interfere with the division of cancer cells and can slow tumor growth. There are several types of interferons, including interferon-alpha, -beta, and gamma. These substances are normally produced by the body. They are also made in the laboratory for use in treating cancer and other diseases. [NIH] Interferon-alpha: One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells when exposed to live or inactivated virus, double-stranded RNA, or bacterial products. It is the major interferon produced by virus-induced leukocyte cultures and, in addition to its pronounced antiviral activity, it causes activation of NK cells. [NIH] Interferon-beta: One of the type I interferons produced by fibroblasts in response to stimulation by live or inactivated virus or by double-stranded RNA. It is a cytokine with antiviral, antiproliferative, and immunomodulating activity. [NIH] Interleukin-1: A soluble factor produced by monocytes, macrophages, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. IL-1 consists of two distinct forms, IL-1 alpha and IL-1 beta which perform the same functions but are distinct proteins. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation. The factor is distinct from interleukin-2. [NIH] Interleukin-10: Factor that is a coregulator of mast cell growth. It is produced by T-cells and B-cells and shows extensive homology with the Epstein-Barr virus BCRFI gene. [NIH] Interleukin-11: Lymphohematopoietic cytokine that has the ability to modulate antigenspecific antibody responses, potentiate megakaryocytes, and regulate bone marrow
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adipogenesis. [NIH] Interleukin-12: A heterodimeric cytokine that stimulates the production of interferon gamma from T-cells and natural killer cells, and also induces differentiation of Th1 helper cells. It is an initiator of cell-mediated immunity. [NIH] Interleukin-15: Cytokine that stimulates the proliferation of T-lymphocytes and shares biological activities with IL-2. IL-15 also can induce B-lymphocyte proliferation and differentiation. [NIH] Interleukin-18: Cytokine which resembles IL-1 structurally and IL-12 functionally. It enhances the cytotoxic activity of NK cells and CTLs, and appears to play a role both as neuroimmunomodulator and in the induction of mucosal immunity. [NIH] Interleukin-2: Chemical mediator produced by activated T lymphocytes and which regulates the proliferation of T cells, as well as playing a role in the regulation of NK cell activity. [NIH] Interleukin-3: A multilineage cell growth factor secreted by lymphocytes, epithelial cells, and astrocytes which stimulates clonal proliferation and differentiation of various types of blood and tissue cells. Also called multi-CSF, it is considered one of the hematopoietic colony stimulating factors. [NIH] Interleukin-8: A cytokine that activates neutrophils and attracts neutrophils and Tlymphocytes. It is released by several cell types including monocytes, macrophages, Tlymphocytes, fibroblasts, endothelial cells, and keratinocytes by an inflammatory stimulus. IL-8 is a member of the beta-thromboglobulin superfamily and structurally related to platelet factor 4. [NIH] Interleukins: Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Internal Medicine: A medical specialty concerned with the diagnosis and treatment of diseases of the internal organ systems of adults. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intervention Studies: Epidemiologic investigations designed to test a hypothesized causeeffect relation by modifying the supposed causal factor(s) in the study population. [NIH] Intestinal: Having to do with the intestines. [NIH] Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intoxication: Poisoning, the state of being poisoned. [EU] Intracellular: Inside a cell. [NIH] Intracranial Hypertension: Increased pressure within the cranial vault. This may result from several conditions, including hydrocephalus; brain edema; intracranial masses; severe systemic hypertension; pseudotumor cerebri; and other disorders. [NIH] Intraepithelial: Within the layer of cells that form the surface or lining of an organ. [NIH] Intramuscular: IM. Within or into muscle. [NIH] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin
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or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]
Involuntary: Reaction occurring without intention or volition. [NIH] Ion Channels: Gated, ion-selective glycoproteins that traverse membranes. The stimulus for channel gating can be a membrane potential, drug, transmitter, cytoplasmic messenger, or a mechanical deformation. Ion channels which are integral parts of ionotropic neurotransmitter receptors are not included. [NIH] Ion Transport: The movement of ions across energy-transducing cell membranes. Transport can be active or passive. Passive ion transport (facilitated diffusion) derives its energy from the concentration gradient of the ion itself and allows the transport of a single solute in one direction (uniport). Active ion transport is usually coupled to an energy-yielding chemical or photochemical reaction such as ATP hydrolysis. This form of primary active transport is called an ion pump. Secondary active transport utilizes the voltage and ion gradients produced by the primary transport to drive the cotransport of other ions or molecules. These may be transported in the same (symport) or opposite (antiport) direction. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] Irritable Bowel Syndrome: A disorder that comes and goes. Nerves that control the muscles in the GI tract are too active. The GI tract becomes sensitive to food, stool, gas, and stress. Causes abdominal pain, bloating, and constipation or diarrhea. Also called spastic colon or mucous colitis. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Ischemic Colitis: Decreased blood flow to the colon. Causes fever, pain, and bloody diarrhea. [NIH] Isoenzyme: Different forms of an enzyme, usually occurring in different tissues. The isoenzymes of a particular enzyme catalyze the same reaction but they differ in some of their properties. [NIH] Jaundice: A clinical manifestation of hyperbilirubinemia, consisting of deposition of bile pigments in the skin, resulting in a yellowish staining of the skin and mucous membranes. [NIH]
Jejunostomy: Surgical formation of an opening through the abdominal wall into the jejunum, usually for enteral hyperalimentation. [NIH] Jejunum: That portion of the small intestine which extends from the duodenum to the ileum; called also intestinum jejunum. [EU] Jet lag: Symptoms produced in human beings by fast travel through large meridian difference. [NIH] Jews: An ethnic group with certain cultural and religious traditions. [NIH] Joint: The point of contact between elements of an animal skeleton with the parts that surround and support it. [NIH] Kallidin: A decapeptide bradykinin homolog produced by the action of tissue and glandular kallikreins on low-molecular-weight kininogen. It is a smooth-muscle stimulant and hypotensive agent that functions through vasodilatation. [NIH] Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Keratinocyte growth factor: A substance that stimulates the growth of epithelial cells that
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line the surface of the mouth and intestinal tract. [NIH] Keratinocytes: Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell. [NIH] Keratitis: Inflammation of the cornea. [NIH] Keratoconus: A disorder characterized by an irregular corneal surface (cone-shaped) resulting in blurred and distorted images. [NIH] Kidney Disease: Any one of several chronic conditions that are caused by damage to the cells of the kidney. People who have had diabetes for a long time may have kidney damage. Also called nephropathy. [NIH] Kilobase: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Kinetics: The study of rate dynamics in chemical or physical systems. [NIH] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Labyrinth: The internal ear; the essential part of the organ of hearing. It consists of an osseous and a membranous portion. [NIH] Lacerations: Torn, ragged, mangled wounds. [NIH] Lacrimal: Pertaining to the tears. [EU] Lacrimal gland: The small almond-shaped structure that produces tears; located just above the outer corner of the eye. [NIH] Lactation: The period of the secretion of milk. [EU] Lactose Intolerance: The disease state resulting from the absence of lactase enzyme in the musocal cells of the gastrointestinal tract, and therefore an inability to break down the disaccharide lactose in milk for absorption from the gastrointestinal tract. It is manifested by indigestion of a mild nature to severe diarrhea. It may be due to inborn defect genetically conditioned or may be acquired. [NIH] Lag: The time elapsing between application of a stimulus and the resulting reaction. [NIH] Laminin: Large, noncollagenous glycoprotein with antigenic properties. It is localized in the basement membrane lamina lucida and functions to bind epithelial cells to the basement membrane. Evidence suggests that the protein plays a role in tumor invasion. [NIH] Laparotomy: A surgical incision made in the wall of the abdomen. [NIH] Large Intestine: The part of the intestine that goes from the cecum to the rectum. The large intestine absorbs water from stool and changes it from a liquid to a solid form. The large intestine is 5 feet long and includes the appendix, cecum, colon, and rectum. Also called colon. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Lavage: A cleaning of the stomach and colon. Uses a special drink and enemas. [NIH] Least-Squares Analysis: A principle of estimation in which the estimates of a set of parameters in a statistical model are those quantities minimizing the sum of squared differences between the observed values of a dependent variable and the values predicted by the model. [NIH] Lens: The transparent, double convex (outward curve on both sides) structure suspended
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between the aqueous and vitreous; helps to focus light on the retina. [NIH] Leptin: A 16-kD peptide hormone secreted from white adipocytes and implicated in the regulation of food intake and energy balance. Leptin provides the key afferent signal from fat cells in the feedback system that controls body fat stores. [NIH] Lesion: An area of abnormal tissue change. [NIH] Lethal: Deadly, fatal. [EU] Leucine: An essential branched-chain amino acid important for hemoglobin formation. [NIH] Leucocyte: All the white cells of the blood and their precursors (myeloid cell series, lymphoid cell series) but commonly used to indicate granulocytes exclusive of lymphocytes. [NIH]
Leukapheresis: The preparation of leukocyte concentrates with the return of red cells and leukocyte-poor plasma to the donor. [NIH] Leukemia: Cancer of blood-forming tissue. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Leukopenia: A condition in which the number of leukocytes (white blood cells) in the blood is reduced. [NIH] Leukotrienes: A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system. [NIH] Library Services: Services offered to the library user. They include reference and circulation. [NIH]
Lichen Planus: An inflammatory, pruritic disease of the skin and mucous membranes, which can be either generalized or localized. It is characterized by distinctive purplish, flattopped papules having a predilection for the trunk and flexor surfaces. The lesions may be discrete or coalesce to form plaques. Histologically, there is a "saw-tooth" pattern of epidermal hyperplasia and vacuolar alteration of the basal layer of the epidermis along with an intense upper dermal inflammatory infiltrate composed predominantly of T-cells. Etiology is unknown. [NIH] Life cycle: The successive stages through which an organism passes from fertilized ovum or spore to the fertilized ovum or spore of the next generation. [NIH] Life Expectancy: A figure representing the number of years, based on known statistics, to which any person of a given age may reasonably expect to live. [NIH] Ligament: A band of fibrous tissue that connects bones or cartilages, serving to support and strengthen joints. [EU] Ligands: A RNA simulation method developed by the MIT. [NIH] Likelihood Functions: Functions constructed from a statistical model and a set of observed data which give the probability of that data for various values of the unknown model parameters. Those parameter values that maximize the probability are the maximum likelihood estimates of the parameters. [NIH] Linear Models: Statistical models in which the value of a parameter for a given value of a factor is assumed to be equal to a + bx, where a and b are constants. The models predict a linear regression. [NIH]
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Linkage: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH] Linkage Disequilibrium: Nonrandom association of linked genes. This is the tendency of the alleles of two separate but already linked loci to be found together more frequently than would be expected by chance alone. [NIH] Linoleic Acids: Eighteen-carbon essential fatty acids that contain two double bonds. [NIH] Lipid: Fat. [NIH] Lipid A: Lipid A is the biologically active component of lipopolysaccharides. It shows strong endotoxic activity and exhibits immunogenic properties. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lipomatosis: A disorder consisting of the accumulation of abnormal localized, or tumor-like fat in the tissues. [NIH] Lipophilic: Having an affinity for fat; pertaining to or characterized by lipophilia. [EU] Lipopolysaccharide: Substance consisting of polysaccaride and lipid. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU] Lipoxygenase: An enzyme of the oxidoreductase class that catalyzes reactions between linoleate and other fatty acids and oxygen to form hydroperoxy-fatty acid derivatives. Related enzymes in this class include the arachidonate lipoxygenases, arachidonate 5lipoxygenase, arachidonate 12-lipoxygenase, and arachidonate 15-lipoxygenase. EC 1.13.11.12. [NIH] Lipoxygenase Inhibitors: Compounds or agents that combine with lipoxygenase and thereby prevent its substrate-enzyme combination with arachidonic acid and the formation of the eicosanoid products hydroxyeicosatetraenoic acid and various leukotrienes. [NIH] Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Liver scan: An image of the liver created on a computer screen or on film. A radioactive substance is injected into a blood vessel and travels through the bloodstream. It collects in the liver, especially in abnormal areas, and can be detected by the scanner. [NIH] Liver Transplantation: The transference of a part of or an entire liver from one human or animal to another. [NIH] Lobe: A portion of an organ such as the liver, lung, breast, or brain. [NIH] Local therapy: Treatment that affects cells in the tumor and the area close to it. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Logistic Models: Statistical models which describe the relationship between a qualitative
Dictionary 429
dependent variable (that is, one which can take only certain discrete values, such as the presence or absence of a disease) and an independent variable. A common application is in epidemiology for estimating an individual's risk (probability of a disease) as a function of a given risk factor. [NIH] Longitudinal study: Also referred to as a "cohort study" or "prospective study"; the analytic method of epidemiologic study in which subsets of a defined population can be identified who are, have been, or in the future may be exposed or not exposed, or exposed in different degrees, to a factor or factors hypothesized to influence the probability of occurrence of a given disease or other outcome. The main feature of this type of study is to observe large numbers of subjects over an extended time, with comparisons of incidence rates in groups that differ in exposure levels. [NIH] Loop: A wire usually of platinum bent at one end into a small loop (usually 4 mm inside diameter) and used in transferring microorganisms. [NIH] Lower Esophageal Sphincter: The muscle between the esophagus and stomach. When a person swallows, this muscle relaxes to let food pass from the esophagus to the stomach. It stays closed at other times to keep stomach contents from flowing back into the esophagus. [NIH]
Luciferase: Any one of several enzymes that catalyze the bioluminescent reaction in certain marine crustaceans, fish, bacteria, and insects. The enzyme is a flavoprotein; it oxidizes luciferins to an electronically excited compound that emits energy in the form of light. The color of light emitted varies with the organism. The firefly enzyme is a valuable reagent for measurement of ATP concentration. (Dorland, 27th ed) EC 1.13.12.-. [NIH] Lumbar: Pertaining to the loins, the part of the back between the thorax and the pelvis. [EU] Lumen: The cavity or channel within a tube or tubular organ. [EU] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [NIH] Lymph node: A rounded mass of lymphatic tissue that is surrounded by a capsule of connective tissue. Also known as a lymph gland. Lymph nodes are spread out along lymphatic vessels and contain many lymphocytes, which filter the lymphatic fluid (lymph). [NIH]
Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphatic system: The tissues and organs that produce, store, and carry white blood cells that fight infection and other diseases. This system includes the bone marrow, spleen, thymus, lymph nodes and a network of thin tubes that carry lymph and white blood cells. These tubes branch, like blood vessels, into all the tissues of the body. [NIH] Lymphoblasts: Interferon produced predominantly by leucocyte cells. [NIH] Lymphocyte: A white blood cell. Lymphocytes have a number of roles in the immune system, including the production of antibodies and other substances that fight infection and diseases. [NIH] Lymphocyte Subsets: A classification of lymphocytes based on structurally or functionally different populations of cells. [NIH] Lymphocyte Transformation: Morphologic alteration of small lymphocytes in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by interleukins, mitogens such as phytohemagglutinins, and by specific antigens. It
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may also occur in vivo, as in graft rejection and chronic myelogenous leukemia. [NIH] Lymphocytic: Referring to lymphocytes, a type of white blood cell. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lymphokines: Soluble protein factors generated by activated lymphocytes that affect other cells, primarily those involved in cellular immunity. [NIH] Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Lysine: An essential amino acid. It is often added to animal feed. [NIH] Lytic: 1. Pertaining to lysis or to a lysin. 2. Producing lysis. [EU] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells. [NIH] Macrophage Colony-Stimulating Factor: A mononuclear phagocyte colony-stimulating factor synthesized by mesenchymal cells. The compound stimulates the survival, proliferation, and differentiation of hematopoietic cells of the monocyte-macrophage series. M-CSF is a disulfide-bonded glycoprotein dimer with a MW of 70 kDa. It binds to a specific high affinity receptor (receptor, macrophage colony-stimulating factor). [NIH] Macula: A stain, spot, or thickening. Often used alone to refer to the macula retinae. [EU] Macula Lutea: An oval area in the retina, 3 to 5 mm in diameter, usually located temporal to the superior pole of the eye and slightly below the level of the optic disk. [NIH] Macular Degeneration: Degenerative changes in the macula lutea of the retina. [NIH] Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques. [NIH] Maintenance therapy: Treatment that is given to help a primary (original) treatment keep working. Maintenance therapy is often given to help keep cancer in remission. [NIH] Major Histocompatibility Complex: The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) transplantation antigens, genes which control the structure of the immune responseassociated (Ia) antigens, the immune response (Ir) genes which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement. [NIH] Malabsorption: Impaired intestinal absorption of nutrients. [EU] Malabsorption syndrome: A group of symptoms such as gas, bloating, abdominal pain, and diarrhea resulting from the body's inability to properly absorb nutrients. [NIH] Malaise: A vague feeling of bodily discomfort. [EU] Malformation: A morphologic developmental process. [EU]
defect
resulting
from
an
intrinsically
abnormal
Malignancy: A cancerous tumor that can invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant tumor: A tumor capable of metastasizing. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]
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Mania: Excitement of psychotic proportions manifested by mental and physical hyperactivity, disorganization of behaviour, and elevation of mood. [EU] Manic: Affected with mania. [EU] Manic-depressive psychosis: One of a group of psychotic reactions, fundamentally marked by severe mood swings and a tendency to remission and recurrence. [NIH] Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] Mastocyte: A mast cell. [EU] Mastocytosis: A group of diseases resulting from proliferation of mast cells. [NIH] Matrilysin: The smallest member of the matrix metalloproteinases. It plays a role in tumor progression. EC 3.4.24.23. [NIH] Matrix metalloproteinase: A member of a group of enzymes that can break down proteins, such as collagen, that are normally found in the spaces between cells in tissues (i.e., extracellular matrix proteins). Because these enzymes need zinc or calcium atoms to work properly, they are called metalloproteinases. Matrix metalloproteinases are involved in wound healing, angiogenesis, and tumor cell metastasis. [NIH] Measles Virus: The type species of morbillivirus and the cause of the highly infectious human disease measles, which affects mostly children. [NIH] Meat: The edible portions of any animal used for food including domestic mammals (the major ones being cattle, swine, and sheep) along with poultry, fish, shellfish, and game. [NIH]
Medial: Lying near the midsaggital plane of the body; opposed to lateral. [NIH] Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen with antibody or by the action of antigen with a sensitized lymphocyte. [EU] Medical Records: Recording of pertinent information concerning patient's illness or illnesses. [NIH] Medicament: A medicinal substance or agent. [EU] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Medroxyprogesterone: (6 alpha)-17-Hydroxy-6-methylpregn-4-ene-3,20-dione. A synthetic progestational hormone used in veterinary practice as an estrus regulator. [NIH] Medroxyprogesterone Acetate: An injectable contraceptive, generally marketed under the name Depo-Provera. [NIH] Megacolon: Pathological enlargement of the colon. [NIH] Megakaryocytes: Very large bone marrow cells which release mature blood platelets. [NIH] Megaloblastic: A large abnormal red blood cell appearing in the blood in pernicious anaemia. [EU] Melanin: The substance that gives the skin its color. [NIH] Melanocytes: Epidermal dendritic pigment cells which control long-term morphological color changes by alteration in their number or in the amount of pigment they produce and store in the pigment containing organelles called melanosomes. Melanophores are larger
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cells which do not exist in mammals. [NIH] Melanoma: A form of skin cancer that arises in melanocytes, the cells that produce pigment. Melanoma usually begins in a mole. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Meningitis: Inflammation of the meninges. When it affects the dura mater, the disease is termed pachymeningitis; when the arachnoid and pia mater are involved, it is called leptomeningitis, or meningitis proper. [EU] Menopause: Permanent cessation of menstruation. [NIH] Menstrual Cycle: The period of the regularly recurring physiologic changes in the endometrium occurring during the reproductive period in human females and some primates and culminating in partial sloughing of the endometrium (menstruation). [NIH] Menstruation: The normal physiologic discharge through the vagina of blood and mucosal tissues from the nonpregnant uterus. [NIH] Mental Disorders: Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function. [NIH] Mental Health: The state wherein the person is well adjusted. [NIH] Mental Processes: Conceptual functions or thinking in all its forms. [NIH] Mentors: Senior professionals who provide guidance, direction and support to those persons desirous of improvement in academic positions, administrative positions or other career development situations. [NIH] Mercaptopurine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH] Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to mercury poisoning. Because of its toxicity, the clinical use of mercury and mercurials is diminishing. [NIH] Mesenchymal: Refers to cells that develop into connective tissue, blood vessels, and lymphatic tissue. [NIH] Mesenteric: Pertaining to the mesentery : a membranous fold attaching various organs to the body wall. [EU] Mesentery: A layer of the peritoneum which attaches the abdominal viscera to the abdominal wall and conveys their blood vessels and nerves. [NIH] Meta-Analysis: A quantitative method of combining the results of independent studies (usually drawn from the published literature) and synthesizing summaries and conclusions which may be used to evaluate therapeutic effectiveness, plan new studies, etc., with application chiefly in the areas of research and medicine. [NIH] Metabolic disorder: A condition in which normal metabolic processes are disrupted, usually because of a missing enzyme. [NIH]
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Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Metalloendopeptidases: Endopeptidases which use a metal, normally zinc, in the catalytic mechanism. This group of enzymes is inactivated by metal chelators. EC 3.4.24. [NIH] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH] Metastatic: Having to do with metastasis, which is the spread of cancer from one part of the body to another. [NIH] Methionine: A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. [NIH] Methyltransferase: A drug-metabolizing enzyme. [NIH] Metronidazole: Antiprotozoal used in amebiasis, trichomoniasis, giardiasis, and as treponemacide in livestock. It has also been proposed as a radiation sensitizer for hypoxic cells. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985, p133), this substance may reasonably be anticipated to be a carcinogen (Merck, 11th ed). [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Mice Minute Virus: The type species of parvovirus prevalent in mouse colonies and found as a contaminant of many transplanted tumors or leukemias. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiological: Pertaining to microbiology : the science that deals with microorganisms, including algae, bacteria, fungi, protozoa and viruses. [EU] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microfilaments: The smallest of the cytoskeletal filaments. They are composed chiefly of actin. [NIH] Microorganism: An organism that can be seen only through a microscope. Microorganisms include bacteria, protozoa, algae, and fungi. Although viruses are not considered living organisms, they are sometimes classified as microorganisms. [NIH] Micro-organism: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microscopy: The application of microscope magnification to the study of materials that cannot be properly seen by the unaided eye. [NIH] Microspheres: Small uniformly-sized spherical particles frequently radioisotopes or various reagents acting as tags or markers. [NIH]
labeled
with
Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] Milligram: A measure of weight. A milligram is approximately 450,000-times smaller than a pound and 28,000-times smaller than an ounce. [NIH] Milliliter: A measure of volume for a liquid. A milliliter is approximately 950-times smaller than a quart and 30-times smaller than a fluid ounce. A milliliter of liquid and a cubic centimeter (cc) of liquid are the same. [NIH] Mineralocorticoids: A group of corticosteroids primarily associated with the regulation of
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water and electrolyte balance. This is accomplished through the effect on ion transport in renal tubules, resulting in retention of sodium and loss of potassium. Mineralocorticoid secretion is itself regulated by plasma volume, serum potassium, and angiotensin II. [NIH] Minority Groups: A subgroup having special characteristics within a larger group, often bound together by special ties which distinguish it from the larger group. [NIH] Miscarriage: Spontaneous expulsion of the products of pregnancy before the middle of the second trimester. [NIH] Mitochondria: Parts of a cell where aerobic production (also known as cell respiration) takes place. [NIH] Mitochondrial Swelling: Increase in volume of mitochondria due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of altered permeability of the membranes of respiring mitochondria. [NIH] Mitosis: A method of indirect cell division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Modeling: A treatment procedure whereby the therapist presents the target behavior which the learner is to imitate and make part of his repertoire. [NIH] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecular mass: The sum of the atomic masses of all atoms in a molecule, based on a scale in which the atomic masses of hydrogen, carbon, nitrogen, and oxygen are 1, 12, 14, and 16, respectively. For example, the molecular mass of water, which has two atoms of hydrogen and one atom of oxygen, is 18 (i.e., 2 + 16). [NIH] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monoclonal: An antibody produced by culturing a single type of cell. It therefore consists of a single species of immunoglobulin molecules. [NIH] Monoclonal antibodies: Laboratory-produced substances that can locate and bind to cancer cells wherever they are in the body. Many monoclonal antibodies are used in cancer detection or therapy; each one recognizes a different protein on certain cancer cells. Monoclonal antibodies can be used alone, or they can be used to deliver drugs, toxins, or radioactive material directly to a tumor. [NIH] Monocyte: A type of white blood cell. [NIH] Monokines: Soluble mediators of the immune response that are neither antibodies nor complement. They are produced largely, but not exclusively, by monocytes and macrophages. [NIH] Mononuclear: A cell with one nucleus. [NIH] Monosomy: The condition in which one chromosome of a pair is missing. In a normally diploid cell it is represented symbolically as 2N-1. [NIH] Monotherapy: A therapy which uses only one drug. [EU]
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Morbillivirus: A genus of the family Paramyxoviridae (subfamily Paramyxovirinae) where all the virions have hemagglutinin but not neuraminidase activity. All members produce both cytoplasmic and intranuclear inclusion bodies. MEASLES VIRUS is the type species. [NIH]
Morphological: Relating to the configuration or the structure of live organs. [NIH] Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Motility: The ability to move spontaneously. [EU] Motion Sickness: Sickness caused by motion, as sea sickness, train sickness, car sickness, and air sickness. [NIH] Mucins: A secretion containing mucopolysaccharides and protein that is the chief constituent of mucus. [NIH] Mucocutaneous: Pertaining to or affecting the mucous membrane and the skin. [EU] Mucosa: A mucous membrane, or tunica mucosa. [EU] Mucosal Lining: The lining of GI tract organs that makes mucus. [NIH] Mucositis: A complication of some cancer therapies in which the lining of the digestive system becomes inflamed. Often seen as sores in the mouth. [NIH] Mucus: The viscous secretion of mucous membranes. It contains mucin, white blood cells, water, inorganic salts, and exfoliated cells. [NIH] Multicenter study: A clinical trial that is carried out at more than one medical institution. [NIH]
Multiple Myeloma: A malignant tumor of plasma cells usually arising in the bone marrow; characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria, and anemia. [NIH] Multiple Organ Failure: A progressive condition usually characterized by combined failure of several organs such as the lungs, liver, kidney, along with some clotting mechanisms, usually postinjury or postoperative. [NIH] Multiple sclerosis: A disorder of the central nervous system marked by weakness, numbness, a loss of muscle coordination, and problems with vision, speech, and bladder control. Multiple sclerosis is thought to be an autoimmune disease in which the body's immune system destroys myelin. Myelin is a substance that contains both protein and fat (lipid) and serves as a nerve insulator and helps in the transmission of nerve signals. [NIH] Muscarinic Agonists: Drugs that bind to and activate muscarinic cholinergic receptors (receptors, muscarinic). Muscarinic agonists are most commonly used when it is desirable to increase smooth muscle tone, especially in the GI tract, urinary bladder and the eye. They may also be used to reduce heart rate. [NIH] Muscle Fibers: Large single cells, either cylindrical or prismatic in shape, that form the basic unit of muscle tissue. They consist of a soft contractile substance enclosed in a tubular sheath. [NIH] Muscular Atrophy: Derangement in size and number of muscle fibers occurring with aging, reduction in blood supply, or following immobilization, prolonged weightlessness, malnutrition, and particularly in denervation. [NIH] Muscular Dystrophies: A general term for a group of inherited disorders which are characterized by progressive degeneration of skeletal muscles. [NIH] Mutagenesis: Process of generating genetic mutations. It may occur spontaneously or be induced by mutagens. [NIH]
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Mutagenic: Inducing genetic mutation. [EU] Mutagens: Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes. [NIH] Mutate: To change the genetic material of a cell. Then changes (mutations) can be harmful, beneficial, or have no effect. [NIH] Myalgia: Pain in a muscle or muscles. [EU] Mycobacterium: A genus of gram-positive, aerobic bacteria. Most species are free-living in soil and water, but the major habitat for some is the diseased tissue of warm-blooded hosts. [NIH]
Mydriatic: 1. Dilating the pupil. 2. Any drug that dilates the pupil. [EU] Myelin: The fatty substance that covers and protects nerves. [NIH] Myelodysplastic syndrome: Disease in which the bone marrow does not function normally. Also called preleukemia or smoldering leukemia. [NIH] Myeloid Cells: Cells which include the monocytes and the granulocytes. [NIH] Myeloma: Cancer that arises in plasma cells, a type of white blood cell. [NIH] Myenteric: On stimulation of an intestinal segment, the segment above contracts and that below relaxes. [NIH] Myocardial infarction: Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Myocardial Ischemia: A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (coronary arteriosclerosis), to obstruction by a thrombus (coronary thrombosis), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (myocardial infarction). [NIH] Myocardial Reperfusion: Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing myocardial reperfusion injury. [NIH] Myocardial Reperfusion Injury: Functional, metabolic, or structural changes in ischemic heart muscle thought to result from reperfusion to the ischemic areas. Changes can be fatal to muscle cells and may include edema with explosive cell swelling and disintegration, sarcolemma disruption, fragmentation of mitochondria, contraction band necrosis, enzyme washout, and calcium overload. Other damage may include hemorrhage and ventricular arrhythmias. One possible mechanism of damage is thought to be oxygen free radicals. Treatment currently includes the introduction of scavengers of oxygen free radicals, and injury is thought to be prevented by warm blood cardioplegic infusion prior to reperfusion. [NIH]
Myocarditis: Inflammation of the myocardium; inflammation of the muscular walls of the heart. [EU] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH]
Dictionary 437
Myopia: That error of refraction in which rays of light entering the eye parallel to the optic axis are brought to a focus in front of the retina, as a result of the eyeball being too long from front to back (axial m.) or of an increased strength in refractive power of the media of the eye (index m.). Called also nearsightedness, because the near point is less distant than it is in emmetropia with an equal amplitude of accommodation. [EU] Myositis: Inflammation of a voluntary muscle. [EU] Myotonic Dystrophy: A condition presenting muscle weakness and wasting which may be progressive. [NIH] Nasogastric: The process of passing a small, flexible plastic tube through the nose or mouth into the stomach or small intestine. [NIH] Natural killer cells: NK cells. A type of white blood cell that contains granules with enzymes that can kill tumor cells or microbial cells. Also called large granular lymphocytes (LGL). [NIH] Nausea: An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses. [NIH] NCI: National Cancer Institute. NCI, part of the National Institutes of Health of the United States Department of Health and Human Services, is the federal government's principal agency for cancer research. NCI conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the NCI Web site at http://cancer.gov. [NIH] Nearsightedness: The common term for myopia. [NIH] Necrosis: A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Necrotizing Enterocolitis: A condition in which part of the tissue in the intestines is destroyed. Occurs mainly in under-weight newborn babies. A temporary ileostomy may be necessary. [NIH] Need: A state of tension or dissatisfaction felt by an individual that impels him to action toward a goal he believes will satisfy the impulse. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Neoplasia: Abnormal and uncontrolled cell growth. [NIH] Neoplasm: A new growth of benign or malignant tissue. [NIH] Neoplastic: Pertaining to or like a neoplasm (= any new and abnormal growth); pertaining to neoplasia (= the formation of a neoplasm). [EU] Nephritis: Inflammation of the kidney; a focal or diffuse proliferative or destructive process which may involve the glomerulus, tubule, or interstitial renal tissue. [EU] Nephropathy: Disease of the kidneys. [EU] Nephrosis: Descriptive histopathologic term for renal disease without an inflammatory component. [NIH] Nephrotic: Pertaining to, resembling, or caused by nephrosis. [EU] Nephrotic Syndrome: Clinical association of heavy proteinuria, hypoalbuminemia, and generalized edema. [NIH] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH]
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Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Networks: Pertaining to a nerve or to the nerves, a meshlike structure of interlocking fibers or strands. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] Neuritis: A general term indicating inflammation of a peripheral or cranial nerve. Clinical manifestation may include pain; paresthesias; paresis; or hypesthesia. [NIH] Neurogenic: Loss of bladder control caused by damage to the nerves controlling the bladder. [NIH] Neurologic: Having to do with nerves or the nervous system. [NIH] Neuromuscular: Pertaining to muscles and nerves. [EU] Neuromuscular Junction: The synapse between a neuron and a muscle. [NIH] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropeptide: A member of a class of protein-like molecules made in the brain. Neuropeptides consist of short chains of amino acids, with some functioning as neurotransmitters and some functioning as hormones. [NIH] Neuroretinitis: Inflammation of the optic nerve head and adjacent retina. [NIH] Neurotoxic: Poisonous or destructive to nerve tissue. [EU] Neurotransmitters: Endogenous signaling molecules that alter the behavior of neurons or effector cells. Neurotransmitter is used here in its most general sense, including not only messengers that act directly to regulate ion channels, but also those that act through second messenger systems, and those that act at a distance from their site of release. Included are neuromodulators, neuroregulators, neuromediators, and neurohumors, whether or not acting at synapses. [NIH] Neutrons: Electrically neutral elementary particles found in all atomic nuclei except light hydrogen; the mass is equal to that of the proton and electron combined and they are unstable when isolated from the nucleus, undergoing beta decay. Slow, thermal, epithermal, and fast neutrons refer to the energy levels with which the neutrons are ejected from heavier nuclei during their decay. [NIH] Neutropenia: An abnormal decrease in the number of neutrophils, a type of white blood cell. [NIH] Neutrophil: A type of white blood cell. [NIH] Neutrophil Infiltration: The diffusion or accumulation of neutrophils in tissues or cells in response to a wide variety of substances released at the sites of inflammatory reactions. [NIH] Niacin: Water-soluble vitamin of the B complex occurring in various animal and plant tissues. Required by the body for the formation of coenzymes NAD and NADP. Has pellagra-curative, vasodilating, and antilipemic properties. [NIH] Nicotine: Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke. [NIH]
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Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells. It is synthesized from arginine by a complex reaction, catalyzed by nitric oxide synthase. Nitric oxide is endothelium-derived relaxing factor. It is released by the vascular endothelium and mediates the relaxation induced by some vasodilators such as acetylcholine and bradykinin. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic guanylate cyclase and thus elevates intracellular levels of cyclic GMP. [NIH]
Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Nonmalignant: Not cancerous. [NIH] Nonverbal Communication: Transmission of emotions, ideas, and attitudes between individuals in ways other than the spoken language. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleic Acid Hybridization: The process whereby two single-stranded polynucleotides form a double-stranded molecule, with hydrogen bonding between the complementary bases in the two strains. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nursing Care: Care given to patients by nursing service personnel. [NIH] Nutritional Status: State of the body in relation to the consumption and utilization of nutrients. [NIH] Nutritional Support: The administration of nutrients for assimilation and utilization by a patient by means other than normal eating. It does not include fluid therapy which normalizes body fluids to restore water-electrolyte balance. [NIH] Observational study: An epidemiologic study that does not involve any intervention, experimental or otherwise. Such a study may be one in which nature is allowed to take its course, with changes in one characteristic being studied in relation to changes in other characteristics. Analytical epidemiologic methods, such as case-control and cohort study designs, are properly called observational epidemiology because the investigator is observing without intervention other than to record, classify, count, and statistically analyze results. [NIH] Occult: Obscure; concealed from observation, difficult to understand. [EU] Occult Blood: Chemical, spectroscopic, or microscopic detection of extremely small amounts of blood. [NIH] Octreotide: A potent, long-acting somatostatin octapeptide analog which has a wide range of physiological actions. It inhibits growth hormone secretion, is effective in the treatment of hormone-secreting tumors from various organs, and has beneficial effects in the
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management of many pathological states including diabetes mellitus, orthostatic hypertension, hyperinsulinism, hypergastrinemia, and small bowel fistula. [NIH] Ocular: 1. Of, pertaining to, or affecting the eye. 2. Eyepiece. [EU] Odds Ratio: The ratio of two odds. The exposure-odds ratio for case control data is the ratio of the odds in favor of exposure among cases to the odds in favor of exposure among noncases. The disease-odds ratio for a cohort or cross section is the ratio of the odds in favor of disease among the exposed to the odds in favor of disease among the unexposed. The prevalence-odds ratio refers to an odds ratio derived cross-sectionally from studies of prevalent cases. [NIH] Odour: A volatile emanation that is perceived by the sense of smell. [EU] Office Visits: Visits made by patients to health service providers' offices for diagnosis, treatment, and follow-up. [NIH] Ointments: Semisolid preparations used topically for protective emollient effects or as a vehicle for local administration of medications. Ointment bases are various mixtures of fats, waxes, animal and plant oils and solid and liquid hydrocarbons. [NIH] Omega-3 fatty acid: A type of fat obtained in the diet and involved in immunity. [NIH] Oncogene: A gene that normally directs cell growth. If altered, an oncogene can promote or allow the uncontrolled growth of cancer. Alterations can be inherited or caused by an environmental exposure to carcinogens. [NIH] Oncogenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Open Reading Frames: Reading frames where successive nucleotide triplets can be read as codons specifying amino acids and where the sequence of these triplets is not interrupted by stop codons. [NIH] Ophthalmologist: A medical doctor specializing in the diagnosis and medical or surgical treatment of visual disorders and eye disease. [NIH] Opsin: A protein formed, together with retinene, by the chemical breakdown of metarhodopsin. [NIH] Optic Chiasm: The X-shaped structure formed by the meeting of the two optic nerves. At the optic chiasm the fibers from the medial part of each retina cross to project to the other side of the brain while the lateral retinal fibers continue on the same side. As a result each half of the brain receives information about the contralateral visual field from both eyes. [NIH]
Optic disc: The circular area (disc) where the optic nerve connects to the retina. [NIH] Optic Disk: The portion of the optic nerve seen in the fundus with the ophthalmoscope. It is formed by the meeting of all the retinal ganglion cell axons as they enter the optic nerve. [NIH]
Optic Nerve: The 2nd cranial nerve. The optic nerve conveys visual information from the retina to the brain. The nerve carries the axons of the retinal ganglion cells which sort at the optic chiasm and continue via the optic tracts to the brain. The largest projection is to the lateral geniculate nuclei; other important targets include the superior colliculi and the suprachiasmatic nuclei. Though known as the second cranial nerve, it is considered part of the central nervous system. [NIH] Optic Neuritis: Inflammation of the optic nerve. Commonly associated conditions include autoimmune disorders such as multiple sclerosis, infections, and granulomatous diseases. Clinical features include retro-orbital pain that is aggravated by eye movement, loss of color vision, and contrast sensitivity that may progress to severe visual loss, an afferent pupillary
Dictionary 441
defect (Marcus-Gunn pupil), and in some instances optic disc hyperemia and swelling. Inflammation may occur in the portion of the nerve within the globe (neuropapillitis or anterior optic neuritis) or the portion behind the globe (retrobulbar neuritis or posterior optic neuritis). [NIH] Orbit: One of the two cavities in the skull which contains an eyeball. Each eye is located in a bony socket or orbit. [NIH] Orbital: Pertaining to the orbit (= the bony cavity that contains the eyeball). [EU] Organ Transplantation: Transference of an organ between individuals of the same species or between individuals of different species. [NIH] Organelles: Specific particles of membrane-bound organized living substances present in eukaryotic cells, such as the mitochondria; the golgi apparatus; endoplasmic reticulum; lysomomes; plastids; and vacuoles. [NIH] Orthostatic: Pertaining to or caused by standing erect. [EU] Osmotic: Pertaining to or of the nature of osmosis (= the passage of pure solvent from a solution of lesser to one of greater solute concentration when the two solutions are separated by a membrane which selectively prevents the passage of solute molecules, but is permeable to the solvent). [EU] Ossification: The formation of bone or of a bony substance; the conversion of fibrous tissue or of cartilage into bone or a bony substance. [EU] Osteoarthritis: A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans. [NIH] Osteoporosis: Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis and age-related (or senile) osteoporosis. [NIH] Ostomy: Surgical construction of an artificial opening (stoma) for external fistulization of a duct or vessel by insertion of a tube with or without a supportive stent. [NIH] Outpatient: A patient who is not an inmate of a hospital but receives diagnosis or treatment in a clinic or dispensary connected with the hospital. [NIH] Ovalbumin: An albumin obtained from the white of eggs. It is a member of the serpin superfamily. [NIH] Ovarian Cysts: General term for cysts and cystic diseases of the ovary. [NIH] Ovarian Follicle: Spheroidal cell aggregation in the ovary containing an ovum. It consists of an external fibro-vascular coat, an internal coat of nucleated cells, and a transparent, albuminous fluid in which the ovum is suspended. [NIH] Ovaries: The pair of female reproductive glands in which the ova, or eggs, are formed. The ovaries are located in the pelvis, one on each side of the uterus. [NIH] Ovary: Either of the paired glands in the female that produce the female germ cells and secrete some of the female sex hormones. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH] Oxidants: Oxidizing agents or electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (oxidation-reduction). In vivo, it appears that phagocyte-generated oxidants function as tumor promoters or cocarcinogens rather than as complete carcinogens perhaps because of the high levels of endogenous antioxidant defenses. It is also thought that oxidative damage in joints may trigger the
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autoimmune response that characterizes the persistence of the rheumatoid disease process. [NIH]
Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]
Oxidation-Reduction: A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471). [NIH] Oxidative metabolism: A chemical process in which oxygen is used to make energy from carbohydrates (sugars). Also known as aerobic respiration, cell respiration, or aerobic metabolism. [NIH] Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] P53 gene: A tumor suppressor gene that normally inhibits the growth of tumors. This gene is altered in many types of cancer. [NIH] Pachymeningitis: Inflammation of the dura mater of the brain, the spinal cord or the optic nerve. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Palliative therapy: Treatment given to relieve symptoms caused by advanced cancer. Palliative therapy does not alter the course of a disease but improves the quality of life. [NIH] Palsy: Disease of the peripheral nervous system occurring usually after many years of increased lead absorption. [NIH] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Pancreatic: Having to do with the pancreas. [NIH] Pancreatic cancer: Cancer of the pancreas, a salivary gland of the abdomen. [NIH] Pancreatic Ducts: Ducts that collect pancreatic juice from the pancreas and supply it to the duodenum. [NIH] Pancreatic Insufficiency: Absence of or reduced pancreatic exocrine secretion into the duodenum and resultant poor digestion of lipids, vitamins, nitrogen, and carbohydrates. [NIH]
Pancreatic Juice: The fluid containing digestive enzymes secreted by the pancreas in response to food in the duodenum. [NIH] Pancreatitis: Acute or chronic inflammation of the pancreas, which may be asymptomatic or symptomatic, and which is due to autodigestion of a pancreatic tissue by its own enzymes. It is caused most often by alcoholism or biliary tract disease; less commonly it may be associated with hyperlipaemia, hyperparathyroidism, abdominal trauma (accidental or operative injury), vasculitis, or uraemia. [EU]
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Pancytopenia: Deficiency of all three cell elements of the blood, erythrocytes, leukocytes and platelets. [NIH] Paneth Cells: Epithelial cells found in the basal part of the intestinal glands (crypts of Lieberkuhn). Paneth cells synthesize and secrete lysozyme and cryptdins. [NIH] Panic: A state of extreme acute, intense anxiety and unreasoning fear accompanied by disorganization of personality function. [NIH] Panic Disorder: A type of anxiety disorder characterized by unexpected panic attacks that last minutes or, rarely, hours. Panic attacks begin with intense apprehension, fear or terror and, often, a feeling of impending doom. Symptoms experienced during a panic attack include dyspnea or sensations of being smothered; dizziness, loss of balance or faintness; choking sensations; palpitations or accelerated heart rate; shakiness; sweating; nausea or other form of abdominal distress; depersonalization or derealization; paresthesias; hot flashes or chills; chest discomfort or pain; fear of dying and fear of not being in control of oneself or going crazy. Agoraphobia may also develop. Similar to other anxiety disorders, it may be inherited as an autosomal dominant trait. [NIH] Panniculitis: General term for inflammation of adipose tissue, usually of the skin, characterized by reddened subcutaneous nodules. [NIH] Par excellence: The petrous portion of the temporal bone, containing the inner ear and wedged in at the base of the skull between the sphenoid and occipital bones. [NIH] Paraffin: A mixture of solid hydrocarbons obtained from petroleum. It has a wide range of uses including as a stiffening agent in ointments, as a lubricant, and as a topical antiinflammatory. It is also commonly used as an embedding material in histology. [NIH] Paralysis: Loss of ability to move all or part of the body. [NIH] Parasite: An animal or a plant that lives on or in an organism of another species and gets at least some of its nutrition from that other organism. [NIH] Parasitic: Having to do with or being a parasite. A parasite is an animal or a plant that lives on or in an organism of another species and gets at least some of its nutrients from it. [NIH] Parathyroid: 1. Situated beside the thyroid gland. 2. One of the parathyroid glands. 3. A sterile preparation of the water-soluble principle(s) of the parathyroid glands, ad-ministered parenterally as an antihypocalcaemic, especially in the treatment of acute hypoparathyroidism with tetany. [EU] Parathyroid Glands: Two small paired endocrine glands in the region of the thyroid gland. They secrete parathyroid hormone and are concerned with the metabolism of calcium and phosphorus. [NIH] Paratuberculosis: An infectious disease caused by Mycobacterium paratuberculosis. Characteristics include chronic debilitation and weight loss. [NIH] Parenteral: Not through the alimentary canal but rather by injection through some other route, as subcutaneous, intramuscular, intraorbital, intracapsular, intraspinal, intrasternal, intravenous, etc. [EU] Parenteral Nutrition: The administering of nutrients for assimilation and utilization by a patient who cannot maintain adequate nutrition by enteral feeding alone. Nutrients are administered by a route other than the alimentary canal (e.g., intravenously, subcutaneously). [NIH] Paresthesias: Abnormal touch sensations, such as burning or prickling, that occur without an outside stimulus. [NIH] Parotid: The space that contains the parotid gland, the facial nerve, the external carotid
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artery, and the retromandibular vein. [NIH] Paroxysmal: Recurring in paroxysms (= spasms or seizures). [EU] Partial remission: The shrinking, but not complete disappearance, of a tumor in response to therapy. Also called partial response. [NIH] Particle: A tiny mass of material. [EU] Parvovirus: A genus of the family Parvoviridae, subfamily Parvovirinae, infecting a variety of vertebrates including humans. Parvoviruses are responsible for a number of important diseases but also can be non-pathogenic in certain hosts. The type species is mice minute virus. [NIH] Patch: A piece of material used to cover or protect a wound, an injured part, etc.: a patch over the eye. [NIH] Pathogen: Any disease-producing microorganism. [EU] Pathogenesis: The cellular events and reactions that occur in the development of disease. [NIH]
Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH] Pathologies: The study of abnormality, especially the study of diseases. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Care Management: Generating, planning, organizing, and administering medical and nursing care and services for patients. [NIH] Patient Compliance: Voluntary cooperation of the patient in following a prescribed regimen. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]
Patient Satisfaction: The degree to which the individual regards the health care service or product or the manner in which it is delivered by the provider as useful, effective, or beneficial. [NIH] Patient Selection: Criteria and standards used for the determination of the appropriateness of the inclusion of patients with specific conditions in proposed treatment plans and the criteria used for the inclusion of subjects in various clinical trials and other research protocols. [NIH] Pediatric Gastroenterologist: A doctor who treats children with digestive diseases. [NIH] Pediatrics: A medical specialty concerned with maintaining health and providing medical care to children from birth to adolescence. [NIH] Peer Group: Group composed of associates of same species, approximately the same age, and usually of similar rank or social status. [NIH] Pelvic: Pertaining to the pelvis. [EU] Penis: The external reproductive organ of males. It is composed of a mass of erectile tissue enclosed in three cylindrical fibrous compartments. Two of the three compartments, the corpus cavernosa, are placed side-by-side along the upper part of the organ. The third compartment below, the corpus spongiosum, houses the urethra. [NIH] Pepsin: An enzyme made in the stomach that breaks down proteins. [NIH]
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Pepsin A: Formed from pig pepsinogen by cleavage of one peptide bond. The enzyme is a single polypeptide chain and is inhibited by methyl 2-diaazoacetamidohexanoate. It cleaves peptides preferentially at the carbonyl linkages of phenylalanine or leucine and acts as the principal digestive enzyme of gastric juice. [NIH] Peptic: Pertaining to pepsin or to digestion; related to the action of gastric juices. [EU] Peptic Ulcer: Ulcer that occurs in those portions of the alimentary tract which come into contact with gastric juice containing pepsin and acid. It occurs when the amount of acid and pepsin is sufficient to overcome the gastric mucosal barrier. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Peptide Chain Elongation: The process whereby an amino acid is joined through a substituted amide linkage to a chain of peptides. [NIH] Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins. [NIH] Peptide Hydrolases: A subclass of enzymes from the hydrolase class that catalyze the hydrolysis of peptide bonds. Exopeptidases and endopeptidases make up the sub-subclasses for this group. EC 3.4. [NIH] Perception: The ability quickly and accurately to recognize similarities and differences among presented objects, whether these be pairs of words, pairs of number series, or multiple sets of these or other symbols such as geometric figures. [NIH] Percutaneous: Performed through the skin, as injection of radiopacque material in radiological examination, or the removal of tissue for biopsy accomplished by a needle. [EU] Perennial: Lasting through the year of for several years. [EU] Perforation: 1. The act of boring or piercing through a part. 2. A hole made through a part or substance. [EU] Perfusion: Bathing an organ or tissue with a fluid. In regional perfusion, a specific area of the body (usually an arm or a leg) receives high doses of anticancer drugs through a blood vessel. Such a procedure is performed to treat cancer that has not spread. [NIH] Perianal: Located around the anus. [EU] Pericardium: The fibroserous sac surrounding the heart and the roots of the great vessels. [NIH]
Perinatal: Pertaining to or occurring in the period shortly before and after birth; variously defined as beginning with completion of the twentieth to twenty-eighth week of gestation and ending 7 to 28 days after birth. [EU] Perineal: Pertaining to the perineum. [EU] Perineum: The area between the anus and the sex organs. [NIH] Periodontal disease: Disease involving the supporting structures of the teeth (as the gums and periodontal membranes). [NIH] Periodontitis: Inflammation of the periodontal membrane; also called periodontitis simplex. [NIH]
Perioperative: Around the time of surgery; usually lasts from the time of going into the hospital or doctor's office for surgery until the time the patient goes home. [NIH] Peripheral blood: Blood circulating throughout the body. [NIH] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic
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nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] Peristalsis: The rippling motion of muscles in the intestine or other tubular organs characterized by the alternate contraction and relaxation of the muscles that propel the contents onward. [NIH] Peritoneal: Having to do with the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Peritoneal Cavity: The space enclosed by the peritoneum. It is divided into two portions, the greater sac and the lesser sac or omental bursa, which lies behind the stomach. The two sacs are connected by the foramen of Winslow, or epiploic foramen. [NIH] Peritoneum: Endothelial lining of the abdominal cavity, the parietal peritoneum covering the inside of the abdominal wall and the visceral peritoneum covering the bowel, the mesentery, and certain of the organs. The portion that covers the bowel becomes the serosal layer of the bowel wall. [NIH] Peritonitis: Inflammation of the peritoneum; a condition marked by exudations in the peritoneum of serum, fibrin, cells, and pus. It is attended by abdominal pain and tenderness, constipation, vomiting, and moderate fever. [EU] Personality Disorders: A major deviation from normal patterns of behavior. [NIH] Petrolatum: A colloidal system of semisolid hydrocarbons obtained from petroleum. It is used as an ointment base, topical protectant, and lubricant. [NIH] Petroleum: Naturally occurring complex liquid hydrocarbons which, after distillation, yield combustible fuels, petrochemicals, and lubricants. [NIH] PH: The symbol relating the hydrogen ion (H+) concentration or activity of a solution to that of a given standard solution. Numerically the pH is approximately equal to the negative logarithm of H+ concentration expressed in molarity. pH 7 is neutral; above it alkalinity increases and below it acidity increases. [EU] Phagocyte: An immune system cell that can surround and kill microorganisms and remove dead cells. Phagocytes include macrophages. [NIH] Phagocytosis: The engulfing of microorganisms, other cells, and foreign particles by phagocytic cells. [NIH] Pharmaceutical Preparations: Drugs intended for human or veterinary use, presented in their finished dosage form. Included here are materials used in the preparation and/or formulation of the finished dosage form. [NIH] Pharmaceutical Solutions: Homogeneous liquid preparations that contain one or more chemical substances dissolved, i.e., molecularly dispersed, in a suitable solvent or mixture of mutually miscible solvents. For reasons of their ingredients, method of preparation, or use, they do not fall into another group of products. [NIH] Pharmacists: Those persons legally qualified by education and training to engage in the practice of pharmacy. [NIH] Pharmacodynamic: Is concerned with the response of living tissues to chemical stimuli, that is, the action of drugs on the living organism in the absence of disease. [NIH] Pharmacokinetic: The mathematical analysis of the time courses of absorption, distribution, and elimination of drugs. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Pharmacotherapy: A regimen of using appetite suppressant medications to manage obesity by decreasing appetite or increasing the feeling of satiety. These medications decrease
Dictionary 447
appetite by increasing serotonin or catecholamine—two brain chemicals that affect mood and appetite. [NIH] Pharyngitis: Inflammation of the throat. [NIH] Pharynx: The hollow tube about 5 inches long that starts behind the nose and ends at the top of the trachea (windpipe) and esophagus (the tube that goes to the stomach). [NIH] Phenolphthalein: An acid-base indicator which is colorless in acid solution, but turns pink to red as the solution becomes alkaline. It is used medicinally as a cathartic. [NIH] Phenotype: The outward appearance of the individual. It is the product of interactions between genes and between the genotype and the environment. This includes the killer phenotype, characteristic of yeasts. [NIH] Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor of melanin, dopamine, noradrenalin, and thyroxine. [NIH] Phosphodiesterase: Effector enzyme that regulates the levels of a second messenger, the cyclic GMP. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phospholipases A: Phosphatide acylhydrolases. Catalyze the hydrolysis of one of the acyl groups of phosphoglycerides or glycerophosphatidates. Phospholipase A1 hydrolyzes the acyl group attached to the 1-position (EC 3.1.1.32) and phospholipase A2 hydrolyzes the acyl group attached to the 2-position (EC 3.1.1.4). [NIH] Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides; glycerophospholipids) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylated: Attached to a phosphate group. [NIH] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Photophobia: Abnormal sensitivity to light. This may occur as a manifestation of eye diseases; migraine; subarachnoid hemorrhage; meningitis; and other disorders. Photophobia may also occur in association with depression and other mental disorders. [NIH] Photoreceptors: Cells specialized to detect and transduce light. [NIH] Physical Examination: Systematic and thorough inspection of the patient for physical signs of disease or abnormality. [NIH] Physical Therapy: The restoration of function and the prevention of disability following disease or injury with the use of light, heat, cold, water, electricity, ultrasound, and exercise. [NIH]
Physician-Patient Relations: The interactions between physician and patient. [NIH] Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]
Physiology: The science that deals with the life processes and functions of organismus, their cells, tissues, and organs. [NIH]
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Phytohemagglutinins: Mucoproteins isolated from the kidney bean (Phaseolus vulgaris); some of them are mitogenic to lymphocytes, others agglutinate all or certain types of erythrocytes or lymphocytes. They are used mainly in the study of immune mechanisms and in cell culture. [NIH] Pigment: A substance that gives color to tissue. Pigments are responsible for the color of skin, eyes, and hair. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH] Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [NIH] Placebos: Any dummy medication or treatment. Although placebos originally were medicinal preparations having no specific pharmacological activity against a targeted condition, the concept has been extended to include treatments or procedures, especially those administered to control groups in clinical trials in order to provide baseline measurements for the experimental protocol. [NIH] Placenta: A highly vascular fetal organ through which the fetus absorbs oxygen and other nutrients and excretes carbon dioxide and other wastes. It begins to form about the eighth day of gestation when the blastocyst adheres to the decidua. [NIH] Plana: The radiographic term applied to a vertebral body crushed to a thin plate. [NIH] Plant Diseases: Diseases of plants. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasma Exchange: Removal of plasma and replacement with various fluids, e.g., fresh frozen plasma, plasma protein fractions (PPF), albumin preparations, dextran solutions, saline. Used in treatment of autoimmune diseases, immune complex diseases, diseases of excess plasma factors, and other conditions. [NIH] Plasma protein: One of the hundreds of different proteins present in blood plasma, including carrier proteins ( such albumin, transferrin, and haptoglobin), fibrinogen and other coagulation factors, complement components, immunoglobulins, enzyme inhibitors, precursors of substances such as angiotension and bradykinin, and many other types of proteins. [EU] Plasmapheresis: Procedure whereby plasma is separated and extracted from anticoagulated whole blood and the red cells retransfused to the donor. Plasmapheresis is also employed for therapeutic use. [NIH] Plasmid: An autonomously replicating, extra-chromosomal DNA molecule found in many bacteria. Plasmids are widely used as carriers of cloned genes. [NIH] Platelet Activating Factor: A phospholipid derivative formed by platelets, basophils, neutrophils, monocytes, and macrophages. It is a potent platelet aggregating agent and
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inducer of systemic anaphylactic symptoms, including hypotension, thrombocytopenia, neutropenia, and bronchoconstriction. [NIH] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug. [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelet Factor 4: A high-molecular-weight proteoglycan-platelet factor complex which is released from blood platelets by thrombin. It acts as a mediator in the heparin-neutralizing capacity of the blood and plays a role in platelet aggregation. At high ionic strength (I=0.75), the complex dissociates into the active component (molecular weight 29,000) and the proteoglycan carrier (chondroitin 4-sulfate, molecular weight 350,000). The molecule exists in the form of a dimer consisting of 8 moles of platelet factor 4 and 2 moles of proteoglycan. [NIH]
Plateletpheresis: The preparation of platelet concentrates with the return of red cells and platelet-poor plasma to the donor. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Platinum: Platinum. A heavy, soft, whitish metal, resembling tin, atomic number 78, atomic weight 195.09, symbol Pt. (From Dorland, 28th ed) It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as "alutiae". [NIH]
Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Pollen: The male fertilizing element of flowering plants analogous to sperm in animals. It is released from the anthers as yellow dust, to be carried by insect or other vectors, including wind, to the ovary (stigma) of other flowers to produce the embryo enclosed by the seed. The pollens of many plants are allergenic. [NIH] Polycystic: An inherited disorder characterized by many grape-like clusters of fluid-filled cysts that make both kidneys larger over time. These cysts take over and destroy working kidney tissue. PKD may cause chronic renal failure and end-stage renal disease. [NIH] Polymerase: An enzyme which catalyses the synthesis of DNA using a single DNA strand as a template. The polymerase copies the template in the 5'-3'direction provided that sufficient quantities of free nucleotides, dATP and dTTP are present. [NIH] Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships. [NIH] Polymorphism: The occurrence together of two or more distinct forms in the same population. [NIH] Polypeptide: A peptide which on hydrolysis yields more than two amino acids; called
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tripeptides, tetrapeptides, etc. according to the number of amino acids contained. [EU] Polyposis: The development of numerous polyps (growths that protrude from a mucous membrane). [NIH] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Polyunsaturated fat: An unsaturated fat found in greatest amounts in foods derived from plants, including safflower, sunflower, corn, and soybean oils. [NIH] Population Control: Includes mechanisms or programs which control the numbers of individuals in a population of humans or animals. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postmenopausal: Refers to the time after menopause. Menopause is the time in a woman's life when menstrual periods stop permanently; also called "change of life." [NIH] Postoperative: After surgery. [NIH] Postoperative Complications: Pathologic processes that affect patients after a surgical procedure. They may or may not be related to the disease for which the surgery was done, and they may or may not be direct results of the surgery. [NIH] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Potentiate: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiating: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Precancerous: A term used to describe a condition that may (or is likely to) become cancer. Also called premalignant. [NIH] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Predisposition: A latent susceptibility to disease which may be activated under certain conditions, as by stress. [EU] Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [NIH] Prednisone: A synthetic anti-inflammatory glucocorticoid derived from cortisone. It is biologically inert and converted to prednisolone in the liver. [NIH] Preeclampsia: A toxaemia of late pregnancy characterized by hypertension, edema, and proteinuria, when convulsions and coma are associated, it is called eclampsia. [EU] Preleukemia: Conditions in which the abnormalities in the peripheral blood or bone
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marrow represent the early manifestations of acute leukemia, but in which the changes are not of sufficient magnitude or specificity to permit a diagnosis of acute leukemia by the usual clinical criteria. [NIH] Premalignant: A term used to describe a condition that may (or is likely to) become cancer. Also called precancerous. [NIH] Premenstrual: Occurring before menstruation. [EU] Prenatal: Existing or occurring before birth, with reference to the fetus. [EU] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] Probe: An instrument used in exploring cavities, or in the detection and dilatation of strictures, or in demonstrating the potency of channels; an elongated instrument for exploring or sounding body cavities. [NIH] Procollagen: A biosynthetic precursor of collagen containing additional amino acid sequences at the amino-terminal ends of the three polypeptide chains. Protocollagen, a precursor of procollagen consists of procollagen peptide chains in which proline and lysine have not yet been hydroxylated. [NIH] Proctocolectomy: An operation to remove the colon and rectum. Also called coloproctectomy. [NIH] Proctocolectomy, Restorative: A surgical procedure involving the excision of the colon and rectum and the formation of an ileoanal reservoir (pouch). In patients with intestinal diseases, such as ulcerative colitis, this procedure avoids the need for an ostomy by allowing for transanal defecation. [NIH] Proctocolitis: Inflammation of the rectum and colon. [NIH] Proctosigmoiditis: Irritation of the rectum and the sigmoid colon. [NIH] Proctosigmoidoscopy: An examination of the rectum and the lower part of the colon using a thin, lighted tube called a sigmoidoscope. [NIH] Prodrug: A substance that gives rise to a pharmacologically active metabolite, although not itself active (i. e. an inactive precursor). [NIH] Progeny: The offspring produced in any generation. [NIH] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] Prognostic factor: A situation or condition, or a characteristic of a patient, that can be used to estimate the chance of recovery from a disease, or the chance of the disease recurring (coming back). [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Progressive disease: Cancer that is increasing in scope or severity. [NIH] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Prone: Having the front portion of the body downwards. [NIH]
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Prophylaxis: An attempt to prevent disease. [NIH] Proportional: Being in proportion : corresponding in size, degree, or intensity, having the same or a constant ratio; of, relating to, or used in determining proportions. [EU] Prospective Studies: Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group. [NIH] Prospective study: An epidemiologic study in which a group of individuals (a cohort), all free of a particular disease and varying in their exposure to a possible risk factor, is followed over a specific amount of time to determine the incidence rates of the disease in the exposed and unexposed groups. [NIH] Prostaglandin: Any of a group of components derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway that are extremely potent mediators of a diverse group of physiologic processes. The abbreviation for prostaglandin is PG; specific compounds are designated by adding one of the letters A through I to indicate the type of substituents found on the hydrocarbon skeleton and a subscript (1, 2 or 3) to indicate the number of double bonds in the hydrocarbon skeleton e.g., PGE2. The predominant naturally occurring prostaglandins all have two double bonds and are synthesized from arachidonic acid (5,8,11,14-eicosatetraenoic acid) by the pathway shown in the illustration. The 1 series and 3 series are produced by the same pathway with fatty acids having one fewer double bond (8,11,14-eicosatrienoic acid or one more double bond (5,8,11,14,17-eicosapentaenoic acid) than arachidonic acid. The subscript a or ß indicates the configuration at C-9 (a denotes a substituent below the plane of the ring, ß, above the plane). The naturally occurring PGF's have the a configuration, e.g., PGF2a. All of the prostaglandins act by binding to specific cell-surface receptors causing an increase in the level of the intracellular second messenger cyclic AMP (and in some cases cyclic GMP also). The effect produced by the cyclic AMP increase depends on the specific cell type. In some cases there is also a positive feedback effect. Increased cyclic AMP increases prostaglandin synthesis leading to further increases in cyclic AMP. [EU] Prostaglandins A: (13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic acid (PGA(1)); (5Z,13E,15S)-15-hydroxy-9-oxoprosta-5,10,13-trien-1-oic acid (PGA(2)); (5Z,13E,15S,17Z)-15hydroxy-9-oxoprosta-5,10,13,17-tetraen-1-oic acid (PGA(3)). A group of naturally occurring secondary prostaglandins derived from PGE. PGA(1) and PGA(2) as well as their 19hydroxy derivatives are found in many organs and tissues. [NIH] Prostaglandins D: Physiologically active prostaglandins found in many tissues and organs. They show pressor activity, are mediators of inflammation, and have potential antithrombotic effects. [NIH] Prostate: A gland in males that surrounds the neck of the bladder and the urethra. It secretes a substance that liquifies coagulated semen. It is situated in the pelvic cavity behind the lower part of the pubic symphysis, above the deep layer of the triangular ligament, and rests upon the rectum. [NIH] Prostatitis: Inflammation of the prostate. [EU] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the
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peptide chain. Quaternary protein structure describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain). [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Protein Subunits: Single chains of amino acids that are the units of a multimeric protein. They can be identical or non-identical subunits. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [NIH] Proteoglycans: Glycoproteins which have a very high polysaccharide content. [NIH] Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Protozoa: A subkingdom consisting of unicellular organisms that are the simplest in the animal kingdom. Most are free living. They range in size from submicroscopic to macroscopic. Protozoa are divided into seven phyla: Sarcomastigophora, Labyrinthomorpha, Apicomplexa, Microspora, Ascetospora, Myxozoa, and Ciliophora. [NIH] Proximal: Nearest; closer to any point of reference; opposed to distal. [EU] Pruritic: Pertaining to or characterized by pruritus. [EU] Pseudotumor Cerebri: A condition marked by raised intracranial pressure and characterized clinically by headaches; nausea; papilledema, peripheral constriction of the visual fields, transient visual obscurations, and pulsatile tinnitus. Obesity is frequently associated with this condition, which primarily affects women between 20 and 44 years of age. Chronic papilledema may lead to optic nerve injury (optic nerve diseases) and visual loss (blindness). [NIH] Psoriasis: A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis. [NIH] Psychiatric: Pertaining to or within the purview of psychiatry. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychoanalysis: The separation or resolution of the psyche into its constituent elements. The term has two separate meanings: 1. a procedure devised by Sigmund Freud, for investigating mental processes by means of free association, dream interpretation and interpretation of resistance and transference manifestations; and 2. a theory of psychology
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developed by Freud from his clinical experience with hysterical patients. (From Campbell, Psychiatric Dictionary, 1996). [NIH] Psychogenic: Produced or caused by psychic or mental factors rather than organic factors. [EU]
Psychology: The science dealing with the study of mental processes and behavior in man and animals. [NIH] Psychomotor: Pertaining to motor effects of cerebral or psychic activity. [EU] Psychophysiology: The study of the physiological basis of human and animal behavior. [NIH]
Psychosis: A mental disorder characterized by gross impairment in reality testing as evidenced by delusions, hallucinations, markedly incoherent speech, or disorganized and agitated behaviour without apparent awareness on the part of the patient of the incomprehensibility of his behaviour; the term is also used in a more general sense to refer to mental disorders in which mental functioning is sufficiently impaired as to interfere grossly with the patient's capacity to meet the ordinary demands of life. Historically, the term has been applied to many conditions, e.g. manic-depressive psychosis, that were first described in psychotic patients, although many patients with the disorder are not judged psychotic. [EU] Psychosomatic: Pertaining to the mind-body relationship; having bodily symptoms of psychic, emotional, or mental origin; called also psychophysiologic. [EU] Psychotherapy: A generic term for the treatment of mental illness or emotional disturbances primarily by verbal or nonverbal communication. [NIH] Psyllium: Dried, ripe seeds of Plantago psyllium, P. indica, and P. ovata (Plantaginaceae). Plantain seeds swell in water and are used as demulcents and bulk laxatives. [NIH] Puberty: The period during which the secondary sex characteristics begin to develop and the capability of sexual reproduction is attained. [EU] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]
Pulmonary: Relating to the lungs. [NIH] Pulmonary Emphysema: Condition of the lungs characterized by increase beyond normal in the size of air spaces distal to the terminal bronchioles, either from dilatation of the alveoli or from destruction of their walls. [NIH] Pulmonary Fibrosis: Chronic inflammation and progressive fibrosis of the pulmonary alveolar walls, with steadily progressive dyspnea, resulting finally in death from oxygen lack or right heart failure. [NIH] Pulmonary hypertension: Abnormally high blood pressure in the arteries of the lungs. [NIH] Pulmonary Sarcoidosis: A disease of unknown etiology characterized by tuberclelike, granulomatous nodules which may affect the skin, the lungs, the lymph nodes, the bones of the distal extremities, the conjunctiva, the lacrimal gland, the retina and the uveal tract. [NIH]
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Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]
Pupil: The aperture in the iris through which light passes. [NIH] Purifying: Respiratory equipment whose function is to remove contaminants from otherwise wholesome air. [NIH] Purines: A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include adenine and guanine, constituents of nucleic acids, as well as many alkaloids such as caffeine and theophylline. Uric acid is the metabolic end product of purine metabolism. [NIH] Purpura: Purplish or brownish red discoloration, easily visible through the epidermis, caused by hemorrhage into the tissues. [NIH] Purulent: Consisting of or containing pus; associated with the formation of or caused by pus. [EU] Pyelonephritis: Inflammation of the kidney and its pelvis, beginning in the interstitium and rapidly extending to involve the tubules, glomeruli, and blood vessels; due to bacterial infection. [EU] Pyoderma: Any purulent skin disease (Dorland, 27th ed). [NIH] Pyoderma Gangrenosum: An idiopathic, rapidly evolving, and severely debilitating disease occurring most commonly in association with chronic ulcerative colitis. It is characterized by the presence of boggy, purplish ulcers with undermined borders, appearing mostly on the legs. The majority of cases are in people between 40 and 60 years old. Its etiology is unknown. [NIH] Pyrazinamide: A pyrazine that is used therapeutically as an antitubercular agent. [NIH] Quality of Life: A generic concept reflecting concern with the modification and enhancement of life attributes, e.g., physical, political, moral and social environment. [NIH] Quiescent: Marked by a state of inactivity or repose. [EU] Quinoxaline: AMPA/Kainate antagonist. [NIH] Race: A population within a species which exhibits general similarities within itself, but is both discontinuous and distinct from other populations of that species, though not sufficiently so as to achieve the status of a taxon. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radiation therapy: The use of high-energy radiation from x-rays, gamma rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy), or it may come from radioactive material placed in the body in the area near cancer cells (internal radiation therapy, implant radiation, or brachytherapy). Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Also called radiotherapy. [NIH] Radioactive: Giving off radiation. [NIH] Radiography: Examination of any part of the body for diagnostic purposes by means of roentgen rays, recording the image on a sensitized surface (such as photographic film). [NIH] Radiological: Pertaining to radiodiagnostic and radiotherapeutic procedures, and interventional radiology or other planning and guiding medical radiology. [NIH]
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Radiology: A specialty concerned with the use of x-ray and other forms of radiant energy in the diagnosis and treatment of disease. [NIH] Radius: The lateral bone of the forearm. [NIH] Random Allocation: A process involving chance used in therapeutic trials or other research endeavor for allocating experimental subjects, human or animal, between treatment and control groups, or among treatment groups. It may also apply to experiments on inanimate objects. [NIH] Randomization: Also called random allocation. Is allocation of individuals to groups, e.g., for experimental and control regimens, by chance. Within the limits of chance variation, random allocation should make the control and experimental groups similar at the start of an investigation and ensure that personal judgment and prejudices of the investigator do not influence allocation. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Randomized Controlled Trials: Clinical trials that involve at least one test treatment and one control treatment, concurrent enrollment and follow-up of the test- and control-treated groups, and in which the treatments to be administered are selected by a random process, such as the use of a random-numbers table. Treatment allocations using coin flips, odd-even numbers, patient social security numbers, days of the week, medical record numbers, or other such pseudo- or quasi-random processes, are not truly randomized and trials employing any of these techniques for patient assignment are designated simply controlled clinical trials. [NIH] Reactive Oxygen Species: Reactive intermediate oxygen species including both radicals and non-radicals. These substances are constantly formed in the human body and have been shown to kill bacteria and inactivate proteins, and have been implicated in a number of diseases. Scientific data exist that link the reactive oxygen species produced by inflammatory phagocytes to cancer development. [NIH] Reagent: A substance employed to produce a chemical reaction so as to detect, measure, produce, etc., other substances. [EU] Reality Testing: The individual's objective evaluation of the external world and the ability to differentiate adequately between it and the internal world; considered to be a primary ego function. [NIH] Reassurance: A procedure in psychotherapy that seeks to give the client confidence in a favorable outcome. It makes use of suggestion, of the prestige of the therapist. [NIH] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Receptors, Muscarinic: One of the two major classes of cholinergic receptors. Muscarinic receptors were originally defined by their preference for muscarine over nicotine. There are several subtypes (usually M1, M2, M3.) that are characterized by their cellular actions, pharmacology, and molecular biology. [NIH] Receptors, Serotonin: Cell-surface proteins that bind serotonin and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Recombinant Fusion Proteins: Proteins that are the result of genetic engineering. A regulatory part or promoter of one or more genes is combined with a structural gene. The
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fusion protein is formed after transcription and translation of the fused gene. This type of fusion protein is used in the study of gene regulation or structure-activity relationships. They might also be used clinically as targeted toxins (immunotoxins). [NIH] Recombination: The formation of new combinations of genes as a result of segregation in crosses between genetically different parents; also the rearrangement of linked genes due to crossing-over. [NIH] Rectal: By or having to do with the rectum. The rectum is the last 8 to 10 inches of the large intestine and ends at the anus. [NIH] Rectovaginal Fistula: Abnormal communication between the rectum and the vagina. [NIH] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Recurrence: The return of a sign, symptom, or disease after a remission. [NIH] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH] Red Nucleus: A pinkish-yellow portion of the midbrain situated in the rostral mesencephalic tegmentum. It receives a large projection from the contralateral half of the cerebellum via the superior cerebellar peduncle and a projection from the ipsilateral motor cortex. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Reflective: Capable of throwing back light, images, sound waves : reflecting. [EU] Reflux: The term used when liquid backs up into the esophagus from the stomach. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Refractive Power: The ability of an object, such as the eye, to bend light as light passes through it. [NIH] Refractory: Not readily yielding to treatment. [EU] Regeneration: The natural renewal of a structure, as of a lost tissue or part. [EU] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Regional enteritis: Inflammation of the intestines, but usually only of the small intestine. Also called Crohn's disease. [NIH] Regression Analysis: Procedures for finding the mathematical function which best describes the relationship between a dependent variable and one or more independent variables. In linear regression (see linear models) the relationship is constrained to be a straight line and least-squares analysis is used to determine the best fit. In logistic regression (see logistic models) the dependent variable is qualitative rather than continuously variable and likelihood functions are used to find the best relationship. In multiple regression the dependent variable is considered to depend on more than a single independent variable. [NIH]
Regurgitation: A backward flowing, as the casting up of undigested food, or the backward flowing of blood into the heart, or between the chambers of the heart when a valve is incompetent. [EU] Relapse: The return of signs and symptoms of cancer after a period of improvement. [NIH] Relative risk: The ratio of the incidence rate of a disease among individuals exposed to a specific risk factor to the incidence rate among unexposed individuals; synonymous with risk ratio. Alternatively, the ratio of the cumulative incidence rate in the exposed to the
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cumulative incidence rate in the unexposed (cumulative incidence ratio). The term relative risk has also been used synonymously with odds ratio. This is because the odds ratio and relative risk approach each other if the disease is rare ( 5 percent of population) and the number of subjects is large. [NIH] Remission: A decrease in or disappearance of signs and symptoms of cancer. In partial remission, some, but not all, signs and symptoms of cancer have disappeared. In complete remission, all signs and symptoms of cancer have disappeared, although there still may be cancer in the body. [NIH] Remission Induction: Therapeutic act or process that initiates a response to a complete or partial remission level. [NIH] Remission induction therapy: The initial chemotherapy a person receives to bring about a remission. [NIH] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [NIH] Renal Osteodystrophy: Decalcification of bone due to hyperparathyroidism secondary to chronic kidney disease. [NIH] Reperfusion: Restoration of blood supply to tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. It is primarily a procedure for treating infarction or other ischemia, by enabling viable ischemic tissue to recover, thus limiting further necrosis. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing reperfusion injury. [NIH] Reperfusion Injury: Functional, metabolic, or structural changes, including necrosis, in ischemic tissues thought to result from reperfusion to ischemic areas of the tissue. The most common instance is myocardial reperfusion injury. [NIH] Resected: Surgical removal of part of an organ. [NIH] Resection: Removal of tissue or part or all of an organ by surgery. [NIH] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Respiratory Burst: A large increase in oxygen uptake by neutrophils and most types of tissue macrophages through activation of an NADPH-cytochrome b-dependent oxidase that reduces oxygen to a superoxide. Individuals with an inherited defect in which the oxidase that reduces oxygen to superoxide is decreased or absent (granulomatous disease, chronic) often die as a result of recurrent bacterial infections. [NIH] Respiratory distress syndrome: A lung disease that occurs primarily in premature infants; the newborn must struggle for each breath and blueing of its skin reflects the baby's inability to get enough oxygen. [NIH] Response rate: The percentage of patients whose cancer shrinks or disappears after treatment. [NIH] Restitution: The restoration to a normal state. [NIH] Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic
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nerve and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH] Retinal: 1. Pertaining to the retina. 2. The aldehyde of retinol, derived by the oxidative enzymatic splitting of absorbed dietary carotene, and having vitamin A activity. In the retina, retinal combines with opsins to form visual pigments. One isomer, 11-cis retinal combines with opsin in the rods (scotopsin) to form rhodopsin, or visual purple. Another, all-trans retinal (trans-r.); visual yellow; xanthopsin) results from the bleaching of rhodopsin by light, in which the 11-cis form is converted to the all-trans form. Retinal also combines with opsins in the cones (photopsins) to form the three pigments responsible for colour vision. Called also retinal, and retinene1. [EU] Retinal Detachment: Separation of the inner layers of the retina (neural retina) from the pigment epithelium. Retinal detachment occurs more commonly in men than in women, in eyes with degenerative myopia, in aging and in aphakia. It may occur after an uncomplicated cataract extraction, but it is seen more often if vitreous humor has been lost during surgery. (Dorland, 27th ed; Newell, Ophthalmology: Principles and Concepts, 7th ed, p310-12). [NIH] Retinitis: Inflammation of the retina. It is rarely limited to the retina, but is commonly associated with diseases of the choroid (chorioretinitis) and of the optic nerve (neuroretinitis). The disease may be confined to one eye, but since it is generally dependent on a constitutional factor, it is almost always bilateral. It may be acute in course, but as a rule it lasts many weeks or even several months. [NIH] Retinoblastoma: An eye cancer that most often occurs in children younger than 5 years. It occurs in hereditary and nonhereditary (sporadic) forms. [NIH] Retinoids: Derivatives of vitamin A. Used clinically in the treatment of severe cystic acne, psoriasis, and other disorders of keratinization. Their possible use in the prophylaxis and treatment of cancer is being actively explored. [NIH] Retinol: Vitamin A. It is essential for proper vision and healthy skin and mucous membranes. Retinol is being studied for cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Retinopathy: 1. Retinitis (= inflammation of the retina). 2. Retinosis (= degenerative, noninflammatory condition of the retina). [EU] Retrobulbar: Behind the pons. [EU] Retrospective: Looking back at events that have already taken place. [NIH] Retrospective study: A study that looks backward in time, usually using medical records and interviews with patients who already have or had a disease. [NIH] Retrovirus: A member of a group of RNA viruses, the RNA of which is copied during viral replication into DNA by reverse transcriptase. The viral DNA is then able to be integrated into the host chromosomal DNA. [NIH] Reversion: A return to the original condition, e. g. the reappearance of the normal or wild type in previously mutated cells, tissues, or organisms. [NIH] Rheumatic Diseases: Disorders of connective tissue, especially the joints and related structures, characterized by inflammation, degeneration, or metabolic derangement. [NIH] Rheumatism: A group of disorders marked by inflammation or pain in the connective tissue structures of the body. These structures include bone, cartilage, and fat. [NIH] Rheumatoid: Resembling rheumatism. [EU]
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Rheumatoid arthritis: A form of arthritis, the cause of which is unknown, although infection, hypersensitivity, hormone imbalance and psychologic stress have been suggested as possible causes. [NIH] Rhinitis: Inflammation of the mucous membrane of the nose. [NIH] Ribose: A pentose active in biological systems usually in its D-form. [NIH] Ribosome: A granule of protein and RNA, synthesized in the nucleolus and found in the cytoplasm of cells. Ribosomes are the main sites of protein synthesis. Messenger RNA attaches to them and there receives molecules of transfer RNA bearing amino acids. [NIH] Rickets: A condition caused by deficiency of vitamin D, especially in infancy and childhood, with disturbance of normal ossification. The disease is marked by bending and distortion of the bones under muscular action, by the formation of nodular enlargements on the ends and sides of the bones, by delayed closure of the fontanelles, pain in the muscles, and sweating of the head. Vitamin D and sunlight together with an adequate diet are curative, provided that the parathyroid glands are functioning properly. [EU] Rigidity: Stiffness or inflexibility, chiefly that which is abnormal or morbid; rigor. [EU] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Risk patient: Patient who is at risk, because of his/her behaviour or because of the type of person he/she is. [EU] Rod: A reception for vision, located in the retina. [NIH] Rosiglitazone: A drug taken to help reduce the amount of sugar in the blood. Rosiglitazone helps make insulin more effective and improves regulation of blood sugar. It belongs to the family of drugs called thiazolidinediones. [NIH] Saccharomyces: A genus of ascomycetous fungi of the family Saccharomycetaceae, order saccharomycetales. [NIH] Saccharomyces cerevisiae: A species of the genus Saccharomyces, family Saccharomycetaceae, order Saccharomycetales, known as "baker's" or "brewer's" yeast. The dried form is used as a dietary supplement. [NIH] Saccharomycetales: An order of fungi in the phylum Ascomycota that multiply by budding. They include the telomorphic ascomycetous yeasts which are found in a very wide range of habitats. [NIH] Salicylate: Non-steroidal anti-inflammatory drugs. [NIH] Salicylic: A tuberculosis drug. [NIH] Salicylic Acids: Derivatives and salts of salicylic acid. [NIH] Saline: A solution of salt and water. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] Sarcoidosis: An idiopathic systemic inflammatory granulomatous disorder comprised of epithelioid and multinucleated giant cells with little necrosis. It usually invades the lungs
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with fibrosis and may also involve lymph nodes, skin, liver, spleen, eyes, phalangeal bones, and parotid glands. [NIH] Sarcoma: A connective tissue neoplasm formed by proliferation of mesodermal cells; it is usually highly malignant. [NIH] Scans: Pictures of structures inside the body. Scans often used in diagnosing, staging, and monitoring disease include liver scans, bone scans, and computed tomography (CT) or computerized axial tomography (CAT) scans and magnetic resonance imaging (MRI) scans. In liver scanning and bone scanning, radioactive substances that are injected into the bloodstream collect in these organs. A scanner that detects the radiation is used to create pictures. In CT scanning, an x-ray machine linked to a computer is used to produce detailed pictures of organs inside the body. MRI scans use a large magnet connected to a computer to create pictures of areas inside the body. [NIH] Schematic: Representative or schematic eye computed from the average of a large number of human eye measurements by Allvar Gullstrand. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a person of schizoid personality. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Schizotypal Personality Disorder: A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions, depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to characterize schizophrenia. [NIH] Sclera: The tough white outer coat of the eyeball, covering approximately the posterior fivesixths of its surface, and continuous anteriorly with the cornea and posteriorly with the external sheath of the optic nerve. [EU] Scleritis: Refers to any inflammation of the sclera including episcleritis, a benign condition affecting only the episclera, which is generally short-lived and easily treated. Classic scleritis, on the other hand, affects deeper tissue and is characterized by higher rates of visual acuity loss and even mortality, particularly in necrotizing form. Its characteristic symptom is severe and general head pain. Scleritis has also been associated with systemic collagen disease. Etiology is unknown but is thought to involve a local immune response. Treatment is difficult and includes administration of anti-inflammatory and immunosuppressive agents such as corticosteroids. Inflammation of the sclera may also be secondary to inflammation of adjacent tissues, such as the conjunctiva. [NIH] Scleroderma: A chronic disorder marked by hardening and thickening of the skin. Scleroderma can be localized or it can affect the entire body (systemic). [NIH] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] Secondary tumor: Cancer that has spread from the organ in which it first appeared to another organ. For example, breast cancer cells may spread (metastasize) to the lungs and cause the growth of a new tumor. When this happens, the disease is called metastatic breast cancer, and the tumor in the lungs is called a secondary tumor. Also called secondary cancer. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the
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elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Secretory: Secreting; relating to or influencing secretion or the secretions. [NIH] Sedative: 1. Allaying activity and excitement. 2. An agent that allays excitement. [EU] Sedatives, Barbiturate: Those derivatives of barbituric or thiobarbituric acid that are used as hypnotics or sedatives. The structural class of all such derivatives, regardless of use, is barbiturates. [NIH] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as epilepsy or "seizure disorder." [NIH] Semen: The thick, yellowish-white, viscid fluid secretion of male reproductive organs discharged upon ejaculation. In addition to reproductive organ secretions, it contains spermatozoa and their nutrient plasma. [NIH] Semicircular canal: Three long canals of the bony labyrinth of the ear, forming loops and opening into the vestibule by five openings. [NIH] Seminal vesicles: Glands that help produce semen. [NIH] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU] Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [NIH] Senna: Preparations of Cassia senna L. and C. angustifolia of the Leguminosae. They contain sennosides, which are anthraquinone type cathartics and are used in many different preparations as laxatives. [NIH] Sepsis: The presence of bacteria in the bloodstream. [NIH] Septal: An abscess occurring at the root of the tooth on the proximal surface. [NIH] Septic: Produced by or due to decomposition by microorganisms; putrefactive. [EU] Sequence Analysis: A multistage process that includes the determination of a sequence (protein, carbohydrate, etc.), its fragmentation and analysis, and the interpretation of the resulting sequence information. [NIH] Sequencing: The determination of the order of nucleotides in a DNA or RNA chain. [NIH] Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines, pyrimidines, and other amino acids. [NIH] Serine Endopeptidases: Any member of the group of endopeptidases containing at the active site a serine residue involved in catalysis. EC 3.4.21. [NIH] Serologic: Analysis of a person's serum, especially specific immune or lytic serums. [NIH] Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-tryptophan. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (receptors, serotonin) explain the broad physiological actions and distribution of this biochemical mediator. [NIH] Serotonin Uptake Inhibitors: Compounds that specifically inhibit the reuptake of serotonin in the brain. This increases the serotonin concentration in the synaptic cleft which then activates serotonin receptors to a greater extent. These agents have been used in treatment of depression, panic disorder, obsessive-compulsive behavior, and alcoholism, as analgesics,
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and to treat obesity and bulimia. Many of the adrenergic uptake inhibitors also inhibit serotonin uptake; they are not included here. [NIH] Serous: Having to do with serum, the clear liquid part of blood. [NIH] Serrata: The serrated anterior border of the retina located approximately 8.5 mm from the limbus and adjacent to the pars plana of the ciliary body. [NIH] Serrated: Having notches or teeth on the edge as a saw has. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Sex Characteristics: Those characteristics that distinguish one sex from the other. The primary sex characteristics are the ovaries and testes and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction. [NIH] Sex Determination: The biological characteristics which distinguish human beings as female or male. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral upset occasioned by some disturbing or unexpected experience; disruption of the circulation, which can upset all body functions: sometimes referred to as circulatory shock. [NIH]
Short Bowel Syndrome: A malabsorption syndrome resulting from extensive operative resection of small bowel. [NIH] Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Sigmoid: 1. Shaped like the letter S or the letter C. 2. The sigmoid colon. [EU] Sigmoid Colon: The lower part of the colon that empties into the rectum. [NIH] Sigmoidoscope: A thin, lighted tube used to view the inside of the colon. [NIH] Sigmoidoscopy: Endoscopic examination, therapy or surgery of the sigmoid flexure. [NIH] Signal Transduction: The intercellular or intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GABA-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptormediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. [NIH] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH]
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Skin Aging: The process of aging due to changes in the structure and elasticity of the skin over time. It may be a part of physiological aging or it may be due to the effects of ultraviolet radiation, usually through exposure to sunlight. [NIH] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Sludge: A clump of agglutinated red blood cells. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smoldering leukemia: Disease in which the bone marrow does not function normally. Also called preleukemia or myelodysplastic syndrome. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]
Soaps: Sodium or potassium salts of long chain fatty acids. These detergent substances are obtained by boiling natural oils or fats with caustic alkali. Sodium soaps are harder and are used as topical anti-infectives and vehicles in pills and liniments; potassium soaps are soft, used as vehicles for ointments and also as topical antimicrobials. [NIH] Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Social Support: Support systems that provide assistance and encouragement to individuals with physical or emotional disabilities in order that they may better cope. Informal social support is usually provided by friends, relatives, or peers, while formal assistance is provided by churches, groups, etc. [NIH] Social Work: The use of community resources, individual case work, or group work to promote the adaptive capacities of individuals in relation to their social and economic environments. It includes social service agencies. [NIH] Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH] Solid tumor: Cancer of body tissues other than blood, bone marrow, or the lymphatic system. [NIH] Solvent: 1. Dissolving; effecting a solution. 2. A liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Somatostatin: A polypeptide hormone produced in the hypothalamus, and other tissues and organs. It inhibits the release of human growth hormone, and also modulates important physiological functions of the kidney, pancreas, and gastrointestinal tract. Somatostatin receptors are widely expressed throughout the body. Somatostatin also acts as a neurotransmitter in the central and peripheral nervous systems. [NIH] Sound wave: An alteration of properties of an elastic medium, such as pressure, particle displacement, or density, that propagates through the medium, or a superposition of such alterations. [NIH]
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Soybean Oil: Oil from soybean or soybean plant. [NIH] Spasmodic: Of the nature of a spasm. [EU] Spastic: 1. Of the nature of or characterized by spasms. 2. Hypertonic, so that the muscles are stiff and the movements awkward. 3. A person exhibiting spasticity, such as occurs in spastic paralysis or in cerebral palsy. [EU] Spasticity: A state of hypertonicity, or increase over the normal tone of a muscle, with heightened deep tendon reflexes. [EU] Spatial disorientation: Loss of orientation in space where person does not know which way is up. [NIH] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] Sperm: The fecundating fluid of the male. [NIH] Sphenoid: An unpaired cranial bone with a body containing the sphenoid sinus and forming the posterior part of the medial walls of the orbits. [NIH] Sphincters: Any annular muscle closing an orifice. [NIH] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Spleen: An organ that is part of the lymphatic system. The spleen produces lymphocytes, filters the blood, stores blood cells, and destroys old blood cells. It is located on the left side of the abdomen near the stomach. [NIH] Spondylitis: Inflammation of the vertebrae. [EU] Spontaneous Abortion: The non-induced birth of an embryo or of fetus prior to the stage of viability at about 20 weeks of gestation. [NIH] Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Sprue: A non febrile tropical disease of uncertain origin. [NIH] Stabilization: The creation of a stable state. [EU] Staging: Performing exams and tests to learn the extent of the cancer within the body, especially whether the disease has spread from the original site to other parts of the body. [NIH]
Standard therapy: A currently accepted and widely used treatment for a certain type of cancer, based on the results of past research. [NIH] Statistically significant: Describes a mathematical measure of difference between groups. The difference is said to be statistically significant if it is greater than what might be
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expected to happen by chance alone. [NIH] Steel: A tough, malleable, iron-based alloy containing up to, but no more than, two percent carbon and often other metals. It is used in medicine and dentistry in implants and instrumentation. [NIH] Stem Cells: Relatively undifferentiated cells of the same lineage (family type) that retain the ability to divide and cycle throughout postnatal life to provide cells that can become specialized and take the place of those that die or are lost. [NIH] Stent: A device placed in a body structure (such as a blood vessel or the gastrointestinal tract) to provide support and keep the structure open. [NIH] Sterile: Unable to produce children. [NIH] Sterility: 1. The inability to produce offspring, i.e., the inability to conceive (female s.) or to induce conception (male s.). 2. The state of being aseptic, or free from microorganisms. [EU] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] Steroid therapy: Treatment with corticosteroid drugs to reduce swelling, pain, and other symptoms of inflammation. [NIH] Stimulant: 1. Producing stimulation; especially producing stimulation by causing tension on muscle fibre through the nervous tissue. 2. An agent or remedy that produces stimulation. [EU]
Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stoma: A surgically created opening from an area inside the body to the outside. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Stool test: A test to check for hidden blood in the bowel movement. [NIH] Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are coiled together. [NIH] Streptococcal: Caused by infection due to any species of streptococcus. [NIH] Streptococci: A genus of spherical Gram-positive bacteria occurring in chains or pairs. They are widely distributed in nature, being important pathogens but often found as normal commensals in the mouth, skin, and intestine of humans and other animals. [NIH] Streptococcus: A genus of gram-positive, coccoid bacteria whose organisms occur in pairs or chains. No endospores are produced. Many species exist as commensals or parasites on man or animals with some being highly pathogenic. A few species are saprophytes and occur in the natural environment. [NIH] Streptomycin: O-2-Deoxy-2-(methylamino)-alpha-L-glucopyranosyl-(1-2)-O-5- deoxy-3-Cformyl-alpha-L-lyxofuranosyl-(1-4)-N,N'-bis(aminoiminomethyl)-D-streptamine. Antibiotic substance produced by the soil actinomycete Streptomyces griseus. It acts by inhibiting the initiation and elongation processes during protein synthesis. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH]
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Stress management: A set of techniques used to help an individual cope more effectively with difficult situations in order to feel better emotionally, improve behavioral skills, and often to enhance feelings of control. Stress management may include relaxation exercises, assertiveness training, cognitive restructuring, time management, and social support. It can be delivered either on a one-to-one basis or in a group format. [NIH] Stricture: The abnormal narrowing of a body opening. Also called stenosis. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] Stromal: Large, veil-like cell in the bone marrow. [NIH] Structure-Activity Relationship: The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups. Other factors contributing to structure-activity relationship include chemical reactivity, electronic effects, resonance, and inductive effects. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU] Subarachnoid: Situated or occurring between the arachnoid and the pia mater. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH] Submaxillary: Four to six lymph glands, located between the lower jaw and the submandibular salivary gland. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]
Substrate: A substance upon which an enzyme acts. [EU] Sucralfate: A basic aluminum complex of sulfated sucrose. It is advocated in the therapy of peptic, duodenal, and prepyloric ulcers, gastritis, reflux esophagitis, and other gastrointestinal irritations. It acts primarily at the ulcer site, where it has cytoprotective, pepsinostatic, antacid, and bile acid-binding properties. The drug is only slightly absorbed by the digestive mucosa, which explains the absence of systemic effects and toxicity. [NIH] Sulfur: An element that is a member of the chalcogen family. It has an atomic symbol S, atomic number 16, and atomic weight 32.066. It is found in the amino acids cysteine and methionine. [NIH] Sulfuric acid: A strong acid that, when concentrated is extemely corrosive to the skin and mucous membranes. It is used in making fertilizers, dyes, electroplating, and industrial explosives. [NIH] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Superoxide Dismutase: An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme
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protects the cell against dangerous levels of superoxide. EC 1.15.1.1. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Support group: A group of people with similar disease who meet to discuss how better to cope with their cancer and treatment. [NIH] Suppositories: A small cone-shaped medicament having cocoa butter or gelatin at its basis and usually intended for the treatment of local conditions in the rectum. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Suppressive: Tending to suppress : effecting suppression; specifically : serving to suppress activity, function, symptoms. [EU] Suppurative: Consisting of, containing, associated with, or identified by the formation of pus. [NIH] Surfactant: A fat-containing protein in the respiratory passages which reduces the surface tension of pulmonary fluids and contributes to the elastic properties of pulmonary tissue. [NIH]
Symphysis: A secondary cartilaginous joint. [NIH] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Symptomatic treatment: Therapy that eases symptoms without addressing the cause of disease. [NIH] Symptomatology: 1. That branch of medicine with treats of symptoms; the systematic discussion of symptoms. 2. The combined symptoms of a disease. [EU] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Synaptic Transmission: The communication from a neuron to a target (neuron, muscle, or secretory cell) across a synapse. In chemical synaptic transmission, the presynaptic neuron releases a neurotransmitter that diffuses across the synaptic cleft and binds to specific synaptic receptors. These activated receptors modulate ion channels and/or secondmessenger systems to influence the postsynaptic cell. Electrical transmission is less common in the nervous system, and, as in other tissues, is mediated by gap junctions. [NIH] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Synovial: Of pertaining to, or secreting synovia. [EU] Synovial Membrane: The inner membrane of a joint capsule surrounding a freely movable joint. It is loosely attached to the external fibrous capsule and secretes synovial fluid. [NIH] Synovitis: Inflammation of a synovial membrane. It is usually painful, particularly on motion, and is characterized by a fluctuating swelling due to effusion within a synovial sac. Synovitis is qualified as fibrinous, gonorrhoeal, hyperplastic, lipomatous, metritic, puerperal, rheumatic, scarlatinal, syphilitic, tuberculous, urethral, etc. [EU] Systemic: Affecting the entire body. [NIH] Systemic disease: Disease that affects the whole body. [NIH] Systemic lupus erythematosus: SLE. A chronic inflammatory connective tissue disease marked by skin rashes, joint pain and swelling, inflammation of the kidneys, inflammation of the fibrous tissue surrounding the heart (i.e., the pericardium), as well as other problems.
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Not all affected individuals display all of these problems. May be referred to as lupus. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Tachycardia: Excessive rapidity in the action of the heart, usually with a heart rate above 100 beats per minute. [NIH] Tacrolimus: A macrolide isolated from the culture broth of a strain of Streptomyces tsukubaensis that has strong immunosuppressive activity in vivo and prevents the activation of T-lymphocytes in response to antigenic or mitogenic stimulation in vitro. [NIH] Tardive: Marked by lateness, late; said of a disease in which the characteristic lesion is late in appearing. [EU] Telangiectasia: The permanent enlargement of blood vessels, causing redness in the skin or mucous membranes. [NIH] Temporal: One of the two irregular bones forming part of the lateral surfaces and base of the skull, and containing the organs of hearing. [NIH] Tendinitis: Inflammation of tendons and of tendon-muscle attachments. [EU] Tenesmus: Straining, especially ineffectual and painful straining at stool or in urination. [EU] Teratogenicity: The power to cause abnormal development. [NIH] Thalamic: Cell that reaches the lateral nucleus of amygdala. [NIH] Thalamic Diseases: Disorders of the centrally located thalamus, which integrates a wide range of cortical and subcortical information. Manifestations include sensory loss, movement disorders; ataxia, pain syndromes, visual disorders, a variety of neuropsychological conditions, and coma. Relatively common etiologies include cerebrovascular disorders; craniocerebral trauma; brain neoplasms; brain hypoxia; intracranial hemorrhages; and infectious processes. [NIH] Thalidomide: A pharmaceutical agent originally introduced as a non-barbiturate hypnotic, but withdrawn from the market because of its known tetratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppresive and anti-angiogenic activity. It inhibits release of tumor necrosis factor alpha from monocytes, and modulates other cytokine action. [NIH] Theophylline: Alkaloid obtained from Thea sinensis (tea) and others. It stimulates the heart and central nervous system, dilates bronchi and blood vessels, and causes diuresis. The drug is used mainly in bronchial asthma and for myocardial stimulation. Among its more prominent cellular effects are inhibition of cyclic nucleotide phosphodiesterases and antagonism of adenosine receptors. [NIH] Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Thermal: Pertaining to or characterized by heat. [EU] Thigh: A leg; in anatomy, any elongated process or part of a structure more or less comparable to a leg. [NIH] Third Ventricle: A narrow cleft inferior to the corpus callosum, within the diencephalon, between the paired thalami. Its floor is formed by the hypothalamus, its anterior wall by the lamina terminalis, and its roof by ependyma. It communicates with the fourth ventricle by the cerebral aqueduct, and with the lateral ventricles by the interventricular foramina. [NIH] Thorax: A part of the trunk between the neck and the abdomen; the chest. [NIH] Threonine: An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins. [NIH]
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Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or intensity of the stimulus discernible in prescribed conditions of stimulation. [NIH] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] Thrombocytopenia: A decrease in the number of blood platelets. [NIH] Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation. [NIH]
Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thromboxanes: Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase. [NIH] Thrombus: An aggregation of blood factors, primarily platelets and fibrin with entrapment of cellular elements, frequently causing vascular obstruction at the point of its formation. Some authorities thus differentiate thrombus formation from simple coagulation or clot formation. [EU] Thymus: An organ that is part of the lymphatic system, in which T lymphocytes grow and multiply. The thymus is in the chest behind the breastbone. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Thyroid Gland: A highly vascular endocrine gland consisting of two lobes, one on either side of the trachea, joined by a narrow isthmus; it produces the thyroid hormones which are concerned in regulating the metabolic rate of the body. [NIH] Thyroiditis: Inflammation of the thyroid gland. [NIH] Thyroxine: An amino acid of the thyroid gland which exerts a stimulating effect on thyroid metabolism. [NIH] Time Management: Planning and control of time to improve efficiency and effectiveness. [NIH]
Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Distribution: Accumulation of a drug or chemical substance in various organs (including those not relevant to its pharmacologic or therapeutic action). This distribution depends on the blood flow or perfusion rate of the organ, the ability of the drug to penetrate organ membranes, tissue specificity, protein binding. The distribution is usually expressed as tissue to plasma ratios. [NIH] Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired drug tolerance; a decreasing response to repeated constant doses of a drug or the need for increasing doses to maintain a constant response. [EU] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH] Tonicity: The normal state of muscular tension. [NIH] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Topical: On the surface of the body. [NIH]
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Toxaemia: 1. The condition resulting from the spread of bacterial products (toxins) by the bloodstream. 2. A condition resulting from metabolic disturbances, e.g. toxaemia of pregnancy. [EU] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicologic: Pertaining to toxicology. [EU] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] Toxins: Specific, characterizable, poisonous chemicals, often proteins, with specific biological properties, including immunogenicity, produced by microbes, higher plants, or animals. [NIH] Trace element: Substance or element essential to plant or animal life, but present in extremely small amounts. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Traction: The act of pulling. [NIH] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] Transdermal: Entering through the dermis, or skin, as in administration of a drug applied to the skin in ointment or patch form. [EU] Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transfer Factor: Factor derived from leukocyte lysates of immune donors which can transfer both local and systemic cellular immunity to nonimmune recipients. [NIH] Transfusion: The infusion of components of blood or whole blood into the bloodstream. The blood may be donated from another person, or it may have been taken from the person earlier and stored until needed. [NIH] Transgenes: Genes that are introduced into an organism using gene transfer techniques. [NIH]
Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Translocation: The movement of material in solution inside the body of the plant. [NIH] Transmitter: A chemical substance which effects the passage of nerve impulses from one cell to the other at the synapse. [NIH] Transplantation: Transference of a tissue or organ, alive or dead, within an individual, between individuals of the same species, or between individuals of different species. [NIH]
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Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Treatment Failure: A measure of the quality of health care by assessment of unsuccessful results of management and procedures used in combating disease, in individual cases or series. [NIH] Triad: Trivalent. [NIH] Trichomoniasis: An infection with the protozoan parasite Trichomonas vaginalis. [NIH] Tricuspid Atresia: Absence of the orifice between the right atrium and ventricle, with the presence of an atrial defect through which all the systemic venous return reaches the left heart. As a result, there is left ventricular hypertrophy because the right ventricle is absent or not functional. [NIH] Tricyclic: Containing three fused rings or closed chains in the molecular structure. [EU] Triglyceride: A lipid carried through the blood stream to tissues. Most of the body's fat tissue is in the form of triglycerides, stored for use as energy. Triglycerides are obtained primarily from fat in foods. [NIH] Trisomy: The possession of a third chromosome of any one type in an otherwise diploid cell. [NIH]
Trophic: Of or pertaining to nutrition. [EU] Tropomyosin: A protein found in the thin filaments of muscle fibers. It inhibits contraction of the muscle unless its position is modified by troponin. [NIH] Troponin: One of the minor protein components of skeletal muscle. Its function is to serve as the calcium-binding component in the troponin-tropomyosin B-actin-myosin complex by conferring calcium sensitivity to the cross-linked actin and myosin filaments. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tuberculosis: Any of the infectious diseases of man and other animals caused by species of Mycobacterium. [NIH] Tuberous Sclerosis: A rare congenital disease in which the essential pathology is the appearance of multiple tumors in the cerebrum and in other organs, such as the heart or kidneys. [NIH] Tumor marker: A substance sometimes found in an increased amount in the blood, other body fluids, or tissues and which may mean that a certain type of cancer is in the body. Examples of tumor markers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and gastrointestinal tract cancers), and PSA (prostate cancer). Also called biomarker. [NIH] Tumor Necrosis Factor: Serum glycoprotein produced by activated macrophages and other mammalian mononuclear leukocytes which has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. It mimics the action of endotoxin but differs from it. It has a molecular weight of less than 70,000 kDa. [NIH] Tumor suppressor gene: Genes in the body that can suppress or block the development of cancer. [NIH] Tumour: 1. Swelling, one of the cardinal signs of inflammations; morbid enlargement. 2. A new growth of tissue in which the multiplication of cells is uncontrolled and progressive; called also neoplasm. [EU] Typhimurium: Microbial assay which measures his-his+ reversion by chemicals which cause base substitutions or frameshift mutations in the genome of this organism. [NIH]
Dictionary 473
Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH] Ulceration: 1. The formation or development of an ulcer. 2. An ulcer. [EU] Ulcerative colitis: Chronic inflammation of the colon that produces ulcers in its lining. This condition is marked by abdominal pain, cramps, and loose discharges of pus, blood, and mucus from the bowel. [NIH] Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [NIH] Unsaturated Fats: A type of fat. [NIH] Uraemia: 1. An excess in the blood of urea, creatinine, and other nitrogenous end products of protein and amino acids metabolism; more correctly referred to as azotemia. 2. In current usage the entire constellation of signs and symptoms of chronic renal failure, including nausea, vomiting anorexia, a metallic taste in the mouth, a uraemic odour of the breath, pruritus, uraemic frost on the skin, neuromuscular disorders, pain and twitching in the muscles, hypertension, edema, mental confusion, and acid-base and electrolyte imbalances. [EU]
Ureters: Tubes that carry urine from the kidneys to the bladder. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]
Uric: A kidney stone that may result from a diet high in animal protein. When the body breaks down this protein, uric acid levels rise and can form stones. [NIH] Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary tract: The organs of the body that produce and discharge urine. These include the kidneys, ureters, bladder, and urethra. [NIH] Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Urogenital: Pertaining to the urinary and genital apparatus; genitourinary. [EU] Urogenital System: All the organs involved in reproduction and the formation and release of urine. It includes the kidneys, ureters, bladder, urethra, and the organs of reproduction ovaries, uterus, fallopian tubes, vagina, and clitoris in women and the testes, seminal vesicles, prostate, seminal ducts, and penis in men. [NIH] Ursodeoxycholic Acid: An epimer of chenodeoxycholic acid. It is a mammalian bile acid found first in the bear and is apparently either a precursor or a product of chenodeoxycholate. Its administration changes the composition of bile and may dissolve gallstones. It is used as a cholagogue and choleretic. [NIH] Urticaria: A vascular reaction of the skin characterized by erythema and wheal formation due to localized increase of vascular permeability. The causative mechanism may be allergy, infection, or stress. [NIH] Uterus: The small, hollow, pear-shaped organ in a woman's pelvis. This is the organ in which a fetus develops. Also called the womb. [NIH] Uvea: The middle coat of the eyeball, consisting of the choroid in the back of the eye and the ciliary body and iris in the front of the eye. [NIH] Uveitis: An inflammation of part or all of the uvea, the middle (vascular) tunic of the eye, and commonly involving the other tunics (the sclera and cornea, and the retina). [EU]
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Vaccination: Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Vacuoles: Any spaces or cavities within a cell. They may function in digestion, storage, secretion, or excretion. [NIH] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Vaginal: Of or having to do with the vagina, the birth canal. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vascular endothelial growth factor: VEGF. A substance made by cells that stimulates new blood vessel formation. [NIH] Vasculitis: Inflammation of a blood vessel. [NIH] Vasoconstriction: Narrowing of the blood vessels without anatomic change, for which constriction, pathologic is used. [NIH] Vasodilatation: A state of increased calibre of the blood vessels. [EU] Vasodilator: An agent that widens blood vessels. [NIH] VE: The total volume of gas either inspired or expired in one minute. [NIH] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venoms: Poisonous animal secretions forming fluid mixtures of many different enzymes, toxins, and other substances. These substances are produced in specialized glands and secreted through specialized delivery systems (nematocysts, spines, fangs, etc.) for disabling prey or predator. [NIH] Venous: Of or pertaining to the veins. [EU] Venous Thrombosis: The formation or presence of a thrombus within a vein. [NIH] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Vertebrae: A bony unit of the segmented spinal column. [NIH] Vertebral: Of or pertaining to a vertebra. [EU] Vesicular: 1. Composed of or relating to small, saclike bodies. 2. Pertaining to or made up of vesicles on the skin. [EU] Vestibule: A small, oval, bony chamber of the labyrinth. The vestibule contains the utricle and saccule, organs which are part of the balancing apparatus of the ear. [NIH] Veterinarians: Individuals with a degree in veterinary medicine that provides them with training and qualifications to treat diseases and injuries of animals. [NIH] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH]
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Vibrio: A genus of Vibrionaceae, made up of short, slightly curved, motile, gram-negative rods. Various species produce cholera and other gastrointestinal disorders as well as abortion in sheep and cattle. [NIH] Vibrio cholerae: The etiologic agent of cholera. [NIH] Villous: Of a surface, covered with villi. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Viral vector: A type of virus used in cancer therapy. The virus is changed in the laboratory and cannot cause disease. Viral vectors produce tumor antigens (proteins found on a tumor cell) and can stimulate an antitumor immune response in the body. Viral vectors may also be used to carry genes that can change cancer cells back to normal cells. [NIH] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Visceral: , from viscus a viscus) pertaining to a viscus. [EU] Visual Acuity: Acuteness or clearness of vision, especially of form vision, which is dependent mainly on the sharpness of the retinal focus. [NIH] Vitamin A: A substance used in cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Vitamin D: The vitamin that mediates intestinal calcium absorption, bone calcium metabolism, and probably muscle activity. It usually acts as a hormone precursor, requiring 2 stages of metabolism before reaching actual hormonal form. It is isolated from fish liver oils and used in the treatment and prevention of rickets. [NIH] Vitreous Hemorrhage: Hemorrhage into the vitreous body. [NIH] Vitreous Humor: The transparent, colorless mass of gel that lies behind the lens and in front of the retina and fills the center of the eyeball. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] Volvulus: A twisting of the stomach or large intestine. May be caused by the stomach being in the wrong position, a foreign substance, or abnormal joining of one part of the stomach or intestine to another. Volvulus can lead to blockage, perforation, peritonitis, and poor blood flow. [NIH] Wakefulness: A state in which there is an enhanced potential for sensitivity and an efficient responsiveness to external stimuli. [NIH] White blood cell: A type of cell in the immune system that helps the body fight infection and disease. White blood cells include lymphocytes, granulocytes, macrophages, and others. [NIH]
Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH] Withdrawal: 1. A pathological retreat from interpersonal contact and social involvement, as may occur in schizophrenia, depression, or schizoid avoidant and schizotypal personality disorders. 2. (DSM III-R) A substance-specific organic brain syndrome that follows the
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cessation of use or reduction in intake of a psychoactive substance that had been regularly used to induce a state of intoxication. [EU] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] Yolk Sac: An embryonic membrane formed from endoderm and mesoderm. In reptiles and birds it incorporates the yolk into the digestive tract for nourishing the embryo. In placental mammals its nutritional function is vestigial; however, it is the source of most of the intestinal mucosa and the site of formation of the germ cells. It is sometimes called the vitelline sac, which should not be confused with the vitelline membrane of the egg. [NIH] Zygote: The fertilized ovum. [NIH] Zymogen: Inactive form of an enzyme which can then be converted to the active form, usually by excision of a polypeptide, e. g. trypsinogen is the zymogen of trypsin. [NIH]
477
INDEX 6 6-Mercaptopurine, 5, 16, 35, 36, 53, 59, 127, 232, 306, 307, 308, 317, 319, 369 A Abdominal Cramps, 302, 355, 369 Aberrant, 62, 63, 66, 127, 216, 246, 258, 266, 369 Abscess, 147, 150, 369, 374, 462 Acatalasia, 369, 385 Acceptor, 369, 428, 442 Accommodation, 369, 437 Acetylcholine, 131, 253, 369, 388, 439 Acute Disease, 16, 369 Acute lymphoblastic leukemia, 369 Acute lymphocytic leukemia, 83, 369 Acute renal, 369, 416 Acute-Phase Proteins, 141, 369 Acyl, 218, 370, 447 Adaptation, 34, 213, 282, 302, 370 Adenine, 370, 455 Adenocarcinoma, 69, 121, 238, 370, 416 Adenoma, 11, 137, 287, 370 Adenomatous Polyposis Coli, 138, 370 Adenosine, 44, 370, 384, 447, 469 Adenovirus, 74, 81, 370 Adenylate Cyclase, 370, 388 Adherens Junctions, 116, 370 Adipocytes, 370, 394, 427 Adipose Tissue, 370, 443 Adjunctive Therapy, 4, 20, 370 Adjustment, 18, 34, 241, 369, 370 Adjuvant, 91, 281, 370, 411 Adjuvant Therapy, 281, 370 Adolescence, 34, 370, 444 Adoptive Transfer, 103, 108, 114, 370 Adrenal Cortex, 371, 395, 396, 418, 451 Adrenal Glands, 371, 374 Adrenergic, 371, 401, 405, 463 Adrenergic Uptake Inhibitors, 371, 463 Adsorption, 139, 371 Adsorptive, 138, 139, 371 Adverse Effect, 5, 10, 56, 77, 202, 301, 303, 371, 401, 463 Aerobic, 371, 434, 436, 442 Aerosol, 371, 380 Aetiology, 216, 221, 233, 262, 371 Afferent, 371, 427, 440
Affinity, 47, 58, 73, 95, 106, 252, 371, 372, 378, 428, 430, 464 Agar, 371, 392, 396, 448 Age Groups, 42, 298, 309, 371 Age of Onset, 105, 206, 309, 371 Age-Adjusted, 287, 371 Aged, 80 and Over, 371, 372 Agonist, 107, 253, 372, 401, 438 Agoraphobia, 372, 420, 443 Agranulocytosis, 10, 372 Airway, 67, 372 Albumin, 47, 290, 366, 372, 441, 448 Alertness, 372, 384 Alexia, 372, 402 Algorithms, 29, 76, 87, 372, 382 Alkaline, 176, 255, 372, 374, 380, 384, 447 Alkaline Phosphatase, 176, 372 Alkalinization, 222, 372 Alkaloid, 372, 390, 438, 469 Alkylating Agents, 372, 388 Allantois, 372, 408 Alleles, 90, 372, 428 Allergen, 372, 399 Allergic Rhinitis, 230, 234, 240, 251, 372, 384 Allogeneic, 373, 414 Allograft, 229, 373 Allylamine, 373 Alopecia, 373, 396 Alpha Particles, 373, 455 Alpha-1, 111, 373 Alternative medicine, 271, 318, 373 Aluminum, 373, 467 Alveoli, 373, 454 Amebiasis, 373, 433 Ameliorating, 93, 222, 244, 245, 373 Amine, 215, 228, 373, 417 Amino Acid Sequence, 225, 240, 249, 265, 373, 376, 407, 412, 451 Amino Acid Substitution, 70, 373 Amino Acids, 213, 255, 265, 373, 406, 412, 438, 440, 445, 449, 453, 460, 462, 467, 471, 473 Aminosalicylic Acids, 10, 16, 373 Amino-terminal, 374, 451 Ammonia, 373, 374, 413 Amnion, 374, 408 Amphetamines, 371, 374, 390
478 Ulcerative Colitis
Amplification, 81, 92, 220, 374 Ampulla, 374, 404, 407 Amyloid, 257, 374 Amyloidosis, 24, 192, 374 Anaerobic, 133, 374 Anaesthesia, 374, 422 Anal Fissure, 348, 374 Anal Fistula, 350, 374 Analgesic, 374, 419 Analog, 256, 263, 374, 439 Analogous, 82, 374, 449, 471 Analytes, 342, 374 Anaphylactic, 240, 374, 449 Anaphylatoxins, 374, 392 Anaphylaxis, 230, 251, 374, 375 Anaplasia, 375 Anatomical, 53, 71, 375, 379, 394, 421, 461 Androgens, 371, 375, 396 Anemia, 6, 20, 29, 66, 157, 213, 231, 274, 280, 291, 302, 313, 320, 338, 356, 375, 409, 435 Anergy, 111, 375 Anesthesia, 372, 375, 402, 403 Anesthetics, 375, 380, 405 Aneuploidy, 85, 375 Angiogenesis, 108, 216, 229, 236, 375, 431 Angioplasty, 228, 375, 436 Animal model, 6, 64, 69, 71, 80, 84, 85, 88, 94, 95, 96, 98, 103, 109, 115, 152, 227, 301, 375 Anions, 372, 375, 425, 467 Annealing, 375, 449 Anode, 375, 396 Anomalies, 46, 375 Anorectal, 49, 375 Anorexia, 235, 241, 253, 278, 290, 374, 375, 410, 473 Antagonism, 376, 384, 469 Antiallergic, 376, 396 Antibacterial, 376, 465 Antibiotic, 35, 49, 202, 219, 261, 305, 376, 390, 406, 465, 466 Antibody therapy, 62, 227, 376 Anticoagulant, 57, 209, 376, 399, 452 Anticonvulsants, 376 Antidepressant, 355, 376, 420 Antidiarrheals, 288, 356, 376 Antigen, 30, 62, 65, 69, 70, 73, 74, 84, 89, 90, 99, 103, 108, 111, 114, 128, 212, 220, 228, 231, 248, 251, 252, 261, 371, 375, 376, 392, 396, 398, 412, 417, 419, 420, 421, 422, 423, 431
Antigen-Antibody Complex, 376, 392 Antigen-presenting cell, 108, 376, 398 Anti-infective, 376, 418, 464 Anti-Inflammatory Agents, 27, 376, 378, 396 Antimetabolite, 369, 376 Antimicrobial, 222, 239, 376, 389, 399 Antimycotic, 377, 390 Antineoplastic, 84, 369, 372, 377, 396 Antioxidant, 34, 59, 179, 180, 188, 377, 441, 442 Antiproliferative, 377, 423 Antipyretic, 377 Antiviral, 377, 399, 421, 423 Anus, 29, 231, 261, 288, 320, 350, 355, 374, 375, 377, 379, 380, 383, 404, 409, 419, 445, 457 Anxiety, 119, 203, 204, 213, 253, 257, 297, 298, 313, 349, 354, 377, 443 Anxiety Disorders, 377, 443 Aphakia, 377, 459 Apheresis, 8, 135, 138, 139, 377 Aplasia, 153, 377 Aplastic anemia, 159, 377 Apoptosis, 58, 101, 113, 121, 218, 240, 377 Appendectomy, 17, 24, 47, 377 Appendicitis, 17, 24, 48, 280, 377 Aqueous, 377, 380, 386, 397, 403, 418, 427 Arachidonate 12-Lipoxygenase, 377, 428 Arachidonate 15-Lipoxygenase, 377, 428 Arachidonate Lipoxygenases, 377, 428 Arachidonic Acid, 75, 215, 224, 225, 238, 240, 250, 256, 377, 378, 402, 427, 428, 452 Arginine, 374, 378, 439 Aromatic, 230, 251, 378, 447 Arterial, 254, 373, 378, 395, 419, 453, 469 Arteries, 378, 382, 383, 395, 433, 436, 454, 470 Arteriolar, 378, 383 Arterioles, 118, 217, 244, 378, 383, 384, 436 Arteriolosclerosis, 378 Arteriosclerosis, 217, 234, 378 Arteritis, 159, 378 Articular, 27, 44, 52, 378, 441 Ascending Colon, 138, 378 Aseptic, 155, 378, 466 Aspartic, 378, 403 Aspartic Endopeptidases, 378, 403 Aspirin, 63, 378 Assay, 72, 83, 101, 102, 111, 253, 378, 420, 472 Astrocytes, 95, 378, 424
Index 479
Astrocytoma, 378, 412 Asymptomatic, 24, 290, 369, 373, 379, 442 Ataxia, 337, 379, 418, 469 Atmospheric Pressure, 379, 418 Atopic, 214, 217, 219, 223, 229, 234, 240, 244, 251, 254, 260, 379 Atopic Eczema, 251, 379 Atresia, 213, 379 Atrial, 379, 395, 472 Atrioventricular, 379, 395 Atrium, 379, 395, 472, 474 Atrophy, 122, 337, 379, 406 Attenuated, 11, 379 Atypical, 221, 251, 252, 379 Autacoids, 379, 421 Autoantibodies, 99, 213, 252, 300, 301, 379 Autoantigens, 70, 379 Autodigestion, 379, 442 Autoimmune disease, 109, 214, 220, 223, 249, 255, 266, 301, 379, 435, 448 Autoimmune Hepatitis, 51, 252, 379 Autoimmunity, 8, 100, 231, 301, 379 Autologous, 62, 228, 248, 379 Autologous bone marrow transplantation, 228, 248, 379 Autolysis, 254, 379 Autonomic, 369, 380, 445 Autopsy, 112, 380 Avian, 227, 380 B Bacteria, 55, 62, 65, 66, 84, 85, 91, 98, 99, 101, 103, 104, 117, 122, 177, 183, 237, 240, 245, 249, 258, 276, 305, 317, 370, 371, 376, 380, 381, 390, 393, 404, 406, 407, 408, 410, 412, 414, 415, 417, 422, 429, 433, 436, 448, 456, 462, 465, 466, 471, 474 Bacterial Infections, 320, 380, 387, 415, 458 Bacterial Physiology, 370, 380 Bactericidal, 240, 252, 380, 406 Bacteriophage, 380, 448, 471 Bacterium, 221, 380, 382, 393, 416 Barbiturate, 380, 469 Barium, 36, 203, 227, 295, 321, 343, 350, 367, 380 Barium enema, 36, 203, 227, 321, 350, 367, 380 Basal Ganglia, 379, 380, 388, 413 Basal Ganglia Diseases, 379, 380, 388 Base, 79, 83, 105, 206, 302, 370, 380, 398, 399, 409, 410, 412, 425, 426, 443, 446, 447, 469, 472, 473
Base Sequence, 380, 410, 412 Basement Membrane, 75, 80, 139, 235, 380, 407, 426 Basophils, 67, 372, 380, 414, 427, 448 Beclomethasone, 41, 380 Benign, 148, 370, 378, 380, 415, 437, 461 Benzene, 381, 418 Benzodiazepines, 253, 381 Benzoic Acid, 238, 381 Bereavement, 310, 381 Beta-Defensins, 144, 381 Beta-pleated, 374, 381 Beta-Thromboglobulin, 381, 424 Bewilderment, 381, 393 Bilateral, 25, 381, 406, 459 Bile, 183, 187, 276, 290, 381, 388, 410, 411, 416, 417, 425, 428, 466, 467, 473 Bile Acids, 187, 381, 411, 466 Bile Acids and Salts, 381 Bile Ducts, 290, 381, 410 Bile Pigments, 381, 425 Biliary, 51, 188, 287, 290, 381, 384, 416, 442 Biliary Tract, 188, 287, 381, 384, 442 Bilirubin, 372, 381, 410, 418 Binding Sites, 30, 118, 381 Bioavailability, 208, 381 Biochemical, 28, 53, 86, 88, 95, 104, 179, 183, 260, 372, 376, 381, 409, 441, 462 Biological response modifier, 381, 382, 423 Biological therapy, 29, 382, 415 Biopsy specimen, 45, 51, 92, 382 Biosynthesis, 215, 225, 250, 378, 382, 390, 462 Biotechnology, 116, 119, 274, 318, 333, 336, 337, 338, 382 Biotransformation, 47, 77, 382 Bipolar Disorder, 253, 382 Bismuth, 41, 382 Bismuth Subsalicylate, 41, 382 Bladder, 382, 397, 435, 438, 452, 473 Blast phase, 382, 389 Blastocyst, 382, 393, 448 Bloating, 290, 350, 382, 421, 425, 430 Blood Coagulation, 382, 384, 470 Blood Glucose, 382, 416, 423 Blood Platelets, 382, 431, 449, 462, 470 Blood pressure, 382, 419, 434, 454, 464 Blood transfusion, 57, 383 Blot, 76, 383, 420 Blotting, Western, 383, 420 Body Composition, 124, 383 Body Fluids, 383, 401, 409, 439, 464, 472
480 Ulcerative Colitis
Body Image, 270, 282, 383, 399 Bone Density, 24, 278, 383 Bone Marrow, 110, 249, 303, 369, 377, 379, 381, 382, 383, 389, 392, 396, 406, 414, 420, 423, 429, 431, 435, 436, 451, 464, 467 Bone Marrow Transplantation, 249, 383 Bone Resorption, 283, 383 Bone scan, 383, 461 Bowel Movement, 57, 284, 292, 346, 350, 351, 355, 383, 394, 400, 466 Bradykinin, 30, 383, 425, 439, 448 Branch, 363, 383, 412, 429, 444, 454, 465, 468, 469 Breakdown, 84, 290, 383, 400, 410, 440 Bromelain, 191, 383 Bronchi, 383, 384, 405, 469, 471 Bronchial, 67, 240, 383, 417, 469 Bronchioles, 373, 383, 454 Bronchitis, 67, 214, 384, 389 Bronchoconstriction, 240, 384, 449 Bronchus, 384 Buccal, 384, 429 Budesonide, 8, 41, 42, 47, 52, 216, 306, 319, 384 Bulimia, 241, 253, 384, 463 Bullous, 124, 147, 384 Butyric Acid, 218, 384 C Cachexia, 214, 234, 235, 241, 384 Cadherins, 228, 248, 370, 384 Caffeine, 309, 384, 455 Calcification, 378, 384 Calcium, 7, 93, 263, 384, 392, 431, 436, 443, 463, 472, 475 Calculi, 384, 414 Capillary, 216, 383, 384, 385, 474 Capillary Permeability, 383, 385 Capsules, 230, 251, 385, 401, 404, 411 Carbohydrate, 223, 385, 396, 413, 450, 462 Carbon Dioxide, 385, 448, 458 Carboxy, 225, 250, 385 Carboxy-terminal, 225, 250, 385 Carcinogen, 385, 433 Carcinogenesis, 11, 86, 113, 140, 142, 152, 385, 387 Carcinogenic, 372, 381, 385, 422, 440, 451, 466 Carcinoma, 34, 48, 57, 73, 78, 87, 122, 131, 145, 147, 385 Cardiac, 73, 229, 253, 373, 384, 385, 395, 405, 410, 436, 466 Cardiovascular, 385, 427, 462
Carotene, 385, 459 Carrier Proteins, 385, 448 Case report, 15, 17, 29, 48, 122, 126, 142, 147, 157, 161, 168, 181, 385, 390 Case series, 385, 390 Case-Control Studies, 33, 101, 385, 405 Catalase, 252, 369, 385 Cataract, 240, 377, 385, 459 Catecholamine, 386, 401, 447 Cathepsins, 88, 386 Catheterization, 375, 386, 436 Cathode, 375, 386, 396, 403 Caudal, 386, 400, 419, 450 Causal, 43, 48, 90, 103, 221, 386, 405, 424 Cecum, 64, 231, 386, 426 Celiac Disease, 220, 310, 386 Cell Adhesion, 129, 221, 228, 232, 248, 384, 386, 423 Cell Adhesion Molecules, 221, 228, 248, 386 Cell Death, 377, 386, 412, 437 Cell Differentiation, 263, 386, 463 Cell Division, 337, 380, 386, 415, 434, 448 Cell membrane, 97, 221, 225, 239, 250, 256, 370, 385, 386, 390, 399, 407, 410, 425, 447 Cell proliferation, 11, 52, 85, 113, 220, 265, 378, 386, 424, 463 Cell Respiration, 386, 434, 442, 458 Cell Size, 386, 409 Cell Survival, 386, 415 Cellulose, 387, 448 Central Nervous System Infections, 387, 415, 418 Centrifugation, 255, 387 Cerebellar, 379, 387, 457 Cerebral, 166, 219, 261, 379, 380, 387, 395, 398, 405, 407, 412, 418, 454, 465, 469 Cerebral hemispheres, 380, 387, 412 Cerebral Palsy, 387, 465 Cerebrospinal, 239, 387, 418 Cerebrospinal fluid, 239, 387, 418 Cerebrovascular, 240, 380, 387, 469 Cerebrum, 387, 472 Cesarean Section, 43, 387 Character, 387, 398, 413 Chemokines, 70, 108, 154, 387 Chemokines, C, 108, 387 Chemopreventive, 79, 160, 387 Chemoprotective, 51, 387 Chemotactic Factors, 387, 392 Chemotaxis, 97, 108, 225, 250, 387 Chemotherapy, 370, 388, 458
Index 481
Chenodeoxycholic Acid, 388, 473 Chest Pain, 73, 388 Chest wall, 44, 388 Chimeras, 110, 388 Chlorambucil, 59, 388 Chlorophyll, 388, 404 Cholangitis, 9, 38, 43, 50, 122, 125, 131, 157, 160, 171, 252, 287, 295, 344, 388 Cholecystectomy, 290, 296, 388 Cholecystostomy, 290, 388 Cholelithiasis, 43, 51, 290, 295, 388 Cholera, 91, 117, 213, 218, 388, 475 Cholera Toxin, 91, 218, 388 Choleretic, 388, 473 Cholesterol, 255, 381, 388, 410, 428, 466 Cholinergic, 253, 256, 257, 388, 435, 438, 456 Chorea, 253, 254, 257, 388 Choreatic Disorders, 388 Chorion, 388, 408 Chorioretinitis, 388, 459 Choroid, 388, 389, 459, 473 Choroiditis, 294, 389 Chromatin, 377, 389 Chromosomal, 83, 85, 90, 153, 374, 375, 389, 448, 459 Chronic Disease, 6, 12, 55, 56, 92, 98, 279, 347, 352, 384, 389, 391 Chronic lymphocytic leukemia, 389 Chronic myelogenous leukemia, 382, 389, 430 Chronic Obstructive Pulmonary Disease, 229, 234, 240, 241, 389 Chronic phase, 115, 216, 389 Chronic renal, 389, 449, 473 Ciliary, 389, 463, 473 Ciliary Body, 389, 463, 473 Ciprofloxacin, 16, 41, 52, 288, 389 Circadian, 306, 389 Circadian Rhythm, 306, 389 Circulatory system, 237, 389 CIS, 61, 389, 459 Citrus, 31, 389 Clamp, 72, 390 Clarithromycin, 16, 390 Clinical Medicine, 143, 187, 390, 450 Clinical study, 167, 171, 178, 207, 390, 395 Clone, 61, 265, 390 Cloning, 108, 118, 382, 390 Clostridium, 107, 156, 270, 302, 390 Clostridium difficile, 107, 156, 270, 302, 390
Clotrimazole, 201, 202, 390 Coagulation, 382, 390, 416, 448, 470 Coca, 390 Cocaine, 253, 390 Cochlea, 390, 422 Cod Liver Oil, 391, 403 Codons, 391, 412, 440 Coenzyme, 275, 391 Cofactor, 391, 453, 470 Cognitive restructuring, 391, 467 Cohort Studies, 391, 405 Colitis, Ulcerative, 218, 391 Collagen, 111, 234, 380, 383, 391, 407, 408, 411, 418, 431, 449, 451, 461 Collagen disease, 391, 418, 461 Collagenases, 235, 391 Collagenous Colitis, 75, 221, 391 Collapse, 375, 383, 391 Colloidal, 372, 391, 403, 407, 446 Colonoscope, 78, 391 Colony-Stimulating Factors, 260, 392, 414 Colorectal Surgery, 33, 392 Colostomy, 40, 311, 343, 392 Combination Therapy, 35, 300, 303, 392 Commensal, 84, 88, 115, 117, 245, 392 Compassionate, 304, 392 Complement, 4, 67, 141, 374, 392, 393, 412, 423, 430, 434, 448 Complementary and alternative medicine, 175, 197, 392 Complementary medicine, 12, 175, 393 Complete remission, 393, 458 Compulsive Behavior, 393, 462 Computational Biology, 333, 336, 393 Computed tomography, 383, 393, 461 Computerized axial tomography, 393, 461 Conception, 38, 49, 296, 346, 348, 393, 394, 408, 466 Concomitant, 39, 133, 391, 393 Cone, 92, 393, 426, 468 Confusion, 46, 393, 400, 419, 473 Congestion, 349, 393, 406 Congestive heart failure, 235, 393 Conjugated, 77, 381, 388, 393, 397 Conjugation, 77, 382, 393 Conjunctiva, 394, 454, 461 Conjunctivitis, 219, 228, 240, 248, 260, 294, 394 Conjunctivitis, Allergic, 228, 248, 394 Connective Tissue, 235, 258, 383, 391, 394, 409, 410, 411, 429, 432, 459, 461, 468 Connective Tissue Cells, 394
482 Ulcerative Colitis
Connexins, 113, 394, 410 Consciousness, 374, 394, 398, 401 Constipation, 60, 71, 254, 277, 288, 394, 425, 446 Constitutional, 42, 394, 459 Constriction, 394, 425, 453, 474 Constriction, Pathologic, 394, 474 Consultation, 72, 203, 270, 299, 354, 394, 407 Consumption, 31, 170, 394, 399, 411, 439, 458 Contact dermatitis, 39, 217, 244, 394 Contamination, 394, 416 Continence, 136, 162, 304, 355, 394 Continent Ileostomy, 32, 40, 56, 304, 346, 350, 355, 394 Contraceptive, 394, 431 Contraindications, ii, 350, 394 Contrast Sensitivity, 394, 440 Control group, 394, 448, 456 Controlled clinical trial, 20, 21, 95, 113, 303, 395, 456 Controlled study, 176, 201, 276, 395 Conventional therapy, 16, 395 Conventional treatment, 395 Convulsions, 380, 395, 402, 419, 450 Coordination, 226, 250, 395, 435 Cor, 132, 395 Cornea, 395, 426, 461, 473 Corneal Ulcer, 236, 395 Corneum, 395, 405, 419 Coronary, 395, 433, 436 Coronary Arteriosclerosis, 395, 436 Coronary Thrombosis, 395, 433, 436 Corpus, 216, 395, 444, 451, 469 Corpus Luteum, 216, 395, 451 Cortex, 379, 395, 407, 457 Corticosteroid, 7, 10, 16, 35, 48, 70, 167, 284, 303, 306, 307, 395, 450, 466 Cortisol, 47, 372, 396 Cortisone, 396, 450 Counterimmunoelectrophoresis, 116, 396 Cranial, 396, 415, 424, 438, 440, 446, 465 Craniocerebral Trauma, 380, 396, 415, 418, 469 Cross-Sectional Studies, 396, 405 Crowding, 78, 396 Culture Media, 100, 371, 396 Curative, 27, 40, 55, 281, 288, 396, 438, 460, 469 Cutaneous, 289, 302, 394, 396, 429
Cyclic, 215, 228, 370, 384, 396, 415, 439, 447, 452, 469 Cyclophosphamide, 59, 155, 396 Cysteine, 88, 387, 396, 397, 403, 467 Cysteine Endopeptidases, 396, 403 Cystine, 88, 396, 397 Cystitis, 67, 168, 397 Cytochrome, 397, 458 Cytochrome b, 397, 458 Cytomegalovirus, 133, 145, 283, 292, 397 Cytoplasm, 86, 252, 377, 380, 386, 388, 397, 405, 414, 460 Cytoprotection, 61, 397 Cytoskeleton, 107, 370, 397, 423 Cytotoxic, 59, 301, 397, 421, 424, 463 Cytotoxicity, 103, 265, 373, 397 Cytotoxins, 91, 397 D Databases, Bibliographic, 333, 397 Decidua, 397, 448 Decision Making, 283, 397 Decompression, 288, 398 Decompression Sickness, 398 Defecation, 71, 185, 304, 355, 398, 451 Defense Mechanisms, 398, 423 Degenerative, 101, 235, 398, 416, 430, 441, 459 Dehydration, 17, 57, 388, 398 Deletion, 61, 69, 110, 377, 398 Delirium, 297, 398 Delusions, 398, 454 Dementia, 95, 228, 234, 248, 253, 254, 257, 398 Demyelinating Diseases, 236, 398 Denaturation, 398, 449 Dendrites, 398, 438 Dendritic, 70, 111, 128, 398, 431 Dendritic cell, 70, 128, 398 Density, 7, 27, 53, 76, 92, 96, 124, 170, 278, 283, 383, 387, 399, 409, 428, 440, 464 Deoxycytidine, 72, 399 Deoxyguanosine, 72, 399 Depersonalization, 399, 443, 461 Depolarization, 399, 463 Derealization, 399, 443 Dermal, 228, 248, 399, 427 Dermatitis, 214, 217, 219, 223, 229, 234, 240, 244, 254, 260, 399, 402 Dermatosis, 129, 147, 289, 399 Desensitization, 107, 399 Detergents, 399, 409 Deuterium, 399, 418
Index 483
Developed Countries, 17, 90, 104, 399 Dextran Sulfate, 78, 104, 178, 180, 188, 399 DHEA, 194, 399 Diabetes Mellitus, 13, 70, 101, 214, 266, 399, 413, 416, 440 Diabetic Retinopathy, 216, 236, 399 Diagnostic Imaging, 320, 399 Diagnostic procedure, 211, 318, 346, 400 Diarrhoea, 221, 400, 410 Diastolic, 400, 419 Diencephalon, 400, 419, 469 Dietary Fiber, 186, 187, 254, 400 Dietitian, 348, 400 Diffusion, 385, 396, 400, 422, 425, 438 Digestive system, 210, 271, 278, 288, 347, 348, 349, 352, 356, 400, 411, 435 Digestive tract, 8, 277, 280, 320, 348, 350, 351, 388, 400, 464, 476 Dihydroxy, 215, 400 Dilatation, 283, 375, 400, 451, 454 Dilation, 217, 244, 288, 383, 400, 418 Diploid, 375, 400, 434, 448, 472 Direct, iii, 37, 84, 95, 102, 110, 227, 265, 292, 295, 323, 352, 390, 400, 401, 412, 450, 457 Disease Progression, 43, 400 Disease Susceptibility, 23, 400 Disinfectant, 400, 406 Disorientation, 393, 398, 400 Disposition, 74, 298, 400 Dissection, 74, 400 Dissociation, 371, 400 Distal, 22, 24, 31, 37, 40, 41, 42, 47, 48, 50, 56, 129, 149, 156, 162, 167, 191, 224, 237, 268, 284, 401, 411, 453, 454 Distention, 365, 401 Diuresis, 384, 401, 469 Diuretic, 238, 255, 401 Dizziness, 231, 401, 443 Dominance, 401, 405 Dopamine, 390, 401, 447 Dorsal, 401, 450 Dosage Forms, 243, 401 Drug Interactions, 64, 325, 326, 401 Drug Tolerance, 401, 470 Drug Toxicity, 32, 401 Duct, 51, 222, 374, 386, 388, 401, 407, 441, 460 Duodenal Ulcer, 237, 401 Duodenitis, 49, 150, 243, 401 Duodenum, 49, 233, 237, 262, 381, 388, 401, 402, 403, 410, 425, 442, 466
Dura mater, 402, 432, 442 Dyes, 374, 380, 402, 409, 467 Dyskinesia, 253, 254, 257, 402 Dyslexia, 253, 254, 257, 402 Dyspareunia, 346, 402 Dyspepsia, 73, 402, 421 Dyspnea, 402, 443, 454 Dystonia, 253, 402 Dystrophy, 337, 402 E Eclampsia, 381, 402, 450 Ectopic, 30, 402 Eczema, 217, 230, 240, 244, 402 Edema, 30, 242, 394, 399, 402, 424, 436, 437, 450, 473 Educational Status, 17, 402 Effector, 88, 89, 103, 249, 260, 369, 392, 402, 438, 447 Effector cell, 249, 402, 438 Effusion, 402, 468 Eicosanoids, 44, 63, 75, 256, 402 Elasticity, 378, 395, 402, 464 Elastin, 234, 391, 402, 407 Elective, 14, 46, 281, 304, 402 Electroacupuncture, 180, 402 Electrocardiogram, 204, 402 Electrolyte, 187, 218, 302, 396, 398, 403, 409, 434, 439, 464, 473 Electrons, 377, 380, 386, 403, 425, 441, 442, 455 Electrophoresis, 83, 87, 252, 403 Electroplating, 403, 467 Embryo, 374, 382, 386, 403, 408, 422, 449, 465, 476 Emetic, 253, 403 Emphysema, 257, 389, 403 Emulsion, 296, 403 Encapsulated, 70, 403 Encephalitis, 403 Encephalomyelitis, 249, 403 Endarterectomy, 375, 403 Endemic, 388, 403, 465 Endocytosis, 107, 223, 403 Endometrium, 216, 397, 403, 432 Endopeptidases, 235, 378, 386, 396, 403, 433, 445, 462 Endoscope, 77, 204, 403 Endoscopy, 6, 21, 33, 39, 73, 131, 135, 136, 146, 159, 161, 178, 270, 350, 351, 404 Endothelial cell, 30, 108, 116, 240, 404, 408, 424, 470
484 Ulcerative Colitis
Endothelium, 30, 67, 116, 232, 261, 404, 439 Endothelium, Lymphatic, 404 Endothelium, Vascular, 404 Endothelium-derived, 404, 439 Endotoxemia, 143, 404 Endotoxic, 229, 404, 428 Endotoxin, 143, 246, 247, 265, 404, 472 End-stage renal, 389, 404, 449 Enema, 16, 41, 47, 202, 205, 209, 285, 313, 316, 343, 404 Energy balance, 404, 427 Enhancer, 61, 404 Enteral Nutrition, 223, 281, 290, 404 Enteric bacteria, 84, 91, 101, 404 Enteric-coated, 19, 404 Enteritis, 99, 270, 404 Enterocolitis, 24, 91, 104, 115, 270, 390, 404 Enterocytes, 97, 404 Environmental Exposure, 404, 440 Environmental Health, 332, 334, 405 Enzymatic, 59, 384, 385, 392, 405, 417, 449, 459 Enzyme Inhibitors, 405, 448 Eosinophil, 67, 149, 405, 414 Eosinophilia, 405, 408 Eosinophilic, 219, 220, 405, 408 Eosinophilic Gastroenteritis, 219, 220, 405 Epidemic, 405, 465 Epidemiologic Studies, 55, 405 Epidemiological, 23, 30, 31, 44, 89, 90, 132, 405 Epidermal, 4, 45, 107, 132, 133, 316, 405, 426, 427, 431 Epidermal Growth Factor, 4, 45, 107, 405 Epidermis, 395, 405, 419, 426, 427, 455 Epigastric, 405, 442 Epinephrine, 371, 401, 405, 473 Episcleritis, 294, 405, 461 Episiotomy, 43, 405 Epistasis, 117, 405 Epithelial, 11, 24, 54, 58, 61, 67, 68, 75, 78, 82, 84, 85, 86, 92, 93, 97, 103, 106, 107, 109, 115, 117, 127, 140, 142, 212, 220, 264, 370, 381, 388, 389, 395, 397, 405, 406, 413, 416, 424, 425, 426, 443 Epitope, 104, 117, 406 Erythema, 133, 192, 289, 366, 394, 406, 473 Erythema Nodosum, 133, 289, 406 Erythrocytes, 375, 383, 406, 443, 448, 457 Erythromycin, 390, 406 Erythropoiesis, 6, 406
Erythropoietin, 6, 291, 406 Escalation, 70, 155, 406 Esophageal, 78, 406, 411 Esophagitis, 219, 220, 260, 406, 411, 467 Esophagitis, Peptic, 219, 260, 406 Esophagus, 78, 82, 231, 233, 261, 262, 379, 400, 406, 411, 416, 429, 447, 457, 466 Essential Tremor, 337, 406 Estrogen, 79, 113, 406 Estrogen receptor, 113, 406 Ethanol, 72, 252, 255, 406 Ethnic Groups, 35, 55, 406 Eukaryotic Cells, 407, 421, 441 Evacuation, 394, 407, 410 Evoke, 407, 466 Excitation, 77, 374, 407, 409 Exocrine, 407, 442 Exocytosis, 88, 223, 225, 250, 407 Exogenous, 79, 371, 382, 402, 407 Exon, 13, 407 Expert Systems, 407, 420 Extender, 280, 407 Extensor, 407, 453 Extracellular Matrix, 80, 87, 111, 220, 228, 248, 394, 407, 408, 423, 431 Extracellular Matrix Proteins, 407, 431 Extracellular Space, 407 Extraction, 255, 377, 387, 407, 459 Eye Infections, 370, 407 F Faecal, 156, 166, 182, 183, 400, 407 Fallopian Tubes, 407, 473 Family Planning, 49, 333, 408 Fasciitis, 44, 408 Fatigue, 268, 288, 320, 348, 408, 416 Fatty acids, 31, 41, 45, 166, 184, 218, 224, 290, 319, 372, 402, 408, 413, 428, 452, 464 Febrile, 408, 465 Fecal Incontinence, 15, 408 Feces, 218, 288, 394, 407, 408, 466 Femoral, 7, 408 Femur, 408 Ferritin, 6, 408 Fertilizers, 408, 467 Fetal Growth Retardation, 46, 408 Fetal Membranes, 236, 408 Fetus, 28, 43, 222, 387, 406, 408, 448, 451, 465, 473 Fibrinogen, 408, 448, 470 Fibroblast Growth Factor, 58, 408 Fibroblasts, 240, 394, 408, 423, 424 Fibronectin, 228, 261, 409
Index 485
Fibrosarcoma, 408, 409 Fibrosis, 51, 65, 80, 212, 222, 234, 338, 373, 409, 454, 461 Fish Oils, 189, 409 Fistula, 20, 53, 295, 356, 409, 410, 440 Flatulence, 277, 290, 313, 409 Flatus, 408, 409, 410 Flexor, 407, 409, 427 Flow Cytometry, 92, 102, 409 Fluid Therapy, 409, 439 Fluorescence, 77, 85, 100, 135, 252, 409 Fluorescent Dyes, 409 Folate, 52, 86, 167, 168, 172, 173, 180, 181, 184, 409 Fold, 90, 92, 93, 409, 432 Folic Acid, 5, 16, 172, 173, 187, 188, 302, 409 Foramen, 409, 446 Forearm, 283, 382, 408, 409, 456 Frameshift, 101, 410, 472 Frameshift Mutation, 101, 410, 472 Free Association, 410, 453 Free Radical Scavengers, 41, 410 Fungi, 237, 377, 393, 407, 410, 415, 433, 460, 476 Fungistatic, 381, 410 G Gallbladder, 43, 131, 290, 296, 369, 381, 388, 400, 410, 411 Gallstones, 43, 290, 295, 381, 388, 410, 473 Ganglia, 369, 380, 410, 438, 446 Gap Junctions, 394, 410, 468 Gas, 277, 313, 374, 385, 398, 400, 409, 410, 418, 421, 425, 430, 439, 474 Gastric, 66, 87, 137, 181, 229, 237, 238, 253, 286, 379, 401, 405, 406, 410, 411, 416, 417, 445 Gastric Acid, 238, 253, 410 Gastric Emptying, 286, 410 Gastric Juices, 410, 445 Gastric Mucosa, 410, 445 Gastrin, 410, 417 Gastritis, 65, 73, 115, 135, 170, 188, 222, 237, 410, 467 Gastroduodenal, 85, 410 Gastroenteritis, 93, 213, 410 Gastroenterologist, 45, 46, 279, 296, 297, 299, 305, 411 Gastroesophageal Reflux, 73, 113, 411 Gastroesophageal Reflux Disease, 73, 113, 411
Gastrointestinal tract, 5, 20, 22, 26, 50, 53, 55, 64, 65, 77, 94, 96, 100, 107, 203, 212, 218, 224, 226, 231, 232, 237, 245, 261, 271, 278, 280, 283, 285, 305, 307, 348, 353, 380, 406, 409, 411, 426, 427, 462, 464, 466, 472 Gastrointestinal Transit, 155, 411 Gastroscopy, 78, 411 Gastrostomy, 280, 404, 411 Gelatin, 168, 224, 396, 411, 413, 468, 469 Gelatinases, 235, 411 Gene Amplification, 153, 411 Gene Expression, 61, 66, 75, 76, 80, 81, 83, 97, 106, 129, 170, 187, 338, 411 Gene Rearrangement, 83, 411 General practitioner, 11, 33, 412 Genes, mos, 23, 412 Genetic Code, 412, 439 Genetic Counseling, 76, 412 Genetic Engineering, 382, 390, 412, 456 Genetic Markers, 13, 35, 412 Genetic testing, 412, 449 Genetics, 22, 23, 30, 35, 45, 76, 80, 83, 91, 141, 142, 153, 269, 270, 309, 351, 393, 401, 412 Genital, 389, 412, 473 Genitourinary, 412, 473 Genotype, 76, 81, 412, 447 Germ Cells, 412, 441, 476 Germ-free, 84, 103, 412 Gestation, 28, 43, 412, 445, 448, 465 Gestational, 408, 412 Giant Cells, 412, 460 Giardiasis, 412, 433 Gland, 371, 396, 412, 429, 442, 443, 448, 452, 461, 466, 467, 470 Glioblastoma, 238, 412 Glomerular, 138, 236, 413, 458 Glomeruli, 413, 455 Glomerulonephritis, 115, 139, 148, 413, 420 Glomerulus, 413, 437 Glucocorticoid, 6, 77, 97, 138, 144, 276, 306, 307, 380, 384, 413, 418, 450 Glucose, 337, 382, 387, 399, 413, 416, 419, 422, 423, 460 Glucose Intolerance, 399, 413 Glucuronic Acid, 413, 416 Glutamic Acid, 409, 413, 451 Glutamine, 16, 41, 45, 138, 195, 413 Gluten, 386, 413 Glycerol, 384, 413, 447
486 Ulcerative Colitis
Glycerophospholipids, 225, 250, 413, 447 Glycine, 240, 381, 388, 413, 462 Glycogen, 241, 413 Glycoprotein, 82, 220, 232, 406, 408, 409, 412, 413, 414, 426, 430, 470, 472 Goblet Cells, 404, 413 Gonadal, 414, 466 Gout, 185, 241, 414 Governing Board, 414, 450 Grade, 73, 86, 104, 126, 129, 135, 152, 157, 414 Grading, 78, 138, 414 Graft, 229, 235, 414, 417, 421, 430, 436 Graft Rejection, 235, 414, 421, 430 Grafting, 414, 421 Gram-negative, 229, 404, 414, 475 Gram-Negative Bacteria, 404, 414 Gram-positive, 390, 414, 436, 466 Gram-Positive Bacteria, 390, 414 Granule, 149, 240, 414, 460 Granulocyte Colony-Stimulating Factor, 392, 414 Granulocyte-Macrophage ColonyStimulating Factor, 392, 414 Granulocytes, 252, 372, 392, 414, 427, 436, 463, 475 Granuloma, 139, 238, 414, 415 Granulomatous Colitis, 91, 275, 415 Granulomatous Disease, Chronic, 415, 458 Grasses, 409, 415 Growth factors, 75, 84, 260, 415 Guanylate Cyclase, 415, 439 H Habitat, 415, 436 Hamartoma, 138, 415 Haploid, 415, 448 Haplotypes, 13, 415 Haptens, 371, 415 Headache, 253, 290, 384, 415, 418, 419 Headache Disorders, 415 Health Education, 320, 415 Health Promotion, 7, 415 Health Services, 73, 82, 415 Health Status, 13, 51, 113, 349, 415 Heart failure, 235, 416, 454 Heartbeat, 57, 416 Heartburn, 277, 288, 382, 416, 421 Hematogenous, 249, 416 Hemoglobin, 6, 47, 290, 375, 406, 416, 427 Hemoglobinuria, 337, 416 Hemolytic, 157, 408, 416
Hemorrhage, 48, 57, 73, 396, 415, 416, 436, 447, 455, 467, 475 Hemorrhoids, 220, 348, 416 Hemostasis, 416, 423, 462 Heparin, 9, 41, 52, 57, 85, 140, 162, 209, 284, 317, 416, 449 Hepatic, 39, 64, 218, 265, 372, 398, 416 Hepatitis, 43, 59, 238, 252, 303, 310, 416 Hepatitis A, 43, 416 Hepatobiliary, 26, 35, 42, 43, 50, 290, 416 Hepatocellular, 161, 416 Hepatocellular carcinoma, 161, 416 Hepatocytes, 369, 416 Hepatovirus, 416 Hereditary, 299, 388, 414, 416, 459 Heredity, 356, 411, 412, 417 Heterodimers, 220, 417, 423 Heterogeneity, 16, 30, 76, 80, 89, 126, 137, 300, 305, 371, 417 Heterogenic, 417 Heterogenous, 252, 417 Heterotrophic, 410, 417 Histamine, 374, 417 Histidine, 240, 417 Histology, 51, 86, 417, 443 Homeostasis, 7, 263, 270, 417 Homogeneous, 252, 264, 265, 378, 417, 446 Homologous, 107, 372, 394, 417, 468 Hormonal, 7, 73, 379, 396, 417, 475 Hormone therapy, 370, 417 Human growth hormone, 4, 417, 464 Humoral, 100, 414, 417 Humour, 417 Hybrid, 390, 417 Hybridization, 74, 76, 417 Hybridoma, 104, 417 Hydrocephalus, 418, 424 Hydrocortisone, 35, 36, 284, 418 Hydrogen Bonding, 418, 439 Hydrogen Peroxide, 71, 385, 418, 428, 467 Hydrolysis, 256, 378, 382, 418, 425, 445, 447, 449, 453 Hydrophobic, 226, 399, 413, 418, 428 Hydroxamic Acids, 235, 418 Hydroxybenzoic Acids, 373, 418 Hydroxylysine, 391, 418 Hydroxyproline, 391, 418 Hyperaemia, 394, 418 Hyperbaric, 41, 119, 142, 176, 182, 187, 189, 418 Hyperbaric oxygen, 41, 119, 142, 176, 182, 187, 189, 418
Index 487
Hyperbilirubinemia, 418, 425 Hyperkinesia, 253, 254, 257, 418 Hyperplasia, 161, 418, 427 Hypersecretion, 253, 419 Hypersensitivity, 61, 219, 228, 230, 234, 248, 251, 260, 372, 375, 394, 399, 405, 419, 427, 460 Hypertension, 177, 192, 241, 253, 378, 419, 424, 440, 450, 473 Hypertrophy, 395, 418, 419, 472 Hyperuricemia, 414, 419 Hypnotic, 380, 419, 469 Hypoglycaemia, 398, 419 Hypotension, 395, 419, 449 Hypotensive, 238, 419, 425 Hypothalamic, 110, 419 Hypothalamus, 110, 400, 419, 448, 464, 469 Hypoxia, 398, 419, 469 Hysterotomy, 387, 419 I Ibuprofen, 77, 419 Ichthyosis, 113, 419 Id, 172, 191, 356, 357, 362, 364, 419 Idiopathic, 8, 15, 65, 71, 80, 90, 96, 100, 102, 110, 153, 182, 242, 270, 289, 296, 419, 455, 460 Ileitis, 122, 201, 231, 261, 419 Ileoanal Pull-Through, 154, 419 Ileoanal Reservoir, 13, 136, 343, 419, 451 Ileum, 20, 36, 243, 263, 304, 349, 353, 386, 419, 420, 425 Image Cytometry, 127, 420 Imidazole, 390, 417, 420 Imipramine, 257, 420 Immune adjuvant, 41, 420 Immune Complex Diseases, 376, 420, 448 Immune function, 12, 25, 55, 68, 81, 420, 421 Immune Sera, 420 Immunity, 9, 11, 69, 94, 101, 114, 115, 245, 397, 420, 421, 424, 430, 440, 471 Immunization, 11, 91, 344, 370, 420, 421 Immunoassay, 242, 420 Immunoblotting, 252, 420 Immunocompromised, 82, 270, 420 Immunodeficiency, 81, 337, 420 Immunofluorescence, 252, 420 Immunogenic, 421, 428 Immunoglobulin, 41, 67, 167, 376, 421, 434 Immunohistochemistry, 74, 106, 120, 421 Immunologic, 36, 53, 73, 79, 89, 102, 213, 242, 370, 387, 420, 421
Immunosuppressant, 27, 369, 372, 421 Immunosuppressive Agents, 10, 41, 49, 59, 223, 224, 302, 350, 421, 461 Immunosuppressive therapy, 8, 19, 25, 35, 46, 54, 57, 97, 289, 421 Immunotherapy, 371, 382, 399, 421 Immunotoxins, 421, 457 Impairment, 95, 379, 381, 398, 402, 407, 421, 432, 454 Implantation, 216, 393, 421 In situ, 74, 75, 76, 85, 100, 421 In Situ Hybridization, 74, 75, 76, 85, 100, 421 In vitro, 64, 69, 72, 75, 87, 95, 111, 265, 421, 449, 469 In vivo, 72, 75, 83, 86, 88, 91, 95, 104, 111, 182, 232, 247, 258, 416, 421, 430, 441, 469, 470 Incision, 391, 405, 419, 421, 424, 426 Incompetence, 411, 421 Indicative, 93, 271, 421, 444, 474 Indigestion, 382, 421, 426 Indomethacin, 77, 421 Induction, 8, 16, 26, 27, 35, 54, 61, 75, 78, 82, 110, 111, 150, 270, 283, 284, 307, 375, 422, 424 Induction therapy, 422 Infancy, 291, 422, 460 Infant, Newborn, 371, 422 Infarction, 418, 422, 458 Infectious Diarrhea, 91, 422 Infertility, 38, 219, 222, 261, 349, 422 Infiltration, 24, 51, 86, 111, 150, 413, 422 Infusion, 29, 70, 422, 436, 471 Ingestion, 100, 254, 276, 422, 449 Initiation, 58, 67, 81, 84, 108, 111, 112, 301, 422, 466, 471 Initiator, 422, 424 Inner ear, 25, 422, 443 Inositol, 225, 250, 422 Insight, 55, 67, 69, 84, 98, 99, 101, 107, 269, 279, 294, 422 Instillation, 177, 423 Insulator, 423, 435 Insulin, 87, 235, 423, 460 Insulin-dependent diabetes mellitus, 423 Insulin-like, 87, 423 Insurance Pools, 292, 423 Integrins, 29, 111, 220, 228, 248, 423 Intercellular Junctions, 67, 423 Interferon, 4, 26, 27, 41, 114, 145, 204, 233, 246, 262, 265, 316, 423, 424, 429
488 Ulcerative Colitis
Interferon-alpha, 41, 423 Interferon-beta, 204, 423 Interleukin-1, 41, 71, 112, 137, 169, 219, 236, 241, 260, 265, 423, 424 Interleukin-10, 112, 169, 423 Interleukin-11, 219, 260, 423 Interleukin-12, 265, 424 Interleukin-15, 236, 424 Interleukin-18, 265, 424 Interleukin-2, 41, 81, 84, 103, 217, 423, 424 Interleukin-3, 392, 424 Interleukin-8, 108, 225, 229, 250, 424 Interleukins, 9, 44, 260, 421, 424, 429 Intermittent, 26, 161, 227, 391, 409, 424 Interstitial, 80, 111, 115, 168, 407, 424, 437, 458 Intervention Studies, 86, 424 Intestinal, 8, 9, 13, 17, 27, 32, 33, 40, 42, 45, 52, 54, 55, 56, 57, 58, 61, 62, 63, 65, 68, 75, 76, 80, 84, 85, 86, 90, 91, 93, 94, 97, 98, 103, 104, 107, 109, 110, 114, 115, 117, 153, 161, 169, 170, 183, 184, 203, 204, 213, 224, 227, 231, 232, 245, 258, 261, 268, 270, 276, 278, 289, 290, 291, 293, 295, 302, 304, 321, 343, 349, 352, 385, 386, 388, 390, 404, 424, 426, 430, 436, 443, 451, 475, 476 Intoxication, 398, 424, 476 Intracranial Hypertension, 148, 415, 418, 424 Intraepithelial, 64, 148, 233, 262, 424 Intramuscular, 307, 424, 443 Intrinsic, 40, 258, 371, 380, 424 Invasive, 66, 69, 78, 88, 92, 99, 232, 420, 424, 430 Involuntary, 380, 388, 406, 408, 425, 436 Ion Channels, 378, 425, 438, 468 Ion Transport, 94, 425, 434 Ions, 380, 400, 403, 418, 425 Ischemia, 63, 95, 379, 425, 436, 458 Ischemic Colitis, 24, 425 Isoenzyme, 176, 425 J Jaundice, 43, 418, 425 Jejunostomy, 404, 425 Jejunum, 243, 388, 425 Jet lag, 253, 425 Jews, 55, 83, 190, 425 K Kallidin, 383, 425 Kb, 76, 90, 332, 425, 426
Keratinocyte growth factor, 4, 145, 155, 425 Keratinocytes, 424, 426 Keratitis, 294, 426 Keratoconus, 236, 426 Kidney Disease, 201, 206, 210, 332, 338, 344, 357, 426, 458 Kilobase, 81, 426 Kinetics, 98, 181, 426 L Labile, 77, 392, 426 Labyrinth, 390, 422, 426, 462, 474 Lacerations, 405, 426 Lacrimal, 426, 454 Lacrimal gland, 426, 454 Lactation, 46, 426 Lactose Intolerance, 5, 290, 309, 426 Lag, 21, 426 Laminin, 380, 407, 426 Laparotomy, 24, 159, 426 Latent, 426, 450 Lavage, 127, 426 Least-Squares Analysis, 426, 457 Lens, 377, 385, 426, 475 Leptin, 110, 213, 427 Lesion, 11, 92, 146, 231, 233, 262, 289, 414, 427, 428, 469, 473 Lethal, 265, 380, 427 Leucine, 427, 445 Leucocyte, 373, 405, 427, 429 Leukapheresis, 135, 203, 377, 427 Leukemia, 223, 337, 369, 389, 427, 451 Leukopenia, 59, 64, 231, 427 Leukotrienes, 94, 225, 250, 256, 378, 402, 427, 428 Library Services, 362, 427 Lichen Planus, 161, 427 Life cycle, 266, 410, 427 Life Expectancy, 38, 427 Ligament, 427, 452 Ligands, 67, 68, 106, 228, 232, 386, 423, 427 Likelihood Functions, 427, 457 Linear Models, 427, 457 Linkage, 23, 30, 40, 76, 77, 80, 83, 88, 90, 96, 101, 412, 428, 445 Linkage Disequilibrium, 76, 80, 83, 96, 101, 428 Linoleic Acids, 45, 428 Lipid, 31, 63, 95, 104, 183, 296, 378, 385, 413, 423, 428, 435, 442, 472 Lipid A, 63, 428 Lipid Peroxidation, 104, 428, 442
Index 489
Lipomatosis, 121, 428 Lipophilic, 106, 256, 428 Lipopolysaccharide, 240, 265, 414, 428 Lipoprotein, 414, 428 Lipoxygenase, 41, 52, 183, 215, 319, 377, 427, 428 Lipoxygenase Inhibitors, 41, 428 Liver scan, 428, 461 Liver Transplantation, 43, 288, 428 Lobe, 417, 428 Local therapy, 226, 307, 428 Localization, 83, 233, 262, 421, 428 Locomotion, 428, 448 Logistic Models, 428, 457 Longitudinal study, 153, 429 Loop, 225, 250, 420, 429 Lower Esophageal Sphincter, 411, 429 Luciferase, 83, 98, 429 Lumbar, 7, 429 Lumen, 81, 86, 222, 237, 404, 429 Lupus, 223, 266, 429, 469 Lymph, 118, 389, 404, 417, 429, 454, 461, 467 Lymph node, 429, 454, 461 Lymphatic, 147, 404, 422, 429, 432, 464, 465, 470 Lymphatic system, 429, 464, 465, 470 Lymphoblasts, 369, 429 Lymphocyte, 41, 68, 69, 91, 97, 100, 102, 111, 115, 220, 227, 249, 376, 424, 429, 430, 431 Lymphocyte Subsets, 69, 227, 429 Lymphocyte Transformation, 100, 429 Lymphocytic, 270, 430 Lymphoid, 92, 114, 293, 303, 376, 427, 430 Lymphokines, 260, 430 Lymphoma, 9, 22, 24, 237, 270, 293, 303, 337, 430 Lysine, 418, 430, 451 Lytic, 430, 462 M Macrophage, 4, 87, 111, 233, 262, 265, 392, 414, 423, 430 Macrophage Colony-Stimulating Factor, 392, 430 Macula, 430 Macula Lutea, 430 Macular Degeneration, 236, 430 Magnetic Resonance Imaging, 430, 461 Maintenance therapy, 16, 19, 35, 41, 56, 57, 130, 285, 286, 302, 305, 307, 430
Major Histocompatibility Complex, 23, 415, 430 Malabsorption, 25, 192, 276, 278, 337, 347, 348, 386, 430, 463 Malabsorption syndrome, 430, 463 Malaise, 59, 241, 430 Malformation, 11, 415, 430 Malignancy, 9, 11, 45, 48, 59, 92, 430 Malignant, 51, 84, 293, 337, 370, 377, 378, 408, 412, 420, 430, 435, 437, 461 Malignant tumor, 430, 435 Malnutrition, 4, 17, 45, 290, 291, 347, 372, 379, 384, 430, 435 Mania, 257, 431 Manic, 382, 431, 454 Manic-depressive psychosis, 431, 454 Manifest, 57, 431 Mastocyte, 240, 431 Mastocytosis, 240, 241, 431 Matrilysin, 158, 431 Matrix metalloproteinase, 148, 158, 235, 241, 431 Measles Virus, 7, 431 Meat, 221, 383, 431 Medial, 378, 431, 440, 465 Mediate, 75, 84, 87, 107, 111, 241, 386, 401, 431 Mediator, 63, 67, 94, 95, 109, 115, 183, 225, 249, 265, 424, 431, 449, 462 Medical Records, 21, 204, 431, 459 Medicament, 264, 431, 468 MEDLINE, 333, 336, 338, 431 Medroxyprogesterone, 220, 431 Medroxyprogesterone Acetate, 220, 431 Megacolon, 36, 41, 48, 143, 268, 284, 302, 306, 431 Megakaryocytes, 423, 431 Megaloblastic, 409, 431 Melanin, 431, 447, 473 Melanocytes, 431, 432 Melanoma, 337, 432 Memory, 214, 375, 398, 432 Meninges, 387, 396, 402, 432 Meningitis, 217, 228, 248, 432, 447 Menopause, 346, 432, 450 Menstrual Cycle, 60, 432, 451 Menstruation, 60, 346, 397, 432, 451 Mental Disorders, 210, 256, 257, 432, 447, 453, 454 Mental Health, iv, 60, 210, 332, 335, 432, 454 Mental Processes, 400, 432, 453, 454
490 Ulcerative Colitis
Mentors, 69, 97, 432 Mercaptopurine, 5, 8, 10, 42, 48, 57, 59, 278, 295, 303, 306, 325, 432 Mercury, 15, 33, 44, 409, 432 Mesenchymal, 109, 405, 414, 430, 432 Mesenteric, 130, 432 Mesentery, 432, 446 Meta-Analysis, 90, 432 Metabolic disorder, 414, 432 Metabolite, 58, 59, 81, 238, 240, 382, 433, 451 Metalloendopeptidases, 403, 433 Metastasis, 220, 228, 236, 248, 386, 431, 433 Metastatic, 216, 282, 433, 461 Methionine, 44, 433, 467 Methyltransferase, 159, 433 Metronidazole, 10, 16, 35, 46, 288, 325, 433 MI, 87, 179, 229, 288, 367, 433 Mice Minute Virus, 433, 444 Microbe, 117, 433, 471 Microbiological, 66, 99, 276, 433 Microbiology, 54, 65, 76, 84, 99, 100, 108, 370, 379, 433 Microfilaments, 370, 433 Microorganism, 243, 391, 433, 444, 475 Micro-organism, 237, 433 Microscopy, 81, 93, 252, 380, 433 Microspheres, 70, 433 Migration, 29, 67, 93, 107, 111, 217, 228, 244, 248, 433 Milligram, 303, 433 Milliliter, 383, 433 Mineralocorticoids, 371, 396, 433 Minority Groups, 16, 434 Miscarriage, 348, 434 Mitochondria, 240, 434, 436, 441 Mitochondrial Swelling, 434, 437 Mitosis, 377, 434 Modeling, 73, 78, 82, 434 Modification, 41, 412, 434, 455 Molecular mass, 225, 250, 434 Monitor, 28, 92, 204, 305, 350, 353, 434, 439 Monoclonal, 3, 22, 29, 68, 70, 73, 207, 264, 420, 421, 434, 455 Monoclonal antibodies, 3, 22, 68, 70, 73, 264, 420, 421, 434 Monocyte, 67, 88, 108, 111, 133, 139, 240, 430, 434 Monokines, 260, 434 Mononuclear, 109, 146, 167, 408, 415, 430, 434, 472 Monosomy, 375, 434
Monotherapy, 5, 19, 434 Morbillivirus, 431, 435 Morphological, 11, 93, 184, 403, 431, 435 Morphology, 68, 134, 218, 249, 386, 435 Motility, 71, 73, 108, 179, 286, 421, 435, 462 Motion Sickness, 435, 437 Mucins, 404, 413, 435 Mucocutaneous, 35, 435 Mucosal Lining, 21, 56, 435 Mucositis, 219, 260, 435 Mucus, 435, 473 Multicenter study, 161, 435 Multiple Myeloma, 228, 248, 435 Multiple Organ Failure, 217, 238, 244, 435 Multiple sclerosis, 27, 101, 204, 214, 219, 223, 228, 235, 236, 248, 249, 261, 266, 435, 440 Muscarinic Agonists, 257, 435 Muscle Fibers, 435, 472 Muscular Atrophy, 337, 435 Muscular Dystrophies, 402, 435 Mutagenesis, 95, 98, 101, 102, 107, 109, 435 Mutagenic, 72, 83, 372, 436 Mutagens, 410, 435, 436 Mutate, 87, 436 Myalgia, 241, 436 Mycobacterium, 99, 118, 221, 292, 436, 443, 472 Mydriatic, 400, 436 Myelin, 398, 435, 436 Myelodysplastic syndrome, 101, 436, 464 Myeloid Cells, 252, 436 Myeloma, 417, 436 Myenteric, 125, 436 Myocardial infarction, 219, 234, 261, 381, 395, 433, 436 Myocardial Ischemia, 238, 436 Myocardial Reperfusion, 436, 458 Myocardial Reperfusion Injury, 436, 458 Myocarditis, 228, 248, 436 Myocardium, 433, 436 Myopia, 236, 437, 457, 459 Myositis, 151, 294, 437 Myotonic Dystrophy, 337, 437 N Nasogastric, 280, 404, 437 Natural killer cells, 424, 437 Nausea, 29, 39, 59, 231, 253, 290, 350, 366, 382, 401, 410, 421, 437, 443, 453, 473 NCI, 1, 77, 209, 331, 389, 437 Nearsightedness, 437
Index 491
Necrosis, 4, 41, 49, 233, 241, 246, 247, 262, 377, 395, 408, 412, 422, 433, 436, 437, 458, 460 Necrotizing Enterocolitis, 213, 219, 260, 437 Need, 3, 21, 25, 34, 36, 40, 41, 43, 44, 45, 50, 58, 65, 87, 97, 99, 100, 104, 106, 112, 214, 222, 230, 232, 242, 257, 259, 267, 272, 275, 276, 279, 281, 293, 294, 303, 310, 311, 312, 319, 320, 326, 334, 345, 347, 349, 352, 355, 358, 371, 389, 413, 431, 437, 451, 470 Neonatal, 94, 437 Neoplasia, 4, 6, 52, 102, 113, 127, 148, 152, 160, 217, 287, 337, 437 Neoplasm, 365, 415, 437, 461, 472 Neoplastic, 11, 46, 59, 75, 85, 102, 113, 122, 184, 375, 418, 430, 437 Nephritis, 115, 228, 229, 238, 248, 437 Nephropathy, 148, 426, 437 Nephrosis, 437 Nephrotic, 142, 168, 181, 437 Nephrotic Syndrome, 142, 168, 181, 437 Nerve, 371, 375, 379, 398, 431, 435, 437, 438, 440, 441, 443, 450, 453, 461, 466, 471 Nervous System, 81, 234, 235, 257, 337, 369, 371, 374, 381, 384, 387, 390, 410, 412, 413, 427, 431, 435, 437, 438, 440, 445, 462, 468, 469 Networks, 18, 216, 420, 438 Neural, 371, 374, 417, 420, 438, 459 Neuritis, 438, 441 Neurogenic, 24, 438 Neurologic, 413, 418, 438 Neuromuscular, 369, 438, 473 Neuromuscular Junction, 369, 438 Neuronal, 101, 110, 239, 253, 438 Neurons, 95, 110, 390, 398, 410, 438, 468 Neuropeptide, 106, 438 Neuroretinitis, 438, 459 Neurotoxic, 95, 438 Neurotransmitters, 438 Neutrons, 373, 438, 455 Neutropenia, 438, 449 Neutrophil, 63, 67, 86, 97, 142, 149, 212, 258, 438 Neutrophil Infiltration, 212, 438 Niacin, 5, 438, 472 Nicotine, 8, 9, 39, 41, 52, 129, 131, 149, 169, 170, 253, 256, 257, 288, 348, 438, 456 Nitric Oxide, 6, 41, 157, 241, 439
Nitrogen, 215, 258, 372, 373, 375, 396, 398, 407, 413, 434, 439, 442, 472 Nonmalignant, 83, 439 Nonverbal Communication, 439, 454 Nuclear, 25, 61, 81, 94, 98, 106, 175, 251, 380, 393, 403, 407, 412, 437, 439 Nuclei, 78, 110, 373, 393, 403, 412, 430, 434, 438, 439, 440, 453 Nucleic acid, 59, 118, 225, 238, 244, 245, 247, 249, 260, 369, 380, 412, 417, 421, 436, 439, 455 Nucleic Acid Hybridization, 118, 417, 439 Nucleus, 377, 380, 389, 396, 397, 399, 407, 434, 438, 439, 453, 466, 469 Nursing Care, 439, 444 Nutritional Status, 12, 45, 350, 439 Nutritional Support, 10, 224, 268, 289, 411, 439 O Observational study, 147, 439 Occult, 102, 141, 291, 439 Occult Blood, 141, 439 Octreotide, 290, 439 Ocular, 26, 35, 219, 236, 241, 260, 294, 440 Odds Ratio, 11, 440, 458 Odour, 378, 440, 473 Office Visits, 316, 440 Ointments, 401, 440, 443, 464 Omega-3 fatty acid, 63, 179, 440 Oncogene, 337, 412, 440 Oncogenic, 226, 250, 423, 440 Opacity, 385, 399, 440 Open Reading Frames, 87, 440 Ophthalmologist, 294, 440 Opsin, 440, 459 Optic Chiasm, 419, 440 Optic disc, 440, 441 Optic Disk, 399, 430, 440 Optic Nerve, 438, 440, 442, 453, 459, 461 Optic Neuritis, 294, 440 Orbit, 441 Orbital, 151, 294, 440, 441 Organ Transplantation, 10, 228, 248, 441 Organelles, 387, 397, 431, 441 Orthostatic, 440, 441 Osmotic, 372, 434, 441 Ossification, 441, 460 Osteoarthritis, 219, 235, 236, 239, 241, 261, 441 Osteoporosis, 7, 24, 25, 28, 40, 52, 124, 214, 219, 261, 263, 278, 283, 346, 441 Ostomy, 55, 136, 162, 351, 441, 451
492 Ulcerative Colitis
Outpatient, 18, 151, 279, 441 Ovalbumin, 104, 441 Ovarian Cysts, 147, 441 Ovarian Follicle, 395, 441 Ovaries, 407, 441, 463, 473 Ovary, 259, 395, 441, 449 Ovum, 395, 397, 412, 427, 441, 451, 476 Oxidants, 87, 95, 441 Oxidation, 218, 369, 377, 382, 397, 428, 441, 442 Oxidation-Reduction, 382, 441, 442 Oxidative metabolism, 427, 442 Oxidative Stress, 58, 95, 102, 442 P P53 gene, 78, 442 Pachymeningitis, 432, 442 Palliative, 20, 28, 77, 288, 442, 469 Palliative therapy, 77, 288, 442 Palsy, 253, 442 Pancreas, 74, 222, 369, 400, 411, 423, 442, 464, 472 Pancreatic, 72, 74, 222, 238, 337, 410, 411, 442 Pancreatic cancer, 72, 337, 442 Pancreatic Ducts, 222, 442 Pancreatic Insufficiency, 223, 442 Pancreatic Juice, 74, 222, 411, 442 Pancreatitis, 39, 59, 95, 120, 219, 222, 261, 295, 303, 442 Pancytopenia, 10, 123, 443 Paneth Cells, 404, 443 Panic, 253, 420, 443, 462 Panic Disorder, 253, 420, 443, 462 Panniculitis, 289, 443 Par excellence, 77, 443 Paraffin, 74, 443 Paralysis, 443, 465 Parasite, 266, 443, 472 Parasitic, 67, 443 Parathyroid, 443, 460 Parathyroid Glands, 443, 460 Paratuberculosis, 99, 118, 221, 443 Parenteral, 4, 8, 20, 36, 45, 214, 280, 283, 284, 290, 295, 443 Parenteral Nutrition, 4, 8, 20, 36, 45, 214, 283, 284, 290, 295, 443 Paresthesias, 438, 443 Parotid, 443, 461 Paroxysmal, 337, 415, 444 Partial remission, 444, 458 Particle, 112, 412, 444, 464, 471 Parvovirus, 153, 433, 444
Patch, 72, 114, 169, 257, 444, 471 Pathogen, 65, 76, 84, 85, 91, 115, 220, 237, 444 Pathologic, 92, 233, 262, 290, 377, 382, 395, 418, 419, 444, 450, 453 Pathologic Processes, 377, 444 Pathologies, 228, 247, 248, 444 Pathophysiology, 8, 30, 54, 76, 94, 95, 111, 117, 144, 168, 182, 268, 292, 309, 444 Patient Care Management, 12, 270, 444 Patient Compliance, 218, 285, 286, 301, 444 Patient Education, 15, 49, 59, 119, 280, 312, 345, 352, 355, 360, 362, 368, 444 Patient Satisfaction, 136, 346, 444 Patient Selection, 20, 306, 444 Pediatric Gastroenterologist, 79, 94, 301, 444 Pediatrics, 20, 83, 107, 113, 156, 270, 444 Peer Group, 34, 444 Pelvic, 15, 46, 161, 302, 346, 444, 452 Penis, 444, 473 Pepsin, 255, 444, 445 Pepsin A, 255, 445 Peptic, 73, 107, 219, 261, 342, 445, 467 Peptic Ulcer, 107, 219, 261, 342, 445 Peptide Chain Elongation, 390, 445 Peptide Fragments, 220, 445 Peptide Hydrolases, 403, 445 Perception, 51, 120, 178, 279, 393, 399, 445, 461 Percutaneous, 131, 290, 445 Perennial, 84, 445 Perforation, 20, 48, 283, 302, 355, 409, 445, 475 Perfusion, 410, 419, 445, 470 Perianal, 35, 445 Pericardium, 445, 468 Perinatal, 7, 445 Perineal, 289, 445 Perineum, 445 Periodontal disease, 236, 241, 445 Periodontitis, 219, 238, 260, 445 Perioperative, 4, 20, 445 Peripheral blood, 62, 66, 76, 97, 100, 146, 167, 274, 423, 445, 450 Peripheral Nervous System, 398, 442, 445, 464, 467 Peristalsis, 238, 446 Peritoneal, 237, 446 Peritoneal Cavity, 237, 446 Peritoneum, 432, 446 Peritonitis, 193, 446, 475
Index 493
Personality Disorders, 297, 446 Petrolatum, 403, 446 Petroleum, 443, 446 PH, 236, 383, 446 Phagocyte, 95, 430, 441, 446 Phagocytosis, 99, 446 Pharmaceutical Preparations, 387, 406, 411, 446 Pharmaceutical Solutions, 401, 446 Pharmacists, 286, 349, 446 Pharmacodynamic, 64, 446 Pharmacokinetic, 64, 104, 208, 446 Pharmacologic, 35, 43, 95, 185, 375, 379, 446, 470, 471 Pharmacotherapy, 226, 296, 446 Pharyngitis, 219, 260, 447 Pharynx, 411, 447 Phenolphthalein, 403, 447 Phenotype, 69, 70, 81, 87, 109, 137, 447 Phenylalanine, 98, 125, 445, 447, 473 Phosphodiesterase, 214, 234, 447 Phospholipases, 225, 249, 447, 463 Phospholipases A, 225, 250, 447 Phospholipids, 224, 225, 250, 256, 408, 422, 428, 447 Phosphorus, 384, 443, 447 Phosphorylated, 106, 225, 250, 391, 447 Phosphorylation, 107, 447 Photophobia, 294, 447 Photoreceptors, 447 Physical Examination, 15, 56, 203, 204, 277, 300, 447 Physical Therapy, 45, 50, 447 Physician-Patient Relations, 282, 447 Physiologic, 73, 290, 298, 304, 372, 382, 399, 432, 447, 452, 456 Physiology, 73, 98, 411, 447 Phytohemagglutinins, 429, 448 Pigment, 381, 431, 432, 448, 459 Pilot study, 27, 105, 106, 143, 145, 169, 178, 182, 190, 206, 448 Pituitary Gland, 395, 408, 448 Placebos, 162, 448 Placenta, 216, 448, 451 Plana, 448, 463 Plant Diseases, 404, 448 Plants, 225, 250, 372, 385, 389, 390, 397, 413, 435, 448, 449, 450, 460, 471 Plaque, 236, 375, 448 Plasma cells, 376, 435, 436, 448 Plasma Exchange, 135, 448 Plasma protein, 217, 244, 372, 404, 448
Plasmapheresis, 377, 448 Plasmid, 83, 411, 448, 474 Platelet Activating Factor, 41, 95, 448 Platelet Activation, 449, 463 Platelet Aggregation, 238, 240, 374, 439, 449, 470 Platelet Factor 4, 424, 449 Plateletpheresis, 377, 449 Platelets, 377, 381, 439, 443, 448, 449, 470 Platinum, 429, 449 Poisoning, 398, 401, 411, 424, 432, 437, 449 Pollen, 99, 449 Polycystic, 338, 449 Polymerase, 13, 72, 99, 449 Polymerase Chain Reaction, 99, 449 Polymorphism, 76, 81, 137, 449 Polypeptide, 225, 245, 246, 249, 261, 373, 374, 385, 391, 405, 408, 417, 445, 449, 451, 453, 464, 476 Polyposis, 73, 75, 113, 136, 154, 162, 370, 392, 450 Polysaccharide, 199, 254, 376, 387, 450, 453 Polyunsaturated fat, 31, 63, 179, 450, 470 Population Control, 31, 450 Posterior, 294, 374, 379, 389, 401, 405, 441, 442, 450, 461, 465 Postmenopausal, 441, 450 Postoperative, 10, 20, 36, 48, 267, 276, 295, 348, 435, 450 Postoperative Complications, 36, 49, 295, 450 Postsynaptic, 450, 463, 468 Potentiate, 423, 450 Potentiating, 221, 450 Potentiation, 450, 463 Practice Guidelines, 37, 48, 335, 356, 450 Precancerous, 46, 77, 387, 450, 451 Predisposition, 23, 450 Prednisolone, 5, 25, 34, 41, 46, 47, 77, 127, 149, 151, 161, 284, 294, 306, 450 Prednisone, 35, 37, 48, 53, 155, 303, 306, 308, 450 Preeclampsia, 43, 219, 261, 450 Preleukemia, 436, 450, 464 Premalignant, 45, 87, 450, 451 Premenstrual, 60, 451 Prenatal, 7, 403, 451 Probe, 23, 77, 84, 116, 451 Procollagen, 132, 451 Proctocolectomy, 14, 24, 44, 46, 49, 55, 132, 134, 138, 146, 147, 152, 153, 155, 158, 224, 281, 304, 314, 350, 355, 356, 451
494 Ulcerative Colitis
Proctocolectomy, Restorative, 46, 451 Proctocolitis, 242, 451 Proctosigmoiditis, 57, 227, 270, 281, 309, 451 Proctosigmoidoscopy, 39, 48, 203, 451 Prodrug, 5, 77, 451 Progeny, 393, 451 Progesterone, 219, 220, 451, 466 Prognostic factor, 5, 451 Progression, 78, 80, 84, 85, 102, 104, 152, 220, 235, 281, 375, 431, 451 Progressive disease, 232, 451 Proline, 248, 391, 418, 451 Promoter, 61, 75, 98, 109, 159, 451, 456 Prone, 87, 313, 451 Prophylaxis, 10, 26, 212, 238, 452, 459, 474 Proportional, 79, 411, 452 Prospective Studies, 51, 452 Prospective study, 130, 145, 429, 452 Prostaglandin, 152, 238, 240, 452, 470 Prostaglandins A, 94, 225, 250, 421, 452 Prostaglandins D, 452 Prostate, 238, 259, 337, 452, 472, 473 Prostatitis, 161, 452 Protease, 133, 240, 255, 258, 392, 452 Protein C, 69, 372, 373, 380, 408, 428, 452, 472 Protein Conformation, 373, 452 Protein S, 59, 246, 247, 260, 274, 338, 382, 390, 406, 412, 417, 453, 460, 466 Protein Subunits, 246, 247, 453 Proteinuria, 236, 435, 437, 450, 453 Proteoglycans, 234, 380, 407, 453 Proteolytic, 373, 392, 408, 453 Protocol, 39, 113, 117, 203, 448, 453 Protons, 373, 418, 453, 455 Protozoa, 393, 433, 453 Proximal, 26, 33, 38, 218, 222, 224, 233, 262, 401, 453, 462 Pruritic, 402, 427, 453 Pseudotumor Cerebri, 424, 453 Psychiatric, 185, 186, 189, 270, 297, 354, 432, 453, 454 Psychiatry, 181, 453 Psychic, 453, 454, 462 Psychoanalysis, 282, 453 Psychogenic, 177, 282, 454 Psychology, 400, 453, 454 Psychomotor, 398, 454 Psychophysiology, 73, 454 Psychosis, 253, 254, 412, 454 Psychosomatic, 185, 186, 187, 189, 190, 454
Psychotherapy, 27, 177, 188, 273, 282, 454, 456 Psyllium, 196, 454 Puberty, 7, 20, 291, 454 Public Health, 7, 97, 335, 454 Public Policy, 333, 454 Publishing, 16, 35, 42, 45, 48, 49, 56, 57, 116, 310, 454 Pulmonary Emphysema, 234, 258, 454 Pulmonary Fibrosis, 228, 248, 454 Pulmonary hypertension, 395, 454 Pulmonary Sarcoidosis, 121, 454 Pulse, 128, 434, 455 Pupil, 395, 400, 436, 441, 455 Purifying, 264, 399, 455 Purines, 44, 380, 455, 462 Purpura, 40, 127, 135, 455 Purulent, 369, 455 Pyelonephritis, 67, 115, 455 Pyoderma, 153, 170, 186, 253, 289, 455 Pyoderma Gangrenosum, 170, 253, 289, 455 Pyrazinamide, 221, 455 Q Quiescent, 24, 81, 455 Quinoxaline, 229, 455 R Race, 38, 39, 433, 455 Radiation, 24, 237, 270, 370, 405, 409, 418, 433, 455, 461, 464, 476 Radiation therapy, 370, 418, 455 Radioactive, 383, 418, 421, 428, 434, 439, 440, 455, 461 Radiography, 7, 270, 283, 295, 299, 343, 367, 455 Radiological, 28, 44, 268, 283, 343, 445, 455 Radiology, 41, 130, 154, 343, 455, 456 Radius, 7, 456 Random Allocation, 456 Randomization, 26, 456 Randomized Controlled Trials, 306, 456 Reactive Oxygen Species, 6, 220, 456 Reagent, 399, 429, 456 Reality Testing, 454, 456 Reassurance, 28, 313, 456 Receptor, 4, 6, 22, 30, 47, 58, 67, 69, 70, 83, 87, 88, 91, 95, 97, 103, 104, 106, 107, 108, 110, 117, 118, 133, 137, 138, 143, 156, 207, 217, 225, 229, 232, 238, 240, 244, 250, 253, 259, 265, 370, 376, 393, 401, 430, 456, 462, 463 Receptors, Muscarinic, 435, 456
Index 495
Receptors, Serotonin, 456, 462 Recombinant, 22, 81, 104, 219, 259, 260, 265, 456, 474 Recombinant Fusion Proteins, 104, 456 Recombination, 393, 411, 412, 457 Rectovaginal Fistula, 295, 457 Recurrence, 10, 24, 26, 120, 267, 276, 321, 346, 348, 382, 389, 431, 457 Red blood cells, 290, 406, 416, 457, 460, 464 Red Nucleus, 379, 457 Refer, 1, 299, 384, 392, 401, 410, 428, 430, 438, 454, 457 Reflective, 222, 457 Reflux, 406, 411, 457, 467 Refraction, 437, 457, 465 Refractive Power, 437, 457 Regeneration, 97, 408, 457 Regimen, 12, 37, 48, 402, 444, 446, 457 Regional enteritis, 15, 242, 243, 272, 313, 457 Regression Analysis, 9, 31, 457 Regurgitation, 411, 416, 457 Relative risk, 4, 21, 22, 90, 457 Remission Induction, 308, 458 Remission induction therapy, 308, 458 Renal failure, 398, 458 Renal Osteodystrophy, 263, 458 Reperfusion, 63, 217, 219, 229, 235, 240, 261, 436, 458 Reperfusion Injury, 63, 217, 219, 229, 235, 261, 458 Resected, 40, 71, 293, 458 Resection, 5, 10, 12, 21, 40, 48, 74, 213, 276, 288, 295, 309, 350, 458, 463 Respiration, 385, 408, 434, 442, 458 Respiratory Burst, 225, 250, 458 Respiratory distress syndrome, 229, 234, 458 Response rate, 27, 36, 276, 458 Restitution, 92, 107, 458 Restoration, 436, 447, 458, 476 Retina, 388, 389, 399, 427, 430, 437, 438, 440, 454, 458, 459, 460, 463, 473, 475 Retinal, 240, 294, 393, 399, 440, 459, 475 Retinal Detachment, 240, 399, 459 Retinitis, 219, 228, 248, 260, 294, 459 Retinoblastoma, 337, 459 Retinoids, 459, 475 Retinol, 167, 459 Retinopathy, 236, 399, 459 Retrobulbar, 441, 459
Retrospective, 5, 9, 12, 22, 38, 60, 126, 168, 459 Retrospective study, 38, 60, 459 Retrovirus, 412, 459 Reversion, 459, 472 Rheumatic Diseases, 146, 217, 459 Rheumatism, 419, 459 Rhinitis, 219, 228, 248, 261, 460 Ribose, 370, 460 Ribosome, 460, 471 Rickets, 263, 460, 475 Rigidity, 448, 460 Risk patient, 52, 460 Rod, 380, 390, 404, 460 Rosiglitazone, 106, 121, 201, 460 S Saccharomyces, 120, 134, 176, 242, 255, 300, 460, 476 Saccharomyces cerevisiae, 134, 242, 300, 460, 476 Saccharomycetales, 460 Salicylate, 460 Salicylic, 37, 460 Salicylic Acids, 460 Saline, 254, 448, 460 Salivary, 397, 400, 442, 460, 467 Salivary glands, 397, 400, 460 Saponins, 460, 466 Sarcoidosis, 99, 266, 289, 460 Sarcoma, 409, 412, 461 Scans, 89, 90, 461 Schematic, 277, 461 Schizoid, 461, 475 Schizophrenia, 253, 254, 257, 461, 475 Schizotypal Personality Disorder, 399, 461, 475 Sclera, 389, 394, 405, 461, 473 Scleritis, 294, 461 Scleroderma, 378, 408, 461 Sclerosis, 249, 253, 254, 337, 378, 391, 435, 461 Screening, 21, 34, 52, 74, 82, 83, 92, 96, 101, 112, 141, 203, 245, 282, 390, 461 Secondary tumor, 433, 461 Secretory, 73, 223, 225, 250, 462, 468 Sedative, 203, 380, 420, 462 Sedatives, Barbiturate, 462 Seizures, 376, 398, 413, 444, 462 Semen, 452, 462 Semicircular canal, 422, 462 Seminal vesicles, 462, 473 Semisynthetic, 390, 421, 462
496 Ulcerative Colitis
Senile, 253, 254, 257, 441, 462 Senna, 178, 196, 462 Sepsis, 46, 214, 229, 235, 462 Septal, 289, 462 Septic, 217, 228, 229, 235, 241, 244, 248, 378, 462 Sequence Analysis, 93, 462 Sequencing, 90, 129, 449, 462 Serine, 87, 240, 258, 403, 412, 462 Serine Endopeptidases, 403, 462 Serologic, 42, 420, 462 Serotonin, 257, 371, 447, 456, 462, 472 Serotonin Uptake Inhibitors, 257, 462 Serous, 404, 463 Serrata, 180, 193, 194, 389, 463 Serrated, 463 Sex Characteristics, 370, 375, 454, 463 Sex Determination, 337, 463 Shock, 100, 217, 229, 234, 235, 240, 241, 244, 265, 375, 404, 418, 463, 472 Short Bowel Syndrome, 213, 214, 277, 463 Sigmoid, 71, 451, 463 Sigmoid Colon, 71, 451, 463 Sigmoidoscope, 451, 463 Sigmoidoscopy, 37, 48, 201, 202, 227, 243, 283, 321, 343, 367, 463 Signal Transduction, 71, 91, 93, 107, 226, 250, 422, 463 Signs and Symptoms, 24, 122, 288, 320, 457, 458, 463, 473 Skeletal, 28, 53, 375, 390, 435, 463, 472 Skeleton, 408, 425, 452, 463, 464 Skin Aging, 236, 464 Skull, 396, 441, 443, 464, 469 Sludge, 290, 464 Smoldering leukemia, 436, 464 Smooth muscle, 373, 374, 379, 384, 394, 417, 435, 464, 467 Soaps, 409, 464 Social Environment, 455, 464 Social Support, 18, 464, 467 Social Work, 286, 464 Sodium, 16, 41, 78, 178, 180, 218, 414, 434, 464 Soft tissue, 383, 408, 409, 463, 464 Solid tumor, 236, 375, 464 Solvent, 381, 406, 413, 441, 446, 464 Somatic, 370, 417, 434, 445, 464 Somatostatin, 439, 464 Sound wave, 457, 464 Soybean Oil, 450, 465 Spasmodic, 369, 465
Spastic, 253, 425, 465 Spasticity, 465 Spatial disorientation, 401, 465 Specialist, 33, 358, 400, 465 Specificity, 22, 62, 69, 73, 89, 112, 225, 249, 371, 377, 384, 403, 451, 465, 470 Spectrum, 16, 44, 57, 62, 68, 72, 78, 103, 242, 272, 308, 313, 390, 465 Sperm, 375, 389, 449, 465 Sphenoid, 443, 465 Sphincters, 304, 408, 465 Spinal cord, 204, 378, 387, 388, 402, 403, 432, 438, 442, 445, 465 Spleen, 265, 374, 397, 417, 429, 461, 465 Spondylitis, 28, 50, 52, 65, 287, 465 Spontaneous Abortion, 38, 43, 465 Sporadic, 11, 75, 78, 87, 121, 137, 156, 269, 285, 459, 465 Sprue, 115, 253, 274, 465 Stabilization, 61, 465 Staging, 7, 12, 461, 465 Standard therapy, 106, 465 Statistically significant, 26, 465 Steel, 390, 466 Stem Cells, 406, 466 Stent, 288, 441, 466 Sterile, 65, 378, 443, 466 Sterility, 396, 422, 466 Steroid, 5, 8, 10, 16, 19, 25, 26, 27, 29, 35, 40, 49, 53, 56, 57, 59, 62, 77, 106, 120, 123, 131, 134, 151, 157, 167, 168, 169, 202, 206, 276, 281, 282, 285, 290, 291, 303, 307, 319, 320, 381, 396, 460, 466 Steroid therapy, 25, 49, 59, 120, 151, 206, 290, 307, 466 Stimulant, 265, 384, 417, 425, 466 Stimulus, 66, 220, 258, 320, 401, 402, 407, 424, 425, 426, 443, 466, 470 Stoma, 40, 313, 441, 466 Stool test, 204, 350, 351, 466 Strand, 83, 449, 466 Streptococcal, 289, 466 Streptococci, 305, 466 Streptococcus, 276, 408, 466 Streptomycin, 221, 466 Stress management, 270, 320, 467 Stricture, 26, 43, 53, 288, 467 Stroke, 210, 228, 229, 248, 253, 332, 467 Stromal, 137, 140, 467 Structure-Activity Relationship, 457, 467 Subacute, 422, 467 Subarachnoid, 415, 447, 467
Index 497
Subclinical, 96, 278, 295, 422, 462, 467 Subcutaneous, 121, 289, 370, 402, 443, 467 Submaxillary, 405, 467 Subspecies, 276, 465, 467 Substance P, 106, 255, 406, 433, 462, 466, 467 Substrate, 91, 225, 250, 405, 428, 467 Sucralfate, 41, 325, 467 Sulfur, 173, 254, 258, 399, 407, 433, 467 Sulfuric acid, 254, 467 Superoxide, 61, 458, 467 Superoxide Dismutase, 61, 467 Support group, 310, 312, 320, 351, 468 Suppositories, 35, 320, 350, 411, 468 Suppression, 29, 47, 64, 71, 91, 95, 108, 157, 228, 248, 303, 347, 396, 468 Suppressive, 77, 238, 468 Suppurative, 24, 468 Surfactant, 222, 468 Symphysis, 452, 468 Symptomatic, 13, 20, 29, 50, 236, 290, 291, 294, 296, 376, 442, 468 Symptomatic treatment, 236, 376, 468 Symptomatology, 297, 468 Synaptic, 438, 462, 463, 468 Synaptic Transmission, 438, 468 Synergistic, 77, 226, 230, 250, 251, 468 Synovial, 236, 468 Synovial Membrane, 468 Synovitis, 241, 468 Systemic disease, 6, 419, 468 Systemic lupus erythematosus, 217, 249, 391, 420, 468 Systolic, 419, 469 T Tachycardia, 57, 469 Tacrolimus, 9, 131, 469 Tardive, 253, 254, 257, 469 Telangiectasia, 337, 469 Temporal, 63, 415, 430, 443, 469 Tendinitis, 44, 469 Tenesmus, 26, 37, 48, 57, 366, 469 Teratogenicity, 46, 469 Thalamic, 379, 469 Thalamic Diseases, 379, 469 Thalidomide, 9, 469 Theophylline, 455, 469 Thermal, 400, 438, 449, 469 Thigh, 408, 469 Third Ventricle, 419, 469 Thorax, 369, 429, 469 Threonine, 462, 469
Threshold, 59, 419, 470 Thrombin, 408, 449, 452, 470 Thrombocytopenia, 59, 449, 470 Thrombomodulin, 452, 470 Thrombosis, 229, 381, 423, 453, 467, 470 Thromboxanes, 378, 402, 470 Thrombus, 395, 422, 436, 449, 470, 474 Thymus, 420, 429, 470 Thyroid, 223, 443, 470, 473 Thyroid Gland, 443, 470 Thyroiditis, 101, 470 Thyroxine, 372, 447, 470 Time Management, 467, 470 Tissue Distribution, 384, 470 Tolerance, 64, 84, 103, 212, 413, 470 Tomography, 393, 470 Tonicity, 402, 470 Tooth Preparation, 370, 470 Topical, 35, 36, 37, 41, 47, 48, 77, 130, 151, 167, 170, 202, 219, 260, 274, 284, 294, 320, 334, 406, 418, 443, 446, 464, 470 Toxaemia, 450, 471 Toxicity, 9, 19, 37, 46, 52, 59, 62, 74, 104, 105, 127, 149, 163, 303, 307, 308, 401, 432, 467, 471 Toxicologic, 104, 471 Toxicology, 7, 104, 334, 471 Toxins, 217, 376, 403, 413, 421, 422, 434, 457, 471, 474 Trace element, 34, 471 Trachea, 383, 384, 447, 470, 471 Traction, 390, 471 Transcription Factors, 61, 75, 106, 471 Transdermal, 39, 52, 129, 131, 170, 471 Transduction, 72, 107, 112, 463, 471 Transfection, 61, 109, 116, 382, 471 Transfer Factor, 420, 471 Transfusion, 218, 284, 407, 471 Transgenes, 112, 471 Translation, 68, 406, 457, 471 Translational, 78, 471 Translocation, 390, 406, 471 Transmitter, 369, 378, 401, 425, 431, 471 Transplantation, 43, 51, 74, 389, 420, 430, 471 Trauma, 217, 244, 369, 398, 406, 437, 442, 472 Treatment Failure, 39, 284, 472 Triad, 240, 472 Trichomoniasis, 433, 472 Tricuspid Atresia, 395, 472 Tricyclic, 371, 420, 472
498 Ulcerative Colitis
Triglyceride, 167, 472 Trisomy, 375, 472 Trophic, 45, 472 Tropomyosin, 259, 264, 301, 472 Troponin, 472 Tryptophan, 391, 462, 472 Tuberculosis, 99, 222, 241, 394, 429, 460, 472 Tuberous Sclerosis, 337, 472 Tumor marker, 369, 472 Tumor Necrosis Factor, 3, 52, 94, 114, 132, 240, 241, 245, 246, 247, 295, 306, 469, 472 Tumor suppressor gene, 102, 442, 472 Tumour, 41, 214, 472 Typhimurium, 93, 240, 472 Tyrosine, 107, 223, 401, 473 U Ulcer, 73, 229, 233, 237, 243, 254, 262, 401, 445, 467, 473 Ulceration, 48, 94, 115, 242, 271, 280, 285, 289, 351, 473 Unconscious, 375, 398, 419, 473 Unsaturated Fats, 409, 473 Uraemia, 442, 473 Ureters, 473 Urethra, 444, 452, 473 Uric, 414, 419, 455, 473 Urinary, 67, 237, 384, 389, 397, 412, 418, 435, 473 Urinary tract, 67, 237, 473 Urine, 7, 180, 204, 283, 382, 392, 394, 401, 405, 416, 453, 473 Urogenital, 28, 237, 412, 473 Urogenital System, 237, 473 Ursodeoxycholic Acid, 86, 473 Urticaria, 126, 128, 219, 240, 261, 375, 473 Uterus, 395, 397, 403, 407, 419, 432, 441, 451, 473, 474 Uvea, 473 Uveitis, 219, 260, 294, 473 V Vaccination, 7, 11, 74, 117, 474 Vaccine, 7, 11, 70, 74, 344, 370, 453, 474 Vacuoles, 403, 441, 474 Vagina, 295, 419, 432, 457, 473, 474 Vaginal, 43, 325, 405, 474 Vascular endothelial growth factor, 30, 474 Vasculitis, 24, 59, 146, 289, 294, 442, 474 Vasoconstriction, 240, 253, 405, 474 Vasodilatation, 240, 425, 474
Vasodilator, 383, 401, 417, 436, 474 VE, 82, 116, 152, 169, 474 Vector, 110, 471, 474 Vein, 203, 424, 439, 444, 474 Venoms, 397, 474 Venous, 166, 218, 381, 416, 453, 472, 474 Venous Thrombosis, 166, 381, 474 Ventricle, 379, 395, 455, 469, 472, 474 Ventricular, 117, 395, 418, 436, 472, 474 Venules, 118, 217, 244, 383, 384, 404, 474 Vertebrae, 465, 474 Vertebral, 287, 448, 474 Vesicular, 379, 474 Vestibule, 390, 422, 462, 474 Veterinarians, 82, 474 Veterinary Medicine, 168, 333, 474 Vibrio, 388, 475 Vibrio cholerae, 388, 475 Villous, 161, 386, 475 Viral, 95, 112, 228, 239, 248, 276, 395, 403, 412, 440, 459, 471, 475 Viral vector, 112, 475 Virulence, 85, 93, 379, 471, 475 Virus, 7, 95, 98, 112, 292, 380, 387, 404, 412, 423, 448, 471, 475 Visceral, 73, 446, 475 Visual Acuity, 394, 461, 475 Vitamin A, 422, 459, 475 Vitamin D, 263, 460, 475 Vitreous Hemorrhage, 399, 475 Vitreous Humor, 459, 475 Vitro, 199, 218, 416, 475 Vivo, 77, 86, 95, 104, 111, 167, 475 Volvulus, 213, 475 W Wakefulness, 398, 475 Windpipe, 384, 447, 470, 475 Withdrawal, 19, 39, 46, 257, 298, 398, 475 Wound Healing, 107, 216, 225, 236, 249, 386, 408, 423, 431, 476 X Xenograft, 375, 476 X-ray, 7, 47, 53, 203, 380, 383, 386, 393, 409, 439, 455, 456, 461, 476 Y Yeasts, 410, 447, 460, 476 Yolk Sac, 408, 476 Z Zygote, 393, 476 Zymogen, 452, 476
Index 499
500 Ulcerative Colitis
