Acute Pancreatitis - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References

ACUTE

PANCREATITIS 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

ii

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., 1960Acute Pancreatitis: 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: 0-497-00022-9 1. Acute Pancreatitis-Popular works. I. Title.

iii

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.

Copyright Notice If a physician wishes to copy limited passages from this book for patient use, this right is automatically granted without written permission from ICON Group International, Inc. (ICON Group). However, all of ICON Group publications have copyrights. With exception to the above, copying our publications in whole or in part, for whatever reason, is a violation of copyright laws and can lead to penalties and fines. Should you want to copy tables, graphs, or other materials, please contact us to request permission (E-mail: [email protected]). ICON Group often grants permission for very limited reproduction of our publications for internal use, press releases, and academic research. Such reproduction requires confirmed permission from ICON Group International, Inc. The disclaimer above must accompany all reproductions, in whole or in part, of this book.

iv

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 acute pancreatitis. 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.

v

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.

vi

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

vii

Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON ACUTE PANCREATITIS .............................................................................. 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Acute Pancreatitis....................................................................... 13 E-Journals: PubMed Central ....................................................................................................... 27 The National Library of Medicine: PubMed ................................................................................ 28 CHAPTER 2. NUTRITION AND ACUTE PANCREATITIS .................................................................... 73 Overview...................................................................................................................................... 73 Finding Nutrition Studies on Acute Pancreatitis ....................................................................... 73 Federal Resources on Nutrition ................................................................................................... 78 Additional Web Resources ........................................................................................................... 79 CHAPTER 3. ALTERNATIVE MEDICINE AND ACUTE PANCREATITIS .............................................. 81 Overview...................................................................................................................................... 81 National Center for Complementary and Alternative Medicine.................................................. 81 Additional Web Resources ........................................................................................................... 86 General References ....................................................................................................................... 87 CHAPTER 4. DISSERTATIONS ON ACUTE PANCREATITIS ................................................................ 89 Overview...................................................................................................................................... 89 Dissertations on Acute Pancreatitis ............................................................................................ 89 Keeping Current .......................................................................................................................... 89 CHAPTER 5. PATENTS ON ACUTE PANCREATITIS ........................................................................... 91 Overview...................................................................................................................................... 91 Patents on Acute Pancreatitis...................................................................................................... 91 Patent Applications on Acute Pancreatitis.................................................................................. 97 Keeping Current ........................................................................................................................ 100 CHAPTER 6. BOOKS ON ACUTE PANCREATITIS ............................................................................ 101 Overview.................................................................................................................................... 101 Book Summaries: Federal Agencies............................................................................................ 101 Chapters on Acute Pancreatitis ................................................................................................. 104 CHAPTER 7. PERIODICALS AND NEWS ON ACUTE PANCREATITIS............................................... 107 Overview.................................................................................................................................... 107 News Services and Press Releases.............................................................................................. 107 Newsletter Articles .................................................................................................................... 109 Academic Periodicals covering Acute Pancreatitis .................................................................... 110 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 113 Overview.................................................................................................................................... 113 NIH Guidelines.......................................................................................................................... 113 NIH Databases........................................................................................................................... 115 Other Commercial Databases..................................................................................................... 117 APPENDIX B. PATIENT RESOURCES ............................................................................................... 119 Overview.................................................................................................................................... 119 Patient Guideline Sources.......................................................................................................... 119 Finding Associations.................................................................................................................. 122 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 125 Overview.................................................................................................................................... 125 Preparation................................................................................................................................. 125 Finding a Local Medical Library................................................................................................ 125 Medical Libraries in the U.S. and Canada ................................................................................. 125 ONLINE GLOSSARIES................................................................................................................ 131

viii Contents

Online Dictionary Directories ................................................................................................... 134 ACUTE PANCREATITIS DICTIONARY ................................................................................. 137 INDEX .............................................................................................................................................. 197

1

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 acute pancreatitis 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 acute pancreatitis, 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 acute pancreatitis, 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 acute pancreatitis. 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 acute pancreatitis, 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 acute pancreatitis. The Editors

1

From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.

3

CHAPTER 1. STUDIES ON ACUTE PANCREATITIS Overview In this chapter, we will show you how to locate peer-reviewed references and studies on acute pancreatitis.

The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and acute pancreatitis, 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 “acute pancreatitis” (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: •

Serial Computed Tomography Is Rarely Necessary in Patients with Acute Pancreatitis: A Prospective Study in 102 Patients Source: Journal of the American College of Surgeons. 193(2): 146-152. August 2001. Contact: Available from Journal of the American College of Surgeons. P.O. Box 2127, Marion, OH 43306-8227. (800) 214-8489 or (740) 382-3322. Fax (740) 382-5866. Summary: Computed tomography (CT) has proved to be helpful in patients with acute pancreatitis for differentiating between mild and severe forms. Follow up of acute pancreatitis with CT has been advocated but rarely studied. This article reports on a study undertaken to determine if late CT performed at day 7 might be helpful in establishing the prognosis or the type of complications, and to select a subgroup of

4

Acute Pancreatitis

patients with pancreatitis in whom CT could be beneficial. Contrast enhanced CT was performed at the admission day and 7 days after admission in 102 patients admitted for acute pancreatitis. The extent of pancreatic inflammation was classified according to Balthazar grade, and intrapancreatic necrosis (tissue death) on these examinations was prospectively assessed and compared with clinical and biologic data and with patient outcomes. Among 102 patients, complications developed in 24 (23 percent). Complications developed in only 8 percent of patients with Ranson score less than 2, making routine early CT unnecessary. For the patients with Ranson score less than 2 and Balthazar grades A and B at day 1 CT, late CT seemed to be useless. Complication was suspected by clinical and biologic tests before day 7 in 22 of 24 complicated patients (94 percent), suggesting that CT could be proposed only in cases of clinical or biologic deterioration. Late CT was correlated with a complicated course in patients with Balthazar grades D and E or intrapancreatic necrosis greater than 50 percent. Late CT was predictive of complications in cases of intrapancreatic necrosis enlarging since the first examination. The authors conclude that in cases of acute pancreatitis, there is little justification for systematic early CT, especially in patients with Ranson score less than 2, and late CT does not need to be performed routinely, but only in cases of clinical or biologic worsening. 2 figures. 4 tables. 26 references. •

Managing Acute Pancreatitis: New ACG Recommendations Source: Journal of Critical Illness. 12(8): 508-510, 511. August 1997. Summary: In early 1997, the American College of Gastroenterology (ACG) issued guidelines for the diagnosis and treatment of acute pancreatitis. The guidelines included the clinical terminology for acute pancreatitis and its complications, the appropriate criteria for determining the severity of the disorder, and the indications for medical and surgical treatment. This article provides summaries of these guidelines and includes recommendations for practical patient care. Topics include diagnostic guidelines, symptoms, laboratory findings, severity criteria, supportive care, and additional interventions. The goals of medical therapy for acute pancreatitis are to provide supportive care and to prevent systemic complications, pancreatic necrosis, and pancreatic infection. In a patient with mild pancreatitis, supportive care and monitoring for complications often are all that is required. However, when severe pancreatitis is present, ICU admission is indicated for the management of systemic complications, and additional diagnostic tests are needed to rule out pancreatic necrosis. A detailed patient care algorithm is provided. 1 figure. 1 table. 1 reference. (AA-M).

•

Acute Pancreatitis: Diagnosis and Management Source: American Family Physician. 52(2): 435-443. August 1995. Summary: In this article, the authors outline the steps in the diagnosis and management of acute pancreatitis, a clinical syndrome characterized by midepigastric pain, nausea, and vomiting. Topics include definitions; etiology; medications associated with acute pancreatitis; pathophysiology; clinical presentation; laboratory tests; diagnostic tests, including serum amylase level, lipase, abdominal radiographs, ultrasonography, and computed tomography; prognostic criteria for acute pancreatitis; treatment; and the role of surgery. The authors note that, once a diagnosis of pancreatitis is confirmed, supportive therapy with intravenous hydration and close observation is effective in the majority of patients. Lack of improvement may indicate the need to search for a local complication such as pseudocyst or abscess. They stress that evidence of the systemic complications of pancreatitis mandates intensive care monitoring. 4 figures. 4 tables. 41 references. (AA-M).

Studies

•

5

Acute Pancreatitis in Peritoneal Dialysis and Haemodialysis: Risk, Clinical Course, Outcome, and Possible Aetiology Source: Gut. 46(3): 385-389. March 2000. Contact: Available from BMJ Publishing Group. P.O. Box 590A, Kennebunkport, ME 04046. (800) 236-6265. Summary: It has been suggested that the incidence of acute pancreatitis (pancreas infection) in patients with end stage renal disease (ESRD, kidney failure) is increased. This article reports on a study undertaken to assess the risk of acute pancreatitis in patients on long term peritoneal dialysis (PD) and long term hemodialysis (HD) compared with the general population, to evaluate its clinical course and outcome, and to identify possible etiological factors. All patients from a large general hospital in The Netherlands who were maintained on long term PD or HD (total dialysis time more than six weeks) from January 1989 to March 1998 were included. In 269 patients on HD (total of 614 person years), one patient developed an attack of acute pancreatitis. Patients on hemodialysis did not show an increased risk for acute pancreatitis compared with the general population. In 128 patients on PD (total of 241 person years), seven patients had nine attacks of acute pancreatitis. Patients on PD had a significantly and highly increased risk for acute pancreatitis. Mortality in this series of nine attacks was 11 percent. No single etiological risk factor could be identified. The authors conclude that the risk of acute pancreatitis in patients on long term PD is significantly and highly increased compared with the general population. 3 tables. 22 references.

•

Acute Pancreatitis: Systemic Complications and Prognostic Assessment Source: Practical Gastroenterology. 15(8): 22, 27-30, 32. Summary: Once a diagnosis of acute pancreatitis (AP) has been made, its severity may range from mild, with abdominal pain, nausea and vomiting, to severe, with multisystem involvement. This article reviews the systemic complications and prognostic assessment of acute pancreatitis. The authors note that the management of AP has paralleled the understanding of the effects of the pancreatic gland's capacity to release hormones, enzymes, and peptides and their clinical manifestations. Advances in critical care permit survival of patients with severe fulminating pancreatitis. Death is primarily due to multisystem failure early on, or sepsis later, as secondary infection sets in. The authors discuss system complications (cardiac, renal, respiratory, and metabolic), infrequent system complications, measuring the severity of AP, peritoneal lavage, computed tomography, and the value of prognostic assessment. 5 tables. 27 references. (AA-M).

•

Recurrent Acute Pancreatitis: An Algorithmic Approach to Identification and Elimination of Inciting Factors Source: Gastroenterology. 120(3): 708-717. 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: Recurrent acute pancreatitis represents a challenging clinical problem associated with significant morbidity, impairment in quality of life, and expense. The evaluation of patients with recurrent acute pancreatitis requires systematic identification or elimination of correctable inciting factors. This article provides a comprehensive yet concise overview of the causes of recurrent acute pancreatitis; a detailed review of data relevant to implicated medications, the controversial issues of

6

Acute Pancreatitis

pancreas divisum and sphincter of Oddi dysfunction, and the role of genetic testing; a guideline for the evaluation of patients during the initial episode of acute pancreatitis; and a consensus algorithm within which putative inciting factors may be identified and eliminated. The guidelines offered pertain only to patients with recurrent acute pancreatitis in the absence of obvious evidence of chronic pancreatitis. Future advances in the treatment of these patients will almost certainly depend on improved imaging modalities, prospective clinical trials assessing the efficacy of endoscopic and surgical intervention, a better understanding of mutations and pathophysiologic mechanisms responsible for recurrent acute pancreatitis, and the development of novel, effective preventive and therapeutic strategies. 2 figures. 6 tables. 96 references. •

Acute Pancreatitis After Abdominal Vascular Surgery Source: Journal of the American College of Surgeons. 191(4): 373-380. October 2000. Contact: Available from Journal of the American College of Surgeons. P.O. Box 2127, Marion, OH 43306-8227. (800) 214-8489 or (740) 382-3322. Fax (740) 382-5866. Summary: Retroperitoneal dissection and ischemia (lack of blood to a body part) have been proposed as risk factors for postoperative pancreatitis. This study was undertaken to determine the incidence and outcomes of pancreatitis after abdominal vascular surgery. The authors collected data on 21 patients who developed pancreatitis after abdominal vascular operations; 21 controls undergoing identical operations were also randomly identified from the authors' operative log. The incidence of pancreatitis among all patients undergoing abdominal vascular operations during the 6 year study period was 1.8 percent. Pancreatitis was diagnosed a mean of 9.8 days (plus or minus 8 days) after operation and was associated with 3 or less Ranson signs in all 21 study subjects. Although there was a trend towards longer hospitalization in the subjects, there was no difference in complication rates between the two groups. Sixteen subjects (76 percent) had no complications. Three developed severe complications, two of whom died of causes unrelated to pancreatitis. One developed a pseudocyst that resolved spontaneously. Cholelithiasis (gallstones) was a causative factor in two subjects; no cause was established in the remaining 19. There was no difference in operative details between the two groups. The authors conclude that pancreatitis is a rare and self limited complication of abdominal vascular surgery. Pancreatitis is costly and inconvenient but rarely serious after abdominal vascular operations. 3 tables. 26 references.

•

Pancreatic and Biliary Disease: Laboratory Diagnostic Tests in Acute Pancreatitis Source: Journal of Clinical Gastroenterology. 34(4): 459-462. 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 diagnosis of acute pancreatitis (inflammation of the pancreas) depends on a combination of clinical assessment and laboratory testing. This article reviews the laboratory diagnostic tests in acute pancreatitis. Although the serum amylase is the cornerstone laboratory test used in establishing the diagnosis of acute pancreatitis, there are limitations in the sensitivity and specificity that may be important for the clinician to recognize. The serum lipase level may be especially useful in patients with alcoholinduced acute pancreatitis. A new urinary test strip that uses trypsinogen-2 may have a role in establishing the diagnosis of acute pancreatitis. In addition, several new laboratory tests and new interpretations of old laboratory tests may assist in establishing the etiology (cause) and severity of acute pancreatitis. The authors summarize important aspects of standard laboratory tests and new laboratory approaches in

Studies

7

establishing the diagnosis, etiology, and severity of acute pancreatitis. 1 table. 36 references. •

Evaluation of Factors That Have Reduced Mortality from Acute Pancreatitis Over the Past 20 Years Source: Journal of Clinical Gastroenterology. 35(1): 50-60. July 2002. Contact: Available from Lippincott Williams and Wilkins, Inc. 12107 Insurance Way, Hagerstown, MD 21740. (800) 638-3030 or (301) 714-2300. Summary: The mortality (death) associated with acute pancreatitis varies markedly in different studies, with most frequently reported mortality rates of 10 to 15 percent for all cases and 15 to 90 percent for attacks regarded as 'severe.' This article reports on a study undertaken to investigate whether there has been a reduction in mortality associated with acute pancreatitis over the past 20 years and the reasons for this reduction. The study featured the authors' 20 year prospective assessment of mortality as it relates to the severity of the disease, complications, and current therapy. The results showed that the initial reduction in mortality related to acute pancreatitis coincided with the recognition and application of the signs of severity. These signs dictated admission to intensive care unit (ICU) therapy, the intensity of ICU monitoring, and the importance of organ specific emergency therapy. Further mortality reduction in the 1990s could be attributed to either a more select study sample or earlier and more selective endoscopic or surgical debridement of infected tissue, endoscopic cyst drainage, and angiographic control of gastrointestinal bleeding. Improved nutritional support by jejunal feeding, earlier use of antibiotic therapy, gut sterilization, early endoscopic retrograde cholangiopancreatography (ERCP) for common bile duct stones, and necrosectomy (removal of dead tissue) for noninfected necrosis have reduced the overall mortality associated with acute pancreatitis to a mean of 5 percent for all cases and 20 percent for severe cases. 1 figure. 7 tables. 44 references.

•

Clinical Highlights: Medical Treatment of Acute Pancreatitis Source: Hospital Medicine. 28(1): 63. January 1992. Summary: This article consists of a chart that summarizes the medical treatment of acute pancreatitis. Grouped into supportive and specific nonoperative techniques, the chart covers intravascular volume, indications for pain relief and nutrition, nasogastric suction, percutaneous peritoneal lavage, and the use of antibiotics. 1 figure.

•

Acute Pancreatitis in the Elderly Source: Practical Gastroenterology. 19(1): 10-12, 14-16, 21-22. January 1995. 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 focuses on acute pancreatitis (AP) in the elderly. The authors note that the initial considerations in managing patients with acute pancreatitis are etiology and severity of the underlying inflammatory process. Drugs and biliary causes are the primary etiologies among elderly patients. Topics include the clinical presentation of AP in the elderly; etiological considerations; prognostic indicators, including single biochemical factors and multiple prognostic criteria; peritoneal lavage; computed tomography; therapy; development of systemic complications; pancreatic necrosis; and biliary pancreatitis. The authors conclude that laparoscopic cholecystectomy with intraoperative cholangiography and common bile duct

8

Acute Pancreatitis

exploration is the treatment of choice in the presence of cholelithiasis; preoperative endoscopic retrograde cholangiopancreatography (ECRP) reserved for severe cases. 5 tables. (AA-M). •

Acute Pancreatitis: Which Route Is Better for Nutritional Support? Source: Journal of Critical Illness. 15(1): 10-11. January 2000. Contact: Available from Cliggott Publishing Company. 55 Holly Hill Lane, Greenwich, CT 06831-0010. (203) 661-0600. Summary: This article is an entry from a regular column in which physicians answer specific clinical problems. In this column, the question concerned the nutritional management of patients with acute pancreatitis and the preferred method of nutritional support (enteral or parenteral route). The author answers by noting that the optimal route and timing of nutritional support in patients with acute pancreatitis is controversial. Deciding when to start nutritional support depends on the patient's nutritional history and severity of pancreatitis. If a patient has adequate nutritional reserve and has mild or moderate pancreatitis, it is appropriate to wait 7 to 10 days before starting either enteral or parenteral nutrition and to give intravenous fluids only. There is insufficient evidence that shows nutrition alone positively affects the outcome of acute pancreatitis. Nutritional support simply supplies fluid, macronutrients (proteins, carbohydrates, and fats) and micronutrients (electrolytes, trace elements, and vitamins) while the patient takes nothing by mouth to minimize pancreatic stimulation. After 7 to 10 days without nutrition, negative nitrogen balance occurs, increasing a patient's risk of infection. At this point, nutritional support should be started if the patient is unable to take adequate oral nutrition. The author briefly summarizes two studies that support enteral over parenteral nutrition in the management of acute pancreatitis. The author cautions that in clinical practice, however, the choice is not always that easy. Patients frequently refuse nasal tubes and often do not tolerate the feedings. The author stresses that each case needs an individualized approach and that enteral nutrition should be used whenever possible. 5 references.

•

Octreotide Treatment in Patients with Severe Acute Pancreatitis Source: Digestive Dieseases and Sciences. 45(11): 2247-2251. November 2000. Contact: Available from Kluwer Academic/Plenum Publishers. 233 Spring Street, New York, NY 10013-1578. (212) 620-8000. Fax (212) 807-1047. Summary: This article reports on a study that investigated the effect of octreotide (Sandostatin) in the treatment of severe acute pancreatitis in a case control study. Experimental and clinical studies on the effect of octreotide in the treatment of acute pancreatitis have shown controversial results. The authors report on their prospective randomized study (begun in 1992) on the effect of octreotide in severe acute pancreatitis, undertaken in three hospitals in Israel. Patients were randomly assigned to conservative treatment either with or without octreotide (0.1 mg subcutaneously three times a day). Of 50 patients, 25 were assigned to octreotide (treatment group) and 25 to conservative treatment only (control group). The two groups were matched with regard to age, sex, etiology, and severity of the disease. The complication rate was lower in the treatment group with regard to sepsis and adult respiratory distress syndrome (ARDS). These decreases could be explained by the immunomodulatory effects of octreotide. The hospital stay was shorter in the treatment group. Two patients died in the treatment group and eight in the control group. These results suggest that octreotide may have a beneficial effect in the treatment of severe acute pancreatitis. 4 tables. 36 references.

Studies

•

9

Acute Pancreatitis in Chronic Renal Failure Source: American Journal of Gastroenterology. 91(12): 2477-2482. December 1996. Summary: This article reports on a study to estimate the frequency and severity of acute pancreatitis (AP) associated with chronic renal failure (CRF) and to find out whether CRF causes AP. The authors studied 532 patients with a first episode of AP during the period of 1982 to 1994. Twenty-one patients had CRF; 511 patients without CRF served as controls. AP was diagnosed clinically and by elevation of amylase and lipase. CT or sonographic confirmation of diagnosis was made in all CRF patients. The cause of AP in the non-CRF group was significantly different from that seen in the CRF group. Incidence of severe AP in the two groups was 47.6 percent in the CRF group versus 21 percent in the non-CRF group. By simplified prognostic criteria, it was 38 versus 10.3 percent, respectively. Overall, CRF patients had more complications compared with non-CRF. CRF patients with severe AP had high mortality when stratified by either Ranson's or simplified prognostic criteria. The authors conclude that AP in CRF is frequently of unknown cause, suggesting the role of either CRF or other factors. Irrespective of cause, AP in CRF is a serious disease, associated with a high morbidity and mortality. 1 figure. 3 tables. 38 references. (AA-M).

•

Diagnosis and Management of Acute Pancreatitis Source: American Family Physician. 62(1): 164-174. July 1, 2000. Contact: Available from American Academy of Family Physicians. 11400 Tomahawk Creek Parkway, Leawood, KS 66211-2672. (800) 274-2237. Website: www.aafp.org. Summary: This article reviews the diagnosis and management of acute pancreatitis, which usually occurs as a result of alcohol abuse or bile duct obstruction. A careful review of the patient's history and appropriate laboratory studies can help the physician identify the etiology (cause) of the condition and thus guide management. Serum (blood) amylase and lipase levels are still used to confirm the diagnosis of acute pancreatitis. Although not routinely available, the serum trypsin level is the most accurate laboratory indicator for pancreatitis. Ultrasonography, computed tomography, and endoscopic retrograde cholangiopancreatography (ERCP) are additional modalities that can help the family physician choose the best treatment approach. Prompt identification of patients who need intensive care referral or subspecialty consultation is crucial. The APACHE II and the multiple organ system failure scales provide prognostic information at the time of admission and may be repeated daily to monitor disease progression. Therapies such as nasogastric suctioning, anticholinergics, and histamine H2 receptor blockers have not been shown to decrease symptoms or hospital stays in patients with acute pancreatitis. Systemic antibiotics have been found to improve outcome in patients with severe disease. With supportive care, most patients have a good clinical outcome. 4 figures. 8 tables. 39 references.

•

Etiology and Pathogenesis of Acute Pancreatitis: Current Concepts Source: Journal of Clinical Gastroenterology. 30(4): 343-356. June 2000. Contact: Available from Lippincott Williams and Wilkins, Inc. 12107 Insurance Way, Hagerstown, MD 21740. (800) 638-3030 or (301) 714-2300. Summary: This article reviews the etiology and pathogenesis of acute pancreatitis, a disorder that has numerous causes and an obscure pathogenesis. Bile duct stones and alcohol abuse together account for about 80 percent of acute pancreatitis. Most episodes of biliary pancreatitis are associated with transient impaction of the stone in the ampulla

10

Acute Pancreatitis

(that causes obstruction of the pancreatic duct, with ductal hypertension) or passage of the stone through and into the duodenum. Other causes of acute pancreatitis are various toxins, drugs, other obstructive causes (such as malignancy [cancer] or fibrotic sphincter of Oddi), metabolic abnormalities, trauma, ischemia, infection, and autoimmune diseases. In 10 percent of cases of acute pancreatitis, no underlying cause can be identified; this condition is known as idiopathic acute pancreatitis. Intra acinar activation of trypsinogen plays a central role in the pathogenesis of acute pancreatitis, resulting in subsequent activation of other proteases, causing the subsequent cell damage. Ischemia (fluid) or reperfusion injury is increasingly recognized as a common and important mechanism is the pathogenesis of acute pancreatitis and especially in the progression from mild edematous to severe necrotizing form of the disease. Increased intracellular calcium concentration also mediates acinar cell damage. Oxygen derived free radicals and may cytokines (e.g., interleukin 1, tumor necrosis factor alpha, platelet activating factor) are considered to be principal mediators in the transformation of acute pancreatitis from a local inflammatory process into a multiorgan illness. The damage to pancreatic cells and blood vessels that the different enzymes and inflammatory substances cause can result in tissue hypoxia (lack of oxygen) and further cellular necrosis (cell death), resulting in a vicious circle in which more pancreatic enzymes are released and more pancreatic injury occurs. 4 figures. 2 tables. 155 references. •

Role of Imaging in Acute Pancreatitis Source: European Journal of Gastroenterology and Hepatology. 9(2): 106-116. February 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 reviews the roles of ultrasound, computed tomography, and magnetic resonance imaging (MRI) in the evaluation and management of acute pancreatitis. The author notes that pancreatitis can remain localized to the pancreas and immediate peripancreatic tissues or can affect structures remote from the pancreatic bed. Thus, the imaging techniques chosen need to cover all organs and pathways likely to be affected. The author reviews the importance of imaging in the diagnosis of pancreatic necrosis, acute fluid collections, pancreatic abscess, pseudocysts, and vascular complications. Ultrasound is useful in the detection of gallstones and any associated compromise to the biliary tree; and in the detection of pancreatic and peripancreatic fluid collections. The role of MRI in the imaging of acute pancreatitis remains uncertain, with supporters of the technique suggesting that MRI is complementary to CT with definite advantages in certain situations. Other authors contend that the role of MRI has not been fully evaluated and currently offers no advantage over CT. The use of interventional techniques as opposed to surgical intervention is also discussed. 8 figures. 35 references (32 annotated).

•

Acute Pancreatitis: Principles of Management Source: Practical Gastroenterology. 20(6): 26, 28, 33-36, 38-39. June 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, the fourth in a series on pancreatic disease, presents principles of management for the care of patients with acute pancreatitis. The authors note that the treatment of these patients depends primarily on the etiology and severity of the disease. The goals of therapy are to control the inflammatory process and manage any

Studies

11

complications that arise. The finding of complications such as respiratory impairment, sepsis, and renal failure importantly influences treatment planning. Intravascular volume repletion and maintenance is vital in acute pancreatitis because it prevents further extension of the inflammatory process. A new treatment modality that involves the use of dextran seems to provide additional benefits in this regard. Patients with acute pancreatitis should be kept fasting until the inflammatory process is deemed to be controlled. Nutritional support with parenteral feeding is indicated for patients with severe pancreatitis and those expected to fast for a prolonged period. Pain, a cardinal symptom in acute pancreatitis, can be treated with parenteral meperidine. Octreotide seems to decrease the exocrine secretory activity of the pancreas. Prophylaxis with antibiotics may be considered for patients with severe forms of the disease. A new specific cytokine antagonist, lexipafant, has been shown to be effective in decreasing complications in severe acute pancreatitis. Endoscopic treatment of severe gallstone pancreatitis in its early stages decreases the frequency of biliary sepsis. Surgical treatment is indicated in cases of infected necrotizing pancreatitis. The optimal treatment for noninfected necrotizing pancreatitis remains to be defined. Intensive medical treatment should be provided initially, with failure to respond requiring a surgical approach. 1 figure. 57 references. (AA-M). •

Acute Pancreatitis: Clinical Classification and Terminology Source: Practical Gastroenterology. 20(5): 8, 9-10, 12, 14, 16, 21-22, 24. May 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, the second in a series on pancreatic disease, considers the clinical classification and terminology of acute pancreatitis. The author contends that the management of acute pancreatitis and its complications has been hampered by imprecise terminology and idiosyncratic definitions. Since optimal therapy requires accuracy in diagnosis, and since accurate diagnosis depends in turn on precise terminology, the need for an international consensus was apparent. Accordingly, a multidisciplinary group of 40 internationally recognized experts in acute pancreatitis was assembled in Atlanta, GA, in 1992 for the stated purposes of constructing a clinically based classification system for acute pancreatitis and creating a plan of management based on the new definitions. This article describes the deliberations and resulting recommendations of this symposium. The author concludes that the Atlanta Symposium's suggested classification and resulting therapeutic approach has been in prospective use for the past 5 years by authorities on acute pancreatitis all over the world and may now be recommended without reservation. One chart outlines the flow diagram for the initial management of patients with acute pancreatitis. 3 figures. 7 references. (AA-M).

•

Acute Pancreatitis: Diagnosis and Evaluation Source: Practical Gastroenterology. 20(6): 8, 13-14, 16, 18, 20, 25. June 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, the third in a series on pancreatic disease, considers the diagnosis and evaluation of acute pancreatitis. The authors note that acute pancreatitis can be diagnosed in the vast majority of patients on the basis of the history and the finding of hyperamylasemia (raised amylase level in the blood). In about 5 to 30 percent of patients, the hyperamylasemia arises from causes other than pancreatitis, thus

12

Acute Pancreatitis

necessitating additional investigations. If differentiation from other catastrophic surgically correctable disease is problematic, an immediate computed tomography (CT) scan or, if CT is not available, laparotomy should be performed. Once the diagnosis of pancreatitis is established, the severity of the attack should be assessed in accord with some grading schema. Severity grading derives importance because it governs prognosis, mortality, and the intensity of therapy. The scoring systems currently in use correctly predict a severe or fulminating attack with an accuracy of about 80 to 90 percent in the 20 percent of patients who present with such attacks. A CT scan should not be used for the sole purpose of assessing severity, as the effect of the contrast material on renal and pancreatic microcirculation is still uncertain. However, CT is essential to uncover and delineate intra abdominal complications if the attack persists. Early etiologic assessment is also important because the detection of potential causes for acute pancreatitis will influence the treatment approach, both immediately and after subsidence of the acute process. 4 tables. 6 references. (AA-M). •

Acute Pancreatitis: Another Piece of the Puzzle? Source: New England Journal of Medicine. 325(6): 423-424. August 8, 1991. Summary: This brief article describes two forms of experimental pancreatitis and hypothesizes a connection between the occurrence of pancreatic cellular injury and calcium levels. The author briefly reviews the history of research work searching for the mechanisms that trigger acute pancreatitis. The author concludes that the observation of a relation between pancreatitis and calcium administration may provide yet another clue to the still puzzling story of the pathogenesis of pancreatitis. Reference is made to another article in the same journal issue that presents research in this area. 10 references.

•

Acute Pancreatitis-A Historical Update Source: Practical Gastroenterology. 16(1): 18-19. January 1992. Summary: This brief article, serving as an introduction to a series of articles on pancreatitis, presents an historical update of the condition. Topics include early references to chronic pancreatitis secondary to alcoholism, the Marseille symposium of 1963, and the non-alcohol-related forms of chronic pancreatitis (senile, hereditary, and idiopathic). 2 figures. 1 table. 14 references.

•

Practice Guidelines in Acute Pancreatitis Source: American Journal of Gastroenterology. 92(3): 377-386. March 1997. Summary: This practice guideline reviews the basis of decisions in the management of patients with acute pancreatitis. The author notes that there are a number of important issues pertaining to these decisions, including the need for a consensus on terminology, the most appropriate criteria for determining severity of acute pancreatitis, choices of medical versus surgical therapy, and options for treating complications, including pancreatic pseudocysts. After a section of definitions, the author provides goals and recommendations for each category. The goals of medical therapy include supportive care, limitation of systemic complications, prevention of pancreatic necrosis, and prevention of pancreatic infection once necrosis takes place. In mild pancreatitis, fluid resuscitation and careful monitoring are the two most important components of treatment. Dynamic contrast-enhanced CT scan is recommended at some point beyond the first 3 days in severe acute pancreatitis to distinguish interstitial from necrotizing disease. In the absence of clinical improvement, guided percutaneous aspiration should be performed to distinguish infected necrosis from severe sterile necrosis. Infected

Studies

13

necrosis requires surgical debridement; severe sterile necrosis can usually be treated medically. Asymptomatic pseudocysts require no specific treatment. Symptomatic pseudocysts can be decompressed by surgical, radiologic, or endoscopic methods. 1 figure. 6 tables. 38 references. (AA-M). •

Management of Acute Pancreatitis: A Critical Assessment as Dr. Bockus Would Have Wished Source: American Journal of Gastroenterology. 90(5): 696-703. May 1995. Summary: This presentation, from the 1994 World Congress of Gastroenterology, reviews the management of acute pancreatitis. Topics covered include etiology and pathogenesis; terminology; severity grading; initial management of acute pancreatitis; peritoneal lavage; necrosis and infection; and biliary pancreatitis. The author focuses on some selected features and certain collateral factors that subtly or overtly influence the nature, breadth, and intensity of the therapeutic measures. 6 figures. 67 references. (AAM).

•

Clinical Update: Management of Acute Pancreatitis Source: Journal of Gastroenterology and Hepatology. 12(3): 189-197. March 1997. Contact: Available from Blackwell Science Pty Ltd. P.O. Box 378, Carlton, Victoria 3053, Australia. Phone: 61 3 9347 0300; Fax: 61 3 9347 5001; E-mail: [email protected]. Web site: http://www.blacksci.co.uk. Summary: This review article considers the management of acute pancreatitis. The authors follow the clinically based classification system adapted at an international symposium in Atlanta in 1992. Acute pancreatitis refers to an acute inflammatory process of the pancreas, with variable involvement of other regional tissues or remote organ systems. The authors emphasize the importance of confirming the diagnosis and establishing the etiology. Improved methods of assessing the biliary tree may reduce the number of patients regarded as having idiopathic pancreatitis. Detailed clinical and laboratory protocols, designed to assess severity, have no major advantage over clinical assessment. The contrast-enhanced computed tomography (CT) scan is important to assess the degree of pancreatic necrosis and to detect local complications. The treatment of pancreatitis continues to be largely supportive. However, controlled studies support the use of antibiotics in severe acute pancreatitis and indicate a possible role for the use of octreotide and antioxidants. The place of endoscopic and surgical intervention is becoming better defined. Once an attack has passed, further investigation is often required in an attempt to prevent further episodes of inflammation. 1 figure. 2 tables. 99 references. (AA-M).

Federally Funded Research on Acute Pancreatitis The U.S. Government supports a variety of research studies relating to acute pancreatitis. 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

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).

14

Acute Pancreatitis

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 acute pancreatitis. 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 acute pancreatitis. The following is typical of the type of information found when searching the CRISP database for acute pancreatitis: •

Project Title: ACUTE PANCREATITIS Principal Investigator & Institution: Steer, Michael L.; Professor of Surgery; Beth Israel Deaconess Medical Center St 1005 Boston, Ma 02215 Timing: Fiscal Year 2002; Project Start 01-JUL-1982; Project End 31-JUL-2003 Summary: (Adapted from investigator's abstract) Currently available evidence indicates that digestive enzyme zymogens such as trypsinogen become prematurely activated within acinar cells of the pancreas during the early stages of acute pancreatitis. Activated digestive enzymes are believed to cause cell injury leading to acinar cell death and pancreatitis. The proposed project will pursue the following specific aims: 1) to define the mechanisms responsible for premature activation of zymogens within the pancreas and the role of those activated digestive enzymes in the evolution of acute pancreatitis; and 2) to determine if the type of acinar cell death (ie, necrosis or apoptosis) during acute pancreatitis regulates the severity of that acute pancreatitis. The specific aim #1 studies will build on the observation that infusion of a supramaximally stimulating dose of the CCK analog caerulein causes intrapancreatic activation of trypsinogen as well as pancreatitis in rats. Furthermore, cathepsin B mediated activation of trypsinogen occurs when isolated acini are incubated in vitro with supramaximally stimulating concentrations of caerulein. In the proposed studies, the intracellular location of trypsinogen activation, the cellular events involved in trypsinogen activation, and the mechanism by which trypsinogen activation leads to cell injury will be determined. In the specific aim #2 studies, several models of experimental pancreatitis in laboratory animals (mice, rats, opossums) will be utilized to evaluate the possibility that apoptosis minimizes the severity of pancreatitis. The mechanisms underlying this phenomenon will be examined and the potential value of treating established pancreatitis by inducing apoptosis will be evaluated. Successful completion of these proposed studies will provide important new insights into the cellular basis for acute pancreatitis and identify methods of either preventing or minimizing the severity of this frequently lethal disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

•

Project Title: APOPTOSIS AND NECROSIS IN PANCREATITIS Principal Investigator & Institution: Gukovskaya, Anna S.; Medicine; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2007 Summary: (provided by applicant): Inflammation and parenchymal tissue damage are hallmarks of pancreatitis. In particular, severe necrosis is a major complication of the disease. Over the past decade, significant progress has been achieved in understanding

Studies

15

the mechanisms of the inflammatory response of pancreatitis. In contrast, very little is known about the mechanisms of pancreatic acinar cell death. Mechanisms of necrosis are largely unknown. Key signals mediating apoptosis have been established; however, their roles in disease processes remain obscure, and they have not been investigated in pancreatitis. The role of cell death pathways in pathologic trypsin activation, an important marker of tissue damage in pancreatitis, has not been explored. Our preliminary data indicate that key necrotic and apoptotic mechanisms: poly (ADPribose) polymerase (PARP), mitochondrial dysfunction, caspases (specific cysteine proteases), and the transcription factor NFkappaB are activated in experimental models of pancreatitis and in pancreatic acinar cells stimulated with cholecystokinin (CCK). For the present application, we hypothesize that in pancreatitis, necrotic and apoptotic signaling pathways are interrelated. Activation of PARP and mitochondrial deenergization leads to ATP depletion and necrosis. On the other hand, effector caspases mediate apoptosis and limit necrosis by inactivating PARP and trypsin. NFkappaB negatively regulates effector caspases and, thus plays an anti-apoptotic role in pancreatitis. Thus PARP, mitochondrial dysfunction, caspases, and NFkappaB play central roles in determining the balance between apoptotic versus necrotic type of acinar cell death and the severity of pancreatitis. We propose the following specific objectives for the present application: 1). Determine the role of PARP in necrosis and apoptosis in experimental pancreatitis and in vitro, in pancreatic acini stimulated with CCK. 2). Determine the role of mitochondrial dysfunction in necrosis and apoptosis in experimental pancreatitis and in vitro, in pancreatic acini stimulated with CCK. 3) Determine the role of caspases in necrosis, apoptosis, and trypsin activation in experimental pancreatitis and in vitro, in pancreatic acini stimulated with CCK. 4). Determine the role of NFkappaB in necrosis and apoptosis in experimental pancreatitis and in vitro, in pancreatic acini stimulated with CCK. Measurements to achieve these goals will include measures of pancreatitis, morphologic characterization of apoptosis and necrosis, intrapancreatic activation of caspases and trypsin, cytochrome c release, mitochondrial membrane potential, ATP levels, and NFkappaB activation by using Western blot and gel shift analyses, enzymatic and fluorimetric assays. The result of the experiments in the proposed specific objectives will be delineation of key molecular mechanisms regulating necrosis and apoptosis in acute pancreatitis, which will lead to novel therapeutic strategies to treat the disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CYSTEINE STRING PROTEIN AND ACUTE PANCREATITIS Principal Investigator & Institution: Groblewski, Guy E.; Nutritional Sciences; University of Wisconsin Madison 750 University Ave Madison, Wi 53706 Timing: Fiscal Year 2003; Project Start 01-MAR-2003; Project End 28-FEB-2005 Summary: (provided by applicant): Acute pancreatitis is an inflammatory disease that is triggered by the premature activation of proteolytic zymogens in acinar cells. As a protective mechanism, zymogens are synthesized as inactive pro-enzymes and packaged in specialized secretory granules destined for exocytosis into the pancreatic duct. During pancreatitis, proteolytic zymogens are prematurely activated in acinar cells by aberrantly mixing with hydrolases present in lysosomes. The mixing of lysosomal hydrolases with zymogens occurs in large cytoplasmic vacuoles as a result of pathogenic alterations in acinar cell membrane trafficking. It is well established that the stress-induced expression of heat shock protein-70 (HSP70) in acini provides a natural protective effect against the pathogenic mixing of lysosomal and secretory granule membrane compartments. This proposal is designed to elucidate the mechanism by

16

Acute Pancreatitis

which HSP70 inhibits the intra-acinar cell activation of zymogens in preventing the onset of acute pancreatitis. HSP70 is a molecular chaperone in the cytosol that requires a co-chaperone protein to stimulate ATPase activation and substrate binding. We have 1) identified an HSP70 co-chaperone protein called cysteine string protein (CSP) in acinar cells, 2) localized this membrane associated molecule throughout the secretory pathway and 3) developed the TAT-fusion protein system to manipulate CSP expression in acinar cells and thereby study its function. We hypothesize that CSP mediates the protective effects of HSP70 against pancreatitis by targeting HSPT0 chaperone activity from the cytosol to the secretory pathway. In Specific Aim 1, mutant forms of CSP that no longer anchor to secretory granule membranes will be overexpressed acinar cells to determine the importance of CSP in targeting HSP70 to these organelles during pancreatitis. In Specific Aim II, short interference RNAs will be used to inhibit CSP expression in pancreatic Iobules and the protective effects of HSP70 on secretagogue-induced acinar cell damage will be evaluated. These studies will allow us to directly evaluate the role of CSP in the secretory pathway of acini under physiological and pathophysiological conditions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DIET, DISEASE, AND PANCREATIC ENZYME SYNTHESIS IN HUMANS Principal Investigator & Institution: O'keefe, Stephen J.; Internal Medicine; Virginia Commonwealth University Richmond, Va 232980568 Timing: Fiscal Year 2002; Project Start 01-JUN-2000; Project End 31-MAY-2004 Summary: Acute pancreatitis is a disease of high mortality, induced by premature activation of digestive enzymes in the pancreas, and accompanied by a severe systemic immunoinflammatory response and protein catabolism. Meeting nutritional needs is difficult because food-induced pancreatic stimulation may exacerbate the disease process, and intravenous nutrition (TPN), while "resting the pancreas," increases the risk of septicemia and mucosal atrophy. Recent controlled clinical trials suggest that tubefeeding with elemental diets has advantages over TPN with regard to cost, safety (less infective complications), and efficacy (more anticatabolic). However, it is unknown in humans whether elemental diets stimulate the pancreas, and the beneficial effects may simply reflect better metabolic control and fewer serious complications. Consequently, Dr. O'Keefe and colleagues plan to measure the effects of duodenal infusions of elemental diets on pancreatic enzyme synthesis and secretion in normal volunteers and patients with acute pancreatitis using a unique method that they have developed, based on the 6-hr intravenous and enteral infusion of two isotope-labeled amino acids and measurement of their uptake into trypsin and amylase proteins extracted from duodenal secretions. The method also allows them to obtain simultaneous measurements of the rates of protein catabolism and utilization of dietary amino acids for the synthesis of mucosal proteins (obtained by endoscopic biopsy). Studies will be conducted in groups of 8 normal volunteers to compare the relative effects of complex and elemental diets given as duodenal infusions, versus TPN, on the normal response to a complex oral diet. The results will then be used to evaluate the responses in 20 patients with acute pancreatitis randomized to receive enteral elemental or TPN. The results of these investigations are expected to provide valuable new information on both the stimulatory effects of food on the human digestive system and the nutritional value of modern nutritional support techniques, and help determine why elemental diets are more effective than TPN in the management of patients with acute pancreatitis. The

Studies

17

results are also expected to form a scientific basis for the design of disease-specific diets for patients with acute pancreatic disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ENOS IS PROTECTIVE IN THE INITIATION OF PANCREATITIS Principal Investigator & Institution: Dimagno, Matthew J.; Internal Medicine; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2002; Project Start 01-JAN-2003; Project End 31-DEC-2004 Summary: (provided by applicant): Pharmacological inhibition of nitric oxide synthase (NOS) or enhancement of nitric oxide (NO) in experimental acute pancreatitis (AP) has yielded mixed results, in part because three NOS isoforms exist: neuronal- (nNOS), endothelial- (eNOS) and inducible- (iNOS). Our preliminary data clarifies the role of NO during the initiation of AP and shows that pharmacologic NOS blockade and eNOS deletion, but not nNOS or iNOS deletion, enhance the initiation of an in vivo caerulein hyperstimulation model of AP. By contrast pharmacologic NOS blockade during in vitro caerulein AP has no effect on conversion of intraacinar trypsinogen to trypsin, a hallmark of AP, suggesting that eNOS-derived NO arises from a non-acinar source and/or acts on a non-acinar target. Our data also suggests that upregulation of endothelial eNOS by Simvastatin and Cytochalasin D may attenuate in vivo caerulein AP. We hypothesize that eNOS-derived NO indirectly inhibits initiation of AP by enhancing pancreatic microvascular perfusion. We plan to confirm whether eNOSderived NO acts on a non-acinar target by using an in vitro caerulein model of AP in isolated eNOS KO acini vs. WT acini. Secondly we plan to assess differences in pancreatic perfusion between eNOS KO mice and WT mice during AP using dyelabeled microspheres. Third we plan to determine whether the enhanced initiation of in vivo AP in eNOS KO mice (compared with WT mice) may be normalized by augmenting pancreatic perfusion with NO donors. Fourth we plan to upregulate eNOS pharmacologically in WT and eNOS KO mice to assess for protection against in vivo caerulein AP. We hope that this study may further clarify the role of NO in the pathogenesis of AP. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

•

Project Title: EXOCRINE PANCREATIC ZYMOGEN ACTIVATION Principal Investigator & Institution: Gorelick, Fred S.; Professor of Medicine; Internal Medicine; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2003; Project Start 15-JUL-1998; Project End 31-MAR-2007 Summary: (provided by applicant): The pathologic proteolytic activation of digestive zymogens within pancreatic acinar cells is a key step in the initiation of pancreatitis. The extracellular and intracellular mechanisms responsible for this activation remain unclear. Supraphysiologic concentrations (>10 fold than required for maximal secretion) of the physiologic ligand, cholecystokinin (CCK), given in vivo cause zymogen activation and pancreatitis. Similarly treated isolated acinar cells respond with zymogen activation and are injured. Factors that can sensitize the acinar cell to the pathologic effects of CCK might be relevant to the pathogenesis of acute pancreatitis. Several experimental studies suggest that CCK-activated pathways contribute to disease. These include pancreatitis induced by ischemia, bile salts, the CDE diet, and ethanol. We hypothesize that: 1) clinically relevant agents or conditions can either act alone or sensitize the acinar cell to the effects of CCK on zymogen activation, and 2) such activation will depend on Ca2+-dependent and independent mechanisms. We find that

18

Acute Pancreatitis

the following relevant factors sensitize the acinar cell to zymogen activation caused by physiologic concentrations of CCK: secretin, VLDL, and short chain fatty acids. With respect to alcohols, sensitization increased with chain length and deceased with branching. At sensitizing concentrations, alcohols caused no detectable changes in either cytosolic Ca2+ signaling or secretion. However, the sensitizing effects of secretin corresponded to effects on CCK induced Ca2+ signaling. Previous studies suggested that a low pH compartment mediated zymogen activation. We find that inhibitors of vacuolar (v) ATPase (bafinomycin and concanomycin) block CCK-induced zymogen activation. Using antibodies to subunits of vATPase, we observed translocation during CCK treatments. Thus, vATPase appears to be activated and contribute to zymogen activation. We plan to examine the cellular signaling pathways stimulated by these sensitizing agents with particular emphasis on Ca2+, cAMP, PKC, and vATPase. Further, we will examine the effects of the sensitizing agents on cell injury and the trafficking of active enzymes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: LIVER-LUNG INTERACTION DURING ACUTE PANCREATITIS Principal Investigator & Institution: Gray, Keith D.; Surgery; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2002; Project Start 05-FEB-2002 Summary: A prominent feature of severe acute systemic inflammatory response syndrome (SIRS) including acute respiratory distress syndrome (ARDS). The physiology of these responses appears remarkably similar to responses to direct liver injury in other settings. Cytokines produced in the liver and lungs, including tumor necrosis factoralpha (TNF-alpha) and interleukin (IL-1), are implicated in the pathogenesis of SIRS and animal experiments have demonstrated them capable of precipitating acute lung injury. During acute pancreatitis, proteases are released into the portal system, exposing the liver to high levels of activated enzymes. Nuclear factor kappa-B (NF-kappaB), a transcriptional regulator of TNF- alpha, IL-1 and other cytokines, is activated in the pancreas within 30 minutes of inducing experimental acute pancreatitis and subsequently within the liver and lung within 24 hours of acute liver injury. Our central hypothesis is that NF-kappaB activation in the pancreas and liver mediates acute lung injury associated with pancreatitis. Using the biliary cerulein/glycodeoxycholic acid model of acute pancreatitis will address two specific aims: 1) to determine whether altering NF-kappaB activation in the liver affects the pulmonary response to severe acute pancreatitis; 2) to determine the role of Kupffer cells in mediating the multisystem effects of pancreatitis by depleting Kupffer cells prior to induction of pancreatitis. These studies may allow the development of strategies to ameliorate multisystem to ameliorate multi-system injury including pulmonary failure, which can be devastating during this illness. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

•

Project Title: MODELS OF TYPE 1 AND TYPE II HEREDITARY PANCREATITIS Principal Investigator & Institution: Ulrich, Charles D.; Internal Medicine; University of Cincinnati 2624 Clifton Ave Cincinnati, Oh 45221 Timing: Fiscal Year 2002; Project Start 01-MAY-2001; Project End 31-MAR-2003 Summary: (Applicant's Abstract): Acute and chronic pancreatitis remain major healthcare problems. The lack of effective preventive and therapeutic strategies in these disease states stems from a lack of understanding regarding disease pathogenesis. The

Studies

19

investigator's group has identified mutations responsible for two delayed-onset, autosomal dominant inherited forms of acute and chronic pancreatitis. An RI 17H mutation in the human cationic trypsinogen gene links with type I hereditary pancreatitis (HP I). An N211 mutation in the same gene links with type II hereditary pancreatitis (HP II). Biochemical data from other groups when combined with the results of there preliminary studies support the hypothesis that the HP I mutation in cationic trypsin renders the molecule resistant to proteolytic digestion, the persistence of mutant trypsin activity resulting in the creation of a "milieu" sufficient for clinicallyapparent acute pancreatitis. The alterations in protein biochemistry responsible for the HP II phenotype remain unclear. In an initial attempt to develop an animal model of HP I, the investigator generated transgenic mice containing a diet-inducible pancreatic acinar cell-specific promoter coupled to either wild-type or HP I mutant human cationic trypsinogen. Unfortunately, these mice fail to develop pancreatitis spontaneously, and all available antibodies to human cationic trypsin cross-react with an identically sized mouse trypsin. The investigator believes that enhanced expression of antibody epitopetagged human cationic trypsinogens will provide him with the best opportunity to develop a successful animal model of hereditary pancreatitis. Toward this end, the investigator proposes (1) studies comparing the biochemical properties of affinitypurified recombinant wild-type, R117H, and N21I human cationic trypsinogen/trypsin (+ I- epitope tag) utilizing a validated in vitro assay system. By design, these studies will also further test the investigator's hypothesis with regard to HP I mutant trypsin, and discern the biochemical alterations induced by the HP II mutation. The investigator will then (2) characterize murine pancreata and acinar cells expressing varying levels of epitope-tagged wild-type, R117H, and N2 11 human cationic trypsinogen/trypsin. The development of these animal models, in combination with the experimental design, should provide him with important insights into the events underlying the delayedonset and pathophysiology of HP I, HP II and non-hereditary forms of acute and chronic pancreatitis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MOLECULAR GENETICS OF HEREDITARY PANCREATITIS Principal Investigator & Institution: Whitcomb, David C.; Chief, Div of Gastroenterology, Hepatolo; Medicine; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2002; Project Start 01-APR-1999; Project End 30-NOV-2003 Summary: Acute and chronic pancreatitis are major health-care problems in the United States causing years of pain and disability. Despite the impact of these diseases, mystery surrounds many of the predisposing causes and early molecular events. Furthermore, the devastating effects of acute pancreatitis and chronic pancreatitis, once established, cannot be reversed. We believe that in the future, advances in the treatment of pancreatic disease rest in the early identification of at-risk individuals as well as in the prevention of limitation of pancreatic injury. Thus, the goal of our program is to determine the molecular mechanisms that predispose to acute and chronic pancreatitis and to identify targets for disrupting pathophysiological processes. We believe that effective preemptive actions will prevent or limit pancreatic injury and thus, result in the reduction of he incidence and severity of acute and chronic pancreatitis. To understand the mechanisms of pancreatitis we will identify previously uncharacterized hereditary pancreatitis families and investigate several striking features of this disease including incomplete penetrance and the mechanisms causing pancreatitis with trypsinogen RR117H and N21I mutations. Answering this question may provide insight

20

Acute Pancreatitis

into the pathophysiology of acute and chronic pancreatitis and identify targets for new therapies, and help identify individuals at risk through genetic testing. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MOLECULAR MECHANISMS OF ACUTE PANCREATITIS Principal Investigator & Institution: Logsdon, Craig D.; Professor; Molecular and Integrative Physiology; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2002; Project Start 10-MAY-1998; Project End 31-AUG-2005 Summary: (provided by applicant): Pancreatitis is an important clinical problem for which treatment is still largely supportive. We have identified the transcription factor NF-KappaB as a molecule that is activated early in the disease contributing to the initiation of an inflammatory cascade. Specific aim #1 is to determine the mechanisms and role of NF-KappaB activation in acute pancreatitis. We will extend our understanding of the significance of NF-KappaB activation by directly activating and inhibiting NF-KappaB within the pancreas using adenoviral expression of active and dominant negative subunits. We hypothesize that NF-KappaB plays a pro-inflammatory role and specifically drives expression of mob-1 and gro-alpha, two important chemokines. We will identify other genes activated by NF-KappaB within pancreatic acinar cells using a combination of adenovirus mediated delivery of an active subunit and oligonucleotide-directed microarray analysis. We will also test the hypothesis that trypsin activation is able to activate NF-KappaB within acinar cells using an adenoviral approach to directly active trypsin within acinar cells. Specific aim #2 is to identify the genes that are induced early in the course of acute pancreatitis. To further identify new molecules that are important in acute pancreatitis, we will utilize oligonucleotide directed microarrays to profile gene expression in rapid onset models of acute pancreatitis. We will specifically focus our search on genes for transcription factors and inflammatory mediators, as these may become targets of therapy for the disease. Specific aim #3 is to determine the mechanisms and role of the transcription factor EGR-1 in acute pancreatitis. Preliminary experiments have shown that the transcription factor EGR-1 is highly induced early in the course of caerulein induced acute pancreatitis. EGR-1 plays an important role in other inflammatory diseases and is a know regulator of tissue factor (TF). We will determine if this transcription factor is also induced in other models of acute pancreatitis, investigate the cellular mechanisms involved in its regulation, and determine the relationship between its activation and the severity of acute pancreatitis. We will also test the hypothesis that EGR-1 drives expression of TF in the pancreas, and identify other targets of this important transcription factor. Specific aim #4 is to determine the roles of pro-inflammatory effectors, mob-1, gro-alpha, TF and CGRP in acute pancreatitis. Of the pro-inflammatory molecules identified as upregulated after treatment of animals with high concentrations of caerulein, we have selected these four as being especially likely to contribute to the severity of acute pancreatitis based upon their known functions in other diseases. Specifically, we will test the hypothesis that mob-1 and gro-alpha are important for chemoattraction of Tcells and neutrophils respectively, that TF is important for initiating blood coagulation in the pancreas, and that CGRP expression in acinar cells contributes to alterations in pancreatic and systemic blood flow. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

Studies

•

Project Title: PANCREATITIS

MOLECULAR

PATHOMECHANISM

OF

21

HEREDITARY

Principal Investigator & Institution: Sahin-Toth, Miklos; Associate Professor; Physiology; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2002; Project Start 01-MAY-2001; Project End 31-JUL-2002 Summary: (Applicant's abstract): The broad, long-term objectives of this application are to understand the mechanism by which mutations in the human cationic trypsinogen gene (PRSS1) lead to hereditary pancreatitis (HP). HP is an autosomal dominant genetic disorder characterized by early-onset recurrent attacks of acute pancreatitis with frequent progression to chronic pancreatitis and occasionally to pancreatic cancer. HP belongs to the inherited forms of idiopathic chronic pancreatitis, a genetically heterogeneous disease group, where mutations have been found not only in PRSS1, but also in the cystic fibrosis transmembrane conductance regulator (CFTR) gene and in the pancreatic secretory trypsin inhibitor gene (SPINK1). HP has been widely recognized as a highly relevant model system for all forms of human pancreatitis. In the majority of cases, three mutations, Arg117-His, Asn2l-,lle, and Ala8-Val, have been identified in PRSSI. The molecular defects caused by the HP mutations will be studied within the context of a current pathogenesis model, which suggests that HP is caused by excessive intrapancreatic trypsin activity via one of 3 mechanisms: (i) increased trypsinogen activation, (ii) decreased trypsin degradation; or (iii) impaired inhibition by pancreatic secretory trypsin inhibitor (PSTI). The principal objective of the experimental design is to study the effects of the HP-mutations in vitro, using recombinant human trypsinogens. Wild-type and mutant trypsinogens will be expressed in Escherichia coli, and purified to homogeneity with ecotin affinity chromatography. Catalytic properties and autocatalytic degradation (autolysis) of trypsins and autoactivation and autocatalytic degradation (zymogenolysis) of trypsinogens will be characterized. In addition, interactions between wild-type and mutant forms of cationic trypsin(ogen) with anionic trypsin(ogen) and mesotrypsin(ogen) will be examined. Finally, inhibition of human trypsin isoforms and HP mutant trypsins by wild-type and mutant PSTI proteins will be studied. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NADPH PANCREATITIS

OXIDASE

INHIBITOR

THERAPY

IN

ACUTE

Principal Investigator & Institution: Weinstein, David; Triage Pharmaceuticals, Llc 1 University Pl, Rm A215 Rensselaer, Ny 12144 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 30-JUN-2003 Summary: (provided by applicant): Triage Pharmaceuticals LLC ("Triage") was chartered in the summer of 1999 to exploit new treatments for vascular leakage related illnesses using NADPH oxidase inhibitors patented by Dr. James Holland, a Triage cofounder. The invention is protected by two issued U.S. patents, granted European and Japanese patents, and a pending Canadian patent application. These cases claim a method of prevention and treatment of diseases related to endothelial hyperpermeability and vascular leakage by therapeutic administration of an NADPH oxidase inhibitor. The scientific rationale for the involvement of NADPH oxidase in mechanisms leading to vascular leakage has been well-documented by Triage in its work on the inhibitory effect of apocynin, a naturally occurring plant extract. In order to further this work, Triage is seeking funding to perform accelerated pharmaceutical development

22

Acute Pancreatitis

and preclinical testing for drug candidates in a vascular leakage disease indication that has a clear, simple, non-costly end-point and treatment duration that should allow determination of clinical efficacy in very short trial periods. Using its current library of potent NADPH oxidase inhibitors, "proof of concept" will be established in the vascular leakage of acute pancreatitis using an established rat model of the disease. PROPOSED COMMERCIAL APPLICATION: There are no currently available drugs for the treatment of the endothelial hyper-permeability and vascular leakage component of vascular diseases, such as acute pancreatitis, diabetes mellitus, atherosclerosis and hypertension. Despite the effectiveness of currently available medical treatments for these vascular diseases, the risks of morbidity and mortality remain high. A combination approach with currently available medical treatment and an orally administered NADPH oxidase inhibitor would significantly improve the treatment of individuals with a high risk for the diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NEURAL REGULATION OF PANCREATIC FUNCTION Principal Investigator & Institution: Kirkwood, Kimberly S.; Surgery; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 941222747 Timing: Fiscal Year 2002; Project Start 15-MAY-1994; Project End 31-JUL-2004 Summary: (Adapted from Applicant's Abstract): Approximately 10% of patients with acute pancreatitis die from uncontrolled pancreatic inflammation that results in massive fluid losses and shock. The regulation of pancreatic inflammation is poorly understood. In the trachea, sensory nerves regulate inflammation by releasing tachykinins that bind to endothelial cells and induce arteriolar vasodilatation, plasma extravasation and neutrophil infiltration. This well-characterized phenomenon is called neurogenic inflammation. The general hypothesis of this proposal is that neurogenic mechanisms are essential to the pathogenesis of acute pancreatitis. Specifically, we hypothesize that a) tachykinins induce plasma extravasation and neutrophil infiltration in the pancreas by interacting with neurokinin receptors, b) the pro-inflammatory effects of tachykinins are terminated by cell surface peptidases, and c) tachykinins and their receptors regulate inflammation in a widely-used model of acute pancreatitis. Due to the recent availability of "knockout" mice in which the genes encoding neurokinin receptors or cell surface peptidases have been deleted by homologous recombination, these experiments will be performed in mice. Pancreatic inflammation will be assessed by 1) quantifying and localizing plasma extravasation using Evans blue and Monastral blue, respectively, 2) identifying and measuring endothelial cell gaps through which plasma extravasates using a silver stain and light microscopy, 3) quantifying and localizing neutrophil infiltration using myeloperoxidase, and 4) defining the extent of edema, and cytoplasmic vacuolization using histological criteria. Specific Aim 1 will define the contribution of exogenous and endogenous tachykinins to the initiation of acute pancreatic inflammation. The time-course and dose-response will be determined, and the neurokinin receptors that mediate these effects will be identified using antagonists and knockout mice, and localized using receptor-specific antisera. Specific Aim 2 will examine the role of peptidases in the termination of tachykinin-induced pancreatic inflammation. The peptidases neutral endopeptidase and angiotensin converting enzyme will be localized in the pancreas using specific antisera, and their importance in tachykinin-induced inflammation will be determined using inhibitors and knockout mice. Specific Aim 3 will define the importance of sensory nerves, and specifically tachykinins, in the pathogenesis of acute pancreatitis. Using neurokinin receptor

Studies

23

antagonists, peptidase inhibitors, and knockout mice, we will delineate the neurogenic mechanisms that regulate inflammation in acute pancreatitis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PANCREAS TRANSCRIPTION FACTORS AND CANCER MODEL SYSTEMS Principal Investigator & Institution: Konieczny, Stephen F.; Associate Professor; Biological Sciences; Purdue University West Lafayette West Lafayette, in 479072040 Timing: Fiscal Year 2002; Project Start 01-MAR-2000; Project End 28-FEB-2005 Summary: (adapted from investigator's abstract): The development of the mammalian pancreas represents an attractive model system to study the molecular signals that direct the commitment and differentiation of epithelial cells along different cell lineages. The pancreas consists of two distinct tissue types which carry out different essential functions. The endocrine pancreas regulates blood sugar levels by secreting glucagon or insulin whereas the exocrine pancreas secretes digestive enzymes into the duodenal part of the small intestine. Although many of the transcription factors responsible for endocrine pancreas formation have been identified and extensively studied, the molecular regulatory circuits that control the establishment and maintenance of the exocrine pancreas are just beginning to be elucidated. Towards a goal of identifying key transcriptional regulators of pancreatic development and function, a novel basic helixloop-helix (bHLH) transcription factor (Mistl) recently was identified that accumulates to high levels in pancreatic exocrine cells. Mistl gene expression is initially detected at mouse embryonic day E10.5 in the developing pancreas and remains expressed to high levels in the acinar cells of the adult. Although the Mistl nuclear protein is capable of binding to specific DNA targets as a homodimer or as a heterodimer with other bHLH transcription factors, it lacks a typical transcription activation domain and instead can serve as a transcriptional repressor in some experimental systems. At this time, a true role for Mistl activity in pancreatic function has not been established, although its expression pattern and DNA binding capabilities suggest that Mistl likely serves as a key regulator of exocrine pancreas gene activity. In order to characterize further the biochemical properties of the Mistl protein and the role of Mistl in pancreatic development, studies are proposed to (1) examine the activity of Mistl using a pancreatic cell line model system, (2) identify pancreas-specific Mistl protein binding partners and (3) utilize mouse genetic approaches to create Mistl homozygous null mice and to identify Mistl target genes. In addition, targeted replacement of the Mistl gene with an activated K-ras allele will be performed to generate novel pancreatic cancer models. A complete characterization of Mistl activity in exocrine pancreatic cells will add critical new information regarding normal pancreatic development and function and may provide future strategies for combating several key human diseases, including acute pancreatitis and pancreatic cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

•

Project Title: ROLE PATHOGENESIS

OF

CCK

RECEPTOR

IN

ACUTE

PANCREATITIS

Principal Investigator & Institution: Samuel, Isaac; Surgery; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2003; Project Start 15-JAN-2003; Project End 30-NOV-2007 Summary: (provided by applicant): Acute pancreatitis is a common disease with significant morbidity and mortality but no specific treatment is available as the

24

Acute Pancreatitis

pathogenic mechanisms are not known. The purpose of this research proposal is to elucidate early events in pathogenesis of gallstone-induced acute pancreatitis. We use the rat model of bile-pancreatic duct ligation-induced acute pancreatitis as an experimental corollary. Bile-pancreatic juice exclusion from gut causes feedback exocrine pancreatic stimulation via cholecystokinin-A receptor (CCK-AR) mechanisms. The role of the CCK-AR in disease pathogenesis is not known. Our preliminary studies provide the first evidence that CCK-AR mediated pancreatic acinar cell hyperstimulation plays a contributory role in disease pathogenesis and that induction of CCK-AR occurs within one hour of duct ligation. We hypothesize that pathological amplification of CCK-AR mediated signal transduction exacerbates disease pathogenesis. We propose experiments to test this hypothesis and pursue these specific aims: 1) Characterize the role of the CCK-AR in duct occlusion-induced acute pancreatitis pathogenesis. 2) Characterize the expression and regulation of the CCK-AR in duct occlusion-induced acute pancreatitis. 3) Characterize the CCK-AR mediated signal transduction pathway in duct occlusion-induced acute pancreatitis. Competitive binding assays with radiolabeled ligand will be done to study receptor number, specificity, and affinity. Receptor sensitivity and activity will be determined by measuring downstream signals (cyclic AMP, inositol phosphate). Differences between the induced and native receptor will be determined both in terms of altered functional characteristics and perturbations in intracellular signal transduction pathways. The possibility that promiscuous G-protein coupling in acute pancreatitis could drastically increase CCK-AR affinity and also perpetuate a grossly amplified intracellular signal may have profound implications in mechanisms of disease pathogenesis. An innovative feature of this proposal is the use of an original surgical model, "The Donor Rat Model", that provides a unique opportunity to investigate disease pathogenesis. The significance and health-relatedness of this research endeavor is its ultimate goal to elucidate mechanisms of disease pathogenesis that provide the rationale to base new treatment protocols intended to reduce the morbidity and mortality of acute pancreatitis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: SURGICAL STUDIES ON METABOLISM OF GI HORMONES Principal Investigator & Institution: Gomez, Guillermo; Surgery; University of Texas Medical Br Galveston 301 University Blvd Galveston, Tx 77555 Timing: Fiscal Year 2002; Project Start 01-MAY-1976; Project End 30-APR-2004 Summary: A major challenge in gastrointestinal research today is to gain a better understanding of the underlying molecular mechanisms for maintenance of the exocrine pancreas and small bowel mucosa. Acute pancreatitis (AP) is a complex and poorly understood disease. Severe acute hemorrhagic or necrotizing pancreatitis in humans results in an exceptionally high morbidity and mortality. Despite the abundance of pancreatitis patients, underlying molecular mechanisms that control the severity of an AP are not known. Likewise, a deficiency in appropriate intestinal regeneration or adaptation following mucosal disease or injury can be clinically relevant. The specialized epithelial cells of the small bowel mucosa constitute an essential organ for nutrient absorption, immune function and regulation of fluid and electrolyte balance. Disruption of the integrity of the intestinal mucosa either through inflammation, infiltration, surgical resection or ischemia results in severe malabsorption and ultimately in clinical malnutrition requiring total parenteral nutritional support. The long term objectives of the proposed work are to understand the roles gastrointestinal (GI) hormones play in the homeostasis of the pancreas, and in controlling GI epithelial restitution and regrowth. The Specific Aims of this research proposal are: 1) to

Studies

25

determine the role of gastrointestinal hormones in the regulation of pancreatic apoptosis and regeneration in experimental models of acute pancreatitis; and, 2) to determine the role of gastrointestinal hormones in the regulation of adaptive hyperplasia of the gut. The proposed studies are designed to precisely define, in a systematic fashion, the components of GI hormone-linked intracellular transduction pathways involved in the regulation of pancreatic apoptosis and regeneration in experimental models of AP; and, the proliferation of GI mucosa associated with adaptive hyperplasia of the gut. In order to accomplish these aims, we will investigate molecular pathways of acinar cell proliferation and apoptosis in three different models of experimental AP, and the intracellular signal transduction pathways mediating the regulation of neurotensin gene expression by insulin-like growth factor-I (IGF-I) and the enhancement of glucagon-like peptide-2 (GLP-2)- stimulated mucosal proliferation by neurotensin. These studies will provide a foundation for the development of innovative therapeutic strategies designed to exploit the unique biological activities of GI hormones on the exocrine pancreas and intestinal mucosa. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: THE CALCIUM-SENSING RECEPTOR IN ACUTE PANCREATITIS Principal Investigator & Institution: Saunders, Christine; Biochemistry; University of Texas Hlth Sci Ctr San Ant 7703 Floyd Curl Dr San Antonio, Tx 78229 Timing: Fiscal Year 2002; Project Start 01-APR-2001; Project End 31-JUL-2002 Summary: (adapted from the application) Acute pancreatitis is an inflammatory disease with significant mortality, affecting about 80,000 Americans a year. The pathophysiologic mechanisms are not thoroughly elucidated, and to date there are few if any effective treatments. Calcium and lipid mediators are integral components of the signaling cascade involved in pancreatic inflammation. Changes in blood calcium levels have been associated with acute pancreatitis, both in humans and in laboratory animals. The recently cloned calcium-sensing receptor (CaSR), a G protein-coupled receptor (GPCR), by virtue of its ability to stimulate inflammatory lipid mediator synthesis, provides a possible mechanism for how calcium, lipid mediators and acute pancreatitis are linked. In fact, recent findings suggest that the CaSR in the pancreas is upregulated during acute pancreatitis in the rat. The hypothesis for the proposed studies is that the pancreatic CaSR is involved in initiating and/or propagating acute pancreatitis by activating PLA2, which stimulates lipid mediators involved in the inflammatory cascade. In this proposal, molecular biologic, biochemical and physiologic approaches will be combined to investigate the role of the pancreatic CaSR in experimental acute pancreatitis. The secretagogue (eg. cerulein) hyperstimulation model in rats is a well established model in which hourly administration of high doses of cerulein for 6 hours induces an edematous acute pancreatitis. Multiple techniques will be used to test the hypothesis by addressing the following specific aims: (1) to identify the pancreatic cells which express the functional CaSR; (2) to determine whether the CaSR is directly involved in acute pancreatitis in the rat; (3) to examine whether cytoskeletal depolymerization during acute pancreatitis provides a mechanism for how the CaSR is upregulated in cerulein-induced pancreatitis; (4) to examine whether there is "cross-talk" between the cholecystokinin A (CCK-A) receptor and the CaSR which might lead to activation of the CaSR in cerulein-treated rats. While the role of the CaSR in inherited diseases is emerging, its function in inflammatory conditions remains unknown. Since the CaSR activates lipid mediator synthesis, its potential role in inflammation seems logical and represents an exciting and novel possibility. Also, this study might serve as a

26

Acute Pancreatitis

paradigm for inflammatory conditions other than pancreatitis, the treatments for which have remained elusive. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: TRANSGENIC MOUSE MODELS OF PANCREATIC EXOCRINE FUNCTION Principal Investigator & Institution: Delisle, Robert C.; Associate Professor; Anatomy and Cell Biology; University of Kansas Medical Center Msn 1039 Kansas City, Ks 66160 Timing: Fiscal Year 2002; Project Start 01-JUN-2002; Project End 31-MAY-2004 Summary: (provided by applicant): This grant application proposes to develop genetically engineered mouse models for acute pancreatitis and cystic fibrosis-related pancreatitis. We will focus on a recently discovered gene, which preliminary data suggest may play a role in development of pancreatitis, and also in the pathogenesis of cystic fibrosis (CF). The gene is called crpd in the mouse and dmbt1 in humans and it encodes the protein Muclin, a high molecular weight, and sulfated glycoprotein. This gene is most highly expressed in the exocrine pancreas, but also as different transcripts in other organs including the intestine, gallbladder, and kidney. The hypothesis is that Muclin is required for normal zymogen granule formation and subsequent solubilization of digestive enzymes upon exocytosis of the granules. We predict that if this gene is a disrupted zymogen granule will fail to mature creating a situation in the acinar cell where the zymogens will be prone to become activated, resulting in pancreatitis. The Muclin-deficient mouse model is intended to explore this hypothesis and, if this is borne out, it will make looking for mutations in this gene in human idiopathic pancreatitis a reasonable endeavor. We also predict that mice over expressing Muclin will exhibit poor release of zymogens after exocytosis and will be prone to CFlike plugging of the acinar lumen, which may predispose to pancreatitis. In CFTR-/mice, a model for CF, the pancreas exhibits over expression of Muclin, which is associated with protein, plugs in the acinar lumen. Mice with a Muclin transgene targeted to the pancreas will allow testing of this hypothesis. The specific aims are to produce genetically engineered mice: 1). Globally deficient in Muclin by targeting the first exon, which is present in all transcripts of this gene. 2). An exocrine cell-specific defective Muclin by targeting the last exon which is translated only in exocrine cell transcripts of the gene and codes for a transmembrane domain that may be important for Muclin' s exocrine function; 3). That over expresses Muclin in the pancreatic acinar cell using the rat elastase promoter to direct cell specific expression. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

•

Project Title: VIDEOSCOPIC COLLECTIONS

DRAINAGE

OF

INFECTED

PANCREATIC

Principal Investigator & Institution: Horvath, Karen D.; Surgery; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-AUG-2005 Summary: (provided by applicant): External drainage and antibiotics are the fundamental principles of treatment for infected pancreatic fluid collections following necrotizing pancreatitis. Without proper therapy, nearly all patients will die. Open surgical necrosectomy, or the process of removing necrotic tissue, is currently the standard of care. While highly effective, the large abdominal incision is associated with significant morbidity. Percutaneous catheter drainage is another type of external drainage with variable success rates. Although minimally invasive, the necrosectum

Studies

27

often contains particulate debris, 10-30mm in size, which are poorly drained via the 410mm catheters. When percutaneous drainage fails, all patients crossover to open surgical necrosectomy. Preliminary data suggest that videoscopic-assisted retroperitoneal debridement (VARD) is a promising new method that combines the benefits of open surgical necrosectomy and percutaneous catheter drainage. Debridement occurs under direct vision through a small flank incision with videoscopic assistance. This project is a multicenter, single-arm, Phase II safety and efficacy study of patients undergoing VARD of infected pancreatic fluid collections. Patients enrolled will be limited to hemodynamically stable patients with documented infected pancreatic necrosis or pancreatic abscess as defined by the Atlanta Symposium. Patients will be strictly classified based on: CT classification, time from onset of pancreatitis to external drainage, and patient disease severity. Five major teaching hospitals will enroll 40 patients over 18 months. All patients will be followed for 6 months from the onset of pancreatitis. Safety issues will be monitored by an External Review Board. The hypothesis is: In patients with infected pancreatic fluid collections following acute pancreatitis, VARD provides a safe and efficacious procedure for draining infected pancreatic fluid collections adequately without need for crossover to open surgical necrosectomy. The specific aims are to assess: 1) safety and efficacy of VARD of infected pancreatic fluid collections; and 2) the clinical and functional outcomes of patients treated with VARD. The long-term goal is to use data obtained from this study as the basis for a multicenter, Phase III, randomized study comparing the VARD to the current standard of care, open surgical necrosectomy. 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 “acute pancreatitis” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for acute pancreatitis in the PubMed Central database: •

Activation of polyamine catabolism in transgenic rats induces acute pancreatitis. by Alhonen L, Parkkinen JJ, Keinanen T, Sinervirta R, Herzig KH, Janne J.; 2000 Jul 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26940

•

Acute pancreatitis following medical abortion: Case report. by Hallberg P, Hallberg E, Amini H.; 2004; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=406515

•

Calcium signaling and acute pancreatitis: Specific response to a promiscuous messenger. by Parekh AB.; 2000 Nov 21; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=34065

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.

28

Acute Pancreatitis

•

Excretion of cephalothin and cefamandole by the normal pancreas and in acute pancreatitis in dogs. by Studley JG, Schentag JJ, Schenk WG Jr.; 1982 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183722

•

Immunoglobulin M antibody response against Mycoplasma pneumoniae lipid antigen in patients with acute pancreatitis. by Leinikki PO, Panzar P, Tykka H.; 1978 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=275159

•

Mobilization of xanthine oxidase from the gastrointestinal tract in acute pancreatitis. by Granell S, Bulbena O, Genesca M, Sabater L, Sastre J, Gelpi E, Closa D.; 2004; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=331409

•

Phosphatidylinositol 3-kinase-dependent activation of trypsinogen modulates the severity of acute pancreatitis. by Singh VP, Saluja AK, Bhagat L, van Acker GJ, Song AM, Soltoff SP, Cantley LC, Steer ML.; 2001 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=209439

•

Protective action of luminal bile salts in necrotizing acute pancreatitis in mice. by Gomez G, Townsend CM Jr, Green DW, Rajaraman S, Uchida T, Greeley GH Jr, Soloway RD, Thompson JC.; 1990 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=296724

•

Role of substance P and the neurokinin 1 receptor in acute pancreatitis and pancreatitis-associated lung injury. by Bhatia M, Saluja AK, Hofbauer B, Frossard JL, Lee HS, Castagliuolo I, Wang CC, Gerard N, Pothoulakis C, Steer ML.; 1998 Apr 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=22564

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 acute pancreatitis, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “acute pancreatitis” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for acute pancreatitis (hyperlinks lead to article summaries):

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.

Studies

29

•

A rare initial manifestation of systemic lupus erythematosus--acute pancreatitis: case report and review of the literature. Author(s): Duncan HV, Achara G. Source: The Journal of the American Board of Family Practice / American Board of Family Practice. 2003 July-August; 16(4): 334-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12949035

•

Acute pancreatitis after a course of clarithromycin. Author(s): Schouwenberg BJ, Deinum J. Source: The Netherlands Journal of Medicine. 2003 July; 61(7): 266-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14567525

•

Acute pancreatitis and exacerbation of hepatitis B following reduced dose of prednisolone. Author(s): Ohshiro Y, Tawata M, Takasu N. Source: Qjm : Monthly Journal of the Association of Physicians. 2003 November; 96(11): 868-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14566043

•

Acute pancreatitis and modified-release clarithromycin. Author(s): Gonzalez Carro P, Perez Roldan F, Legaz Huidobro ML, Moraleda de Acuna M, Nieto Garcia JC. Source: The Annals of Pharmacotherapy. 2004 March; 38(3): 508-9. Epub 2004 January 30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14755067

•

Acute pancreatitis caused by meglumine antimoniate given for the treatment of visceral leishmaniasis. Author(s): Lambertucci JR, Franca BM, Queiroz Ede M. Source: Revista Da Sociedade Brasileira De Medicina Tropical. 2004 January-February; 37(1): 74-5. Epub 2004 March 19. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15042193

•

Acute pancreatitis complicating 50% full-thickness burns in a 5-year-old child. Author(s): Wilson MD, Sugden P, Durrani A, Dziewulski P. Source: Burns : Journal of the International Society for Burn Injuries. 2003 September; 29(6): 619-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12927993

•

Acute pancreatitis due to hydrocortisone in a patient with ulcerative colitis. Author(s): Khanna S, Kumar A. Source: Journal of Gastroenterology and Hepatology. 2003 September; 18(9): 1110-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12911675

30

Acute Pancreatitis

•

Acute pancreatitis induced by diffuse pancreatic invasion of adult T-cell leukemia/lymphoma cells. Author(s): Mori A, Kikuchi Y, Motoori S, Watanabe J, Shinozaki M, Eguchi M. Source: Digestive Diseases and Sciences. 2003 October; 48(10): 1979-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14627344

•

Acute pancreatitis occurring in the early postpartum period: a case report. Author(s): Fukami T, Chaen H, Imura H, Sudou K, Eguchi F. Source: Journal of Perinatal Medicine. 2003; 31(4): 345-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12951894

•

Acute pancreatitis. Author(s): Parker M. Source: Emergency Nurse : the Journal of the Rcn Accident and Emergency Nursing Association. 2004 March; 11(10): 28-35. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15045929

•

Acute pancreatitis: molecular biology update. Author(s): Whitcomb DC. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2003 December; 7(8): 940-2. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14675701

•

Acute pancreatitis: symptoms, diagnosis and management. Author(s): Turner B. Source: Nurs Times. 2003 November 18-24; 99(46): 38-40. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14666821

•

Adrenal insufficiency in severe acute pancreatitis. Author(s): De Waele JJ, Hoste E, Decruyenaere J, Colardyn F. Source: Pancreas. 2003 October; 27(3): 244-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14508130

•

Alstrom syndrome with acute pancreatitis: a case report. Author(s): Wu WC, Chen SC, Dia CY, Yu ML, Hsieh MY, Lin ZY, Wang LY, Tsai JF, Chang WY, Chuang WL. Source: Kaohsiung J Med Sci. 2003 July; 19(7): 358-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12926522

Studies

31

•

Ampullary carcinoid tumor presenting as acute pancreatitis in a patient with von Recklinghausen's disease: case report and review of the literature. Author(s): Mayoral W, Salcedo J, Al-Kawas F. Source: Endoscopy. 2003 October; 35(10): 854-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14551865

•

Analysis and prevention of factors predisposing to infections associated with severe acute pancreatitis. Author(s): Sun B, Li HL, Gao Y, Xu J, Jiang HC. Source: Hepatobiliary Pancreat Dis Int. 2003 May; 2(2): 303-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14599990

•

Angiographic features in acute pancreatitis: the severity of abdominal vessel ischemic change reflects the severity of acute pancreatitis. Author(s): Inoue K, Hirota M, Beppu T, Ishiko T, Kimura Y, Maeda K, Ogawa M. Source: Jop [electronic Resource] : Journal of the Pancreas. 2003 November; 4(6): 207-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14614201

•

Antibiotic therapy for prophylaxis against infection of pancreatic necrosis in acute pancreatitis. Author(s): Bassi C, Larvin M, Villatoro E. Source: Cochrane Database Syst Rev. 2003; (4): Cd002941. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14583957

•

Apoptosis versus necrosis in acute pancreatitis. Author(s): Bhatia M. Source: American Journal of Physiology. Gastrointestinal and Liver Physiology. 2004 February; 286(2): G189-96. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14715516

•

Are cytokines the cause of distant organ injury in acute pancreatitis? Author(s): Fernandez-del Castillo C, Alsfasser G. Source: Surgery. 2003 November; 134(5): 846-7; Author Reply 847. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14674420

•

Bacteremia in acute pancreatitis of different etiologies. Author(s): Chang KK, Lin XZ, Chen CY, Shin JS, Yang CC, Chen CY. Source: J Formos Med Assoc. 1995 December; 94(12): 713-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8541731

32

Acute Pancreatitis

•

Bacterial translocation and its prevention in acute pancreatitis. Author(s): Dervenis C, Smailis D, Hatzitheoklitos E. Source: Journal of Hepato-Biliary-Pancreatic Surgery. 2003; 10(6): 415-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14714160

•

Bacterial translocation in acute pancreatitis. Author(s): Thomson A. Source: Journal of Gastroenterology and Hepatology. 2003 October; 18(10): 1214. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12974914

•

Bactericidal/permeability-increasing protein and group I and II phospholipase A2 during the induction phase of human acute pancreatitis. Author(s): Kemppainen E, Hietaranta A, Puolakkainen P, Sainio V, Halttunen J, Haapiainen R, Kivilaakso E, Nevalainen T. Source: Pancreas. 1999 January; 18(1): 21-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9888656

•

Balthazar computed tomography severity index is superior to Ranson criteria and APACHE II and III scoring systems in predicting acute pancreatitis outcome. Author(s): Chatzicostas C, Roussomoustakaki M, Vardas E, Romanos J, Kouroumalis EA. Source: Journal of Clinical Gastroenterology. 2003 March; 36(3): 253-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12590238

•

Baseline hypoxemia as a prognostic marker for pulmonary complications and outcome in patients with acute pancreatitis. Author(s): Polyzogopoulou E, Bikas C, Danikas D, Koutras A, Kalfarentzos F, Gogos CA. Source: Digestive Diseases and Sciences. 2004 January; 49(1): 150-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14992450

•

Behavior of serum interleukin 12 in human acute pancreatitis. Author(s): Pezzilli R, Miniero R, Cappelletti O, Barakat B. Source: Pancreas. 1999 April; 18(3): 247-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10206482

•

Bifid pancreas. An unusual anomaly associated with acute pancreatitis. Author(s): Krishnamurty VS, Rajendran S, Korsten MA. Source: International Journal of Pancreatology : Official Journal of the International Association of Pancreatology. 1994 October-December; 16(2-3): 179-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7868944

Studies

33

•

Biliary sludge and acute pancreatitis. Author(s): Lee SP. Source: Hosp Pract (Off Ed). 1994 May 15; 29(5): 45-52. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8175937

•

Bilirubinate granules: main pathologic bile component in patients with idiopathic acute pancreatitis. Author(s): Perez-Martin G, Gomez-Cerezo J, Codoceo R, Olveira A, Conde P, Garces MC, Barbado FJ, Vazquez JJ. Source: The American Journal of Gastroenterology. 1998 March; 93(3): 360-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9517640

•

Biochemical evaluation of patients with acute pancreatitis. Author(s): Ignjatovic S, Majkic-Singh N, Mitrovic M, Gvozdenovic M. Source: Clinical Chemistry and Laboratory Medicine : Cclm / Fescc. 2000 November; 38(11): 1141-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11156345

•

Biochemical model of logistic regression for early prediction of the etiology of acute pancreatitis. Author(s): Tourne I, Viedma JA, Perez-Mateo M. Source: Rev Esp Enferm Dig. 1997 December; 89(12): 885-96. English, Spanish. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9494376

•

Biochemical parameters in the early differentiation of the etiology of acute pancreatitis. Author(s): Stimac D, Rubinic M, Lenac T, Kovac D, Vcev A, Miletic D. Source: The American Journal of Gastroenterology. 1996 November; 91(11): 2355-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8931417

•

Blood concentrations of polymorphonuclear leucocyte elastase and interleukin-6 are indicators for the occurrence of multiple organ failures at the early stage of acute pancreatitis. Author(s): Ikei S, Ogawa M, Yamaguchi Y. Source: Journal of Gastroenterology and Hepatology. 1998 December; 13(12): 1274-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9918438

•

Blood tests for detection of alcoholic cause of acute pancreatitis. Author(s): Jaakkola M, Sillanaukee P, Lof K, Koivula T, Nordback I. Source: Lancet. 1994 May 28; 343(8909): 1328-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7910327

34

Acute Pancreatitis

•

Blue toe syndrome: a rare complication of acute pancreatitis. Author(s): Bhalla A, Gupta S, Jain AP, Jajoo UN, Gupta OP, Kalantri SP. Source: Jop [electronic Resource] : Journal of the Pancreas. 2003 January; 4(1): 17-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12555011

•

Bockus Lecture: World Congress of Gastroenterology, Los Angeles, CA--October 3, 1994. The management of acute pancreatitis: a critical assessment as Dr. Bockus would have wished. Author(s): Berk JE. Source: The American Journal of Gastroenterology. 1995 May; 90(5): 696-703. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7733071

•

Body composition, physiological function and psychological changes in patients with predicted severe acute pancreatitis. Author(s): Gupta R, Rajani R, Primrose JN, Johnson CD. Source: Pancreatology : Official Journal of the International Association of Pancreatology (Iap). [et Al.]. 2001; 1(1): 58-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12120269

•

Bouveret's syndrome complicated by acute pancreatitis. Author(s): Fenchel RF, Krige JE, Bornman PC. Source: Digestive Surgery. 1999; 16(6): 525-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10805556

•

Buprenorphine or procaine for pain relief in acute pancreatitis. A prospective randomized study. Author(s): Jakobs R, Adamek MU, von Bubnoff AC, Riemann JF. Source: Scandinavian Journal of Gastroenterology. 2000 December; 35(12): 1319-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11199374

•

Calcitonin precursors: early markers of gut barrier dysfunction in patients with acute pancreatitis. Author(s): Ammori BJ, Becker KL, Kite P, Snider RH, Nylen ES, White JC, Barclay GR, Larvin M, McMahon MJ. Source: Pancreas. 2003 October; 27(3): 239-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14508129

•

Can roxithromycin and betamethasone induce acute pancreatitis? A case report. Author(s): Renkes P, Petitpain N, Cosserat F, Bangratz S, Trechot P. Source: Jop [electronic Resource] : Journal of the Pancreas. 2003 September; 4(5): 184-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14526130

Studies

35

•

Carbofuran-induced acute pancreatitis. Author(s): Rizos E, Liberopoulos E, Kosta P, Efremidis S, Elisaf M. Source: Jop [electronic Resource] : Journal of the Pancreas. 2004 January; 5(1): 44-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14730122

•

Carcinoid of the ampulla of Vater presenting as acute pancreatitis. Author(s): Mergener K, Gottfried MR, Feldman JM, Branch MS. Source: The American Journal of Gastroenterology. 1996 November; 91(11): 2426-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8931432

•

Childhood acute pancreatitis in a children's hospital. Author(s): Goh SK, Chui CH, Jacobsen AS. Source: Singapore Med J. 2003 September; 44(9): 453-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14740774

•

Chylous cardiac tamponade in acute pancreatitis. Author(s): Arendt T, Bastian A, Lins M, Klause N, Schmidt WE, Folsch UR. Source: Digestive Diseases and Sciences. 1996 October; 41(10): 1972-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8888709

•

Circulating intact parathyroid hormone levels in acute pancreatitis. Author(s): McKay C, Beastall GH, Imrie CW, Baxter JN. Source: The British Journal of Surgery. 1994 March; 81(3): 357-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8173897

•

Clinical effects of continuous high volume hemofiltration on severe acute pancreatitis complicated with multiple organ dysfunction syndrome. Author(s): Wang H, Li WQ, Zhou W, Li N, Li JS. Source: World Journal of Gastroenterology : Wjg. 2003 September; 9(9): 2096-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12970914

•

Clinical evaluation of serum interleukin 10 in patients with acute pancreatitis. Author(s): Han XC, Zhang YC, Wang Y, Jia MK. Source: Hepatobiliary Pancreat Dis Int. 2003 February; 2(1): 135-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14607666

•

Clinical study on nutrition support in patients with severe acute pancreatitis. Author(s): Zhao G, Wang CY, Wang F, Xiong JX. Source: World Journal of Gastroenterology : Wjg. 2003 September; 9(9): 2105-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12970916

36

Acute Pancreatitis

•

Clinical value of lipopolysaccharide-binding protein (LBP) determinations in acute pancreatitis. Author(s): Rau B, Steinbach G, Kruger CM, Baumgart K, Schilling M, Beger HG. Source: Langenbeck's Archives of Surgery / Deutsche Gesellschaft Fur Chirurgie. 2003 July; 388(3): 181-8. Epub 2003 July 11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12856185

•

Colon involvement in acute pancreatitis. Author(s): Chen CY, Lin XZ, Lin CY, Chang TT, Shin JS, Yang CC, Lin PW, Tsai HM. Source: Journal of Clinical Gastroenterology. 1994 April; 18(3): 243-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8034928

•

Compartmentalization of the inflammatory response during acute pancreatitis: correlation with local and systemic complications. Author(s): Dugernier TL, Laterre PF, Wittebole X, Roeseler J, Latinne D, Reynaert MS, Pugin J. Source: American Journal of Respiratory and Critical Care Medicine. 2003 July 15; 168(2): 148-57. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12851244

•

Compartments that cause the real damage in severe acute pancreatitis. Author(s): Raraty MG, Neoptolemos JP. Source: American Journal of Respiratory and Critical Care Medicine. 2003 July 15; 168(2): 141-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12851239

•

Computed tomography and magnetic resonance imaging in the assessment of acute pancreatitis. Author(s): Arvanitakis M, Delhaye M, De Maertelaere V, Bali M, Winant C, Coppens E, Jeanmart J, Zalcman M, Van Gansbeke D, Deviere J, Matos C. Source: Gastroenterology. 2004 March; 126(3): 715-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14988825

•

Controversies in clinical pancreatology. Recurrent "idiopathic" acute pancreatitis: should a laparoscopic cholecystectomy be the first procedure of choice? Author(s): Steinberg WM, Geenen JE, Bradley EL 3rd, Barkin JS. Source: Pancreas. 1996 November; 13(4): 329-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8899791

Studies

37

•

Controversies in clinical pancreatology: should the sphincter of Oddi be measured in patients with idiopathic recurrent acute pancreatitis, and should sphincterotomy be performed if the pressure is high? Author(s): Steinberg WM. Source: Pancreas. 2003 August; 27(2): 118-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12883258

•

Current aspects of the pathophysiology of acute pancreatitis and therapeutic effects of an inflammatory cell infiltration inhibitor. Author(s): Manabe T. Source: Journal of Gastroenterology. 2003; 38(3): 305-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12693385

•

Cytokine release, pancreatic injury, and risk of acute pancreatitis after spinal fusion surgery. Author(s): He Z, Tonb DJ, Dabney KW, Miller F, Shah SA, Brenn BR, Theroux MC, Mehta DI. Source: Digestive Diseases and Sciences. 2004 January; 49(1): 143-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14992449

•

Cytokines (IL-6, IL-8, TNF): early and reliable predictors of severe acute pancreatitis. Author(s): Pooran N, Indaram A, Singh P, Bank S. Source: Journal of Clinical Gastroenterology. 2003 September; 37(3): 263-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12960727

•

Dapsone-induced acute pancreatitis. Author(s): Jha SH, Reddy JA, Dave JK. Source: The Annals of Pharmacotherapy. 2003 October; 37(10): 1438-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14519046

•

Decreased HLA (human leucocyte antigen)-DR expression on peripheral blood monocytes predicts the development of organ failure in patients with acute pancreatitis. Author(s): Mentula P, Kylanpaa-Back ML, Kemppainen E, Takala A, Jansson SE, Kautiainen H, Puolakkainen P, Haapiainen R, Repo H. Source: Clinical Science (London, England : 1979). 2003 October; 105(4): 409-17. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12780344

•

Depletion of serum L-arginine in patients with acute pancreatitis. Author(s): Sandstrom P, Gasslander T, Sundqvist T, Franke J, Svanvik J. Source: Pancreas. 2003 October; 27(3): 261-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14508133

38

Acute Pancreatitis

•

Detection of abnormal union of pancreaticobiliary junction by magnetic resonance cholangiopancreatography in a girl with acute pancreatitis. Author(s): Suzuki R, Shimizu T, Suzuki M, Yamashiro Y. Source: Pediatrics International : Official Journal of the Japan Pediatric Society. 2002 April; 44(2): 183-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11896881

•

Detection of choledocholithiasis by EUS in acute pancreatitis: a prospective evaluation in 100 consecutive patients. Author(s): Liu CL, Lo CM, Chan JK, Poon RT, Lam CM, Fan ST, Wong J. Source: Gastrointestinal Endoscopy. 2001 September; 54(3): 325-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11522972

•

Development and use of a new staging system for severe acute pancreatitis based on a nationwide survey in Japan. Author(s): Ogawa M, Hirota M, Hayakawa T, Matsuno S, Watanabe S, Atomi Y, Otsuki M, Kashima K, Koizumi M, Harada H, Yamamoto M, Nishimori I. Source: Pancreas. 2002 November; 25(4): 325-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12409824

•

Diabetic hypertriglyceridemia-induced acute pancreatitis masquerading as biliary pancreatitis. Author(s): Huang DB, Raskin P. Source: Journal of Diabetes and Its Complications. 2002 March-April; 16(2): 180-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12039403

•

Diagnosis and early management of acute pancreatitis. Author(s): Powell JJ, Parks RW. Source: Hosp Med. 2003 March; 64(3): 150-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12669481

•

Diagnostic value of pancreatic elastase-1 in human acute pancreatitis. Author(s): Wereszczynska-Siemiatkowska U, Jedynak M, Mroczko B, Siemiatkowski A. Source: Arch Immunol Ther Exp (Warsz). 2003; 51(3): 195-200. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12894874

•

Diclofenac reduces the incidence of acute pancreatitis after endoscopic retrograde cholangiopancreatography. Author(s): Oiofinlade O. Source: Gastroenterology. 2004 February; 126(2): 632; Author Reply 632. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14765402

Studies

39

•

Diclofenac reduces the incidence of acute pancreatitis after endoscopic retrograde cholangiopancreatography. Author(s): Murray B, Carter R, Imrie C, Evans S, O'Suilleabhain C. Source: Gastroenterology. 2003 June; 124(7): 1786-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12806612

•

Discrepancies between population-based data and adverse reaction reports in assessing drugs as causes of acute pancreatitis. Author(s): Lancashire RJ, Cheng K, Langman MJ. Source: Alimentary Pharmacology & Therapeutics. 2003 April 1; 17(7): 887-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12656691

•

Do we need a computed tomography examination in all patients with acute pancreatitis within 72 h after admission to hospital for the detection of pancreatic necrosis? Author(s): Lankisch PG, Struckmann K, Assmus C, Lehnick D, Maisonneuve P, Lowenfels AB. Source: Scandinavian Journal of Gastroenterology. 2001 April; 36(4): 432-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11336171

•

Does anion gap predict severity in acute pancreatitis? Author(s): Escofet X, Kang SP, Woods WG, Khan AZ. Source: Journal of Clinical Gastroenterology. 2001 October; 33(4): 343-4. Erratum In: J Clin Gastroenterol 2001 November-December; 33(5): 427. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11588556

•

Does mortality occur early or late in acute pancreatitis? Author(s): Mutinga M, Rosenbluth A, Tenner SM, Odze RR, Sica GT, Banks PA. Source: International Journal of Pancreatology : Official Journal of the International Association of Pancreatology. 2000 October; 28(2): 91-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11128978

•

Drainage for acute pancreatitis. Author(s): Kimura W, Fuse A, Usuba O, Mizutani M, Matsukura A, Makuuchi M. Source: Hepatogastroenterology. 2001 March-April; 48(38): 434-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11379326

•

Duodenal duplication cysts: A rare cause of acute pancreatitis in children. Author(s): Keller MS, Weber TR, Sotelo-Avila C, Brink DS, Luisiri A. Source: Surgery. 2001 July; 130(1): 112-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11436024

40

Acute Pancreatitis

•

Duodenal lesions following severe acute pancreatitis: review of 10 years' clinical experience. Author(s): Chen CY, Lu CL, Chang FY, Lee SD. Source: Hepatogastroenterology. 2001 May-June; 48(39): 869-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11462944

•

Duodenal necrosis associated with acute pancreatitis. Author(s): Takeyama Y, Ueda T, Hori Y, Shinkai M, Ajiki T, Kuroda Y. Source: Pancreas. 2001 March; 22(2): 217-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11249081

•

Dynamic nature of early organ dysfunction determines outcome in acute pancreatitis. Author(s): Buter A, Imrie CW, Carter CR, Evans S, McKay CJ. Source: The British Journal of Surgery. 2002 March; 89(3): 298-302. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11872053

•

Early activation of peripheral lymphocytes in human acute pancreatitis. Author(s): Pezzilli R, Maldini M, Morselli-Labate AM, Barakat B, Romboli E, Beltrandi E, Migliori M, Tomassetti P, Corinaldesi R. Source: Journal of Clinical Gastroenterology. 2003 April; 36(4): 360-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12642746

•

Early assessment of severity in acute pancreatitis. Author(s): Taxonera Samso C. Source: Rev Esp Enferm Dig. 2002 September; 94(9): 515-22. English, Spanish. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12587231

•

Early measurement of procalcitonin does not predict severity in patients with acute pancreatitis. Author(s): Frasquet J, Saez J, Trigo C, Martinez J, Such J, Perez-Mateo M. Source: The British Journal of Surgery. 2003 September; 90(9): 1129-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12945081

•

Early multi-system organ failure associated with acute pancreatitis: a plea for a conservative therapeutic strategy. Author(s): Dugernier T, Reynaert M, Laterre PF. Source: Acta Gastroenterol Belg. 2003 April-June; 66(2): 177-83. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12891929

Studies

41

•

Early physiological response to intensive care as a clinically relevant approach to predicting the outcome in severe acute pancreatitis. Author(s): Flint R, Windsor JA. Source: Archives of Surgery (Chicago, Ill. : 1960). 2004 April; 139(4): 438-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15078714

•

Early prediction of severe acute pancreatitis by urinary trypsinogen activation peptide. Author(s): Liu ZS, Jiang CQ, Qian Q, Sun Q, Fan LF, Ai ZL. Source: Hepatobiliary Pancreat Dis Int. 2002 May; 1(2): 285-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14612286

•

Early severity indexes in acute pancreatitis. Author(s): Johnson CD. Source: Acta Gastroenterol Belg. 2003 April-June; 66(2): 174-6. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12891928

•

Enalapril-associated acute pancreatitis: recurrence after rechallenge. Author(s): Maringhini A, Termini A, Patti R, Ciambra M, Biffarella P, Pagliaro L. Source: The American Journal of Gastroenterology. 1997 January; 92(1): 166-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8995963

•

Endoscopic pancreaticoduodenostomy for treatment of pancreatic duct disconnection because of severe acute pancreatitis. Author(s): Zein CO, Baron TH, Morgan DE. Source: Gastrointestinal Endoscopy. 2003 July; 58(1): 130-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12838241

•

Endoscopic sphincterotomy and recurrence of acute pancreatitis in gallstone patients considered unfit for surgery. Author(s): Uomo G, Manes G, Laccetti M, Cavallera A, Rabitti PG. Source: Pancreas. 1997 January; 14(1): 28-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8981504

•

Endotoxin, cellular immune dysfunction and acute pancreatitis. Author(s): Curley PJ. Source: Annals of the Royal College of Surgeons of England. 1996 November; 78(6): 5315. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8943639

42

Acute Pancreatitis

•

Enteral nutrition during acute pancreatitis: feasibility study of a self-propeeling spiral distal end jejunal tube. Author(s): Karsenti D, Viguier J, Bourlier P, d'alteroche L, Barbieux JP, Metman EH, Dorval E. Source: Gastroenterologie Clinique Et Biologique. 2003 June; 27(6-7): 614-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12910227

•

Enteral nutrition in severe acute pancreatitis: future development. Author(s): Dervenis C. Source: Jop [electronic Resource] : Journal of the Pancreas. 2004 March; 5(2): 60-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15007186

•

Enteral nutrition in treatment of severe acute pancreatitis. Author(s): Shi D, Zhang CW, Jiang JS, Xie ZJ, Zou SC. Source: Hepatobiliary Pancreat Dis Int. 2002 February; 1(1): 146-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14607646

•

Enterolith ileus complicating afferent loop syndrome simulating acute pancreatitis. Author(s): Sarli L, Iusco D, Violi V, Roncoroni L. Source: Int Surg. 2003 July-September; 88(3): 129-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14584766

•

ERCP and acute pancreatitis. Author(s): Fiocca F, Santagati A, Ceci V, Donatelli G, Pasqualini MJ, Moretti MG, Speranza V, Di Giuli M, Minervini S, Sportelli G, Giri S. Source: Eur Rev Med Pharmacol Sci. 2002 January-February; 6(1): 13-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12608652

•

Etiology and age have only a limited influence on the course of acute pancreatitis. Author(s): Lankisch PG, Burchard-Reckert S, Petersen M, Lehnick D, Schirren CA, Stockmann F, Kohler H. Source: Pancreas. 1996 November; 13(4): 344-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8899794

•

Etiology of acute pancreatitis--a multi-center study in Taiwan. Author(s): Chang MC, Su CH, Sun MS, Huang SC, Chiu CT, Chen MC, Lee KT, Lin CC, Lin JT. Source: Hepatogastroenterology. 2003 September-October; 50(53): 1655-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14571809

Studies

43

•

Evaluation of Pankrin, a new serum test for diagnosis of acute pancreatitis. Author(s): Keim V, Teich N, Bodeker H, Mossner J. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 2003 June; 332(1-2): 45-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12763279

•

Evolving concepts in the pathophysiology of acute pancreatitis. Author(s): Zyromski N, Murr MM. Source: Surgery. 2003 March; 133(3): 235-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12660632

•

Factors influencing morbidity and mortality in acute pancreatitis; an analysis of 279 cases. Author(s): de Beaux AC, Palmer KR, Carter DC. Source: Gut. 1995 July; 37(1): 121-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7672660

•

Factors predicting mortality in severe acute pancreatitis. Author(s): Company L, Saez J, Martinez J, Aparicio JR, Laveda R, Grino P, Perez-Mateo M. Source: Pancreatology : Official Journal of the International Association of Pancreatology (Iap). [et Al.]. 2003; 3(2): 144-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12748423

•

Factors predisposing to severe acute pancreatitis: evaluation and prevention. Author(s): Sun B, Li HL, Gao Y, Xu J, Jiang HC. Source: World Journal of Gastroenterology : Wjg. 2003 May; 9(5): 1102-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12717866

•

Failure of the Hong Kong criteria to predict the severity of acute pancreatitis. Author(s): Heath DI, Meng WC, Anderson JH, Leung KL, Lau WY, Li AK. Source: International Journal of Pancreatology : Official Journal of the International Association of Pancreatology. 1997 December; 22(3): 201-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9444551

•

Fatal acute pancreatitis caused by valproic acid. Author(s): Evans RJ, Miranda RN, Jordan J, Krolikowski FJ. Source: The American Journal of Forensic Medicine and Pathology : Official Publication of the National Association of Medical Examiners. 1995 March; 16(1): 62-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7771387

44

Acute Pancreatitis

•

Fatal acute pancreatitis with cystic formation in reactive systemic AA amyloidosis secondary to rheumatoid arthritis. Author(s): Matsuda M, Sakurai S, Suzuki A, Kadoya M, Ikeda S. Source: Intern Med. 2003 September; 42(9): 888-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14518683

•

Fatal acute pancreatitis. Characteristics of patients never reaching hospital. Author(s): Andersson R, Andren-Sandberg A. Source: Pancreatology : Official Journal of the International Association of Pancreatology (Iap). [et Al.]. 2003; 3(1): 64-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12649566

•

Fatal outcome in acute pancreatitis: its occurrence and early prediction. Author(s): Blum T, Maisonneuve P, Lowenfels AB, Lankisch PG. Source: Pancreatology : Official Journal of the International Association of Pancreatology (Iap). [et Al.]. 2001; 1(3): 237-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12120201

•

Fatal sepsis associated with acute pancreatitis caused by Moraxella catarrhalis in a child. Author(s): Ohkusu K, Nakamura A, Horie H, Udagawa A. Source: The Pediatric Infectious Disease Journal. 2001 September; 20(9): 914-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11734777

•

Fibrotic stricture of the extrapancreatic biliary tract: a new complication of acute pancreatitis. Two cases. Author(s): Delcenserie R, Joly JP, Lenne C, Kannoun MM, Sevestre H, Capron JP, Dupas JL. Source: Pancreas. 1995 January; 10(1): 100-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7899453

•

Flexible approach to nutritional support in severe acute pancreatitis. Author(s): De Beaux AC, Plester C, Fearon KC. Source: Nutrition (Burbank, Los Angeles County, Calif.). 1994 May-June; 10(3): 246-8; Discussion 249. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7919677

•

Formalized therapeutic guideline for hyperlipidemic severe acute pancreatitis. Author(s): Mao EQ, Tang YQ, Zhang SD. Source: World Journal of Gastroenterology : Wjg. 2003 November; 9(11): 2622-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14606112

Studies

45

•

Frank Brooks memorial Lecture: The early intraacinar cell events which occur during acute pancreatitis. Author(s): Steer ML. Source: Pancreas. 1998 July; 17(1): 31-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9667517

•

Frequency and risk factors of recurrent pain during refeeding in patients with acute pancreatitis: a multivariate multicentre prospective study of 116 patients. Author(s): Levy P, Heresbach D, Pariente EA, Boruchowicz A, Delcenserie R, Millat B, Moreau J, Le Bodic L, de Calan L, Barthet M, Sauvanet A, Bernades P. Source: Gut. 1997 February; 40(2): 262-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9071942

•

Fulminant acute pancreatitis and infected necrosis: results of open management of the abdomen and "planned" reoperations. Author(s): Bosscha K, Hulstaert PF, Hennipman A, Visser MR, Gooszen HG, van Vroonhoven TJ, v d Werken C. Source: Journal of the American College of Surgeons. 1998 September; 187(3): 255-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9740182

•

Fungaemia due to Candida pelliculosa in a case of acute pancreatitis. Author(s): Neumeister B, Rockemann M, Marre R. Source: Mycoses. 1992 November-December; 35(11-12): 309-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1302804

•

Fungal infections in patients with severe acute pancreatitis and the use of prophylactic therapy. Author(s): De Waele JJ, Vogelaers D, Blot S, Colardyn F. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 2003 July 15; 37(2): 208-13. Epub 2003 Jul 09. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12856213

•

Further evidence for endothelin as an important mediator of pancreatic and intestinal ischemia in severe acute pancreatitis. Author(s): Inoue K, Hirota M, Kimura Y, Kuwata K, Ohmuraya M, Ogawa M. Source: Pancreas. 2003 April; 26(3): 218-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12657945

•

Gabexate mesilate in acute pancreatitis: miracle or mirage? Author(s): Bradley EL 3rd. Source: Dig Liver Dis. 2001 January-February; 33(1): 12-3. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11303968

46

Acute Pancreatitis

•

Gabexate mesilate in acute pancreatitis: neither a miracle nor a mirage, merely the search of optimal dosage. Author(s): Pezzilli R. Source: Dig Liver Dis. 2001 August-September; 33(6): 502. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11572579

•

Gadolinium arteriography complicated by acute pancreatitis and acute renal failure. Author(s): Schenker MP, Solomon JA, Roberts DA. Source: Journal of Vascular and Interventional Radiology : Jvir. 2001 March; 12(3): 393. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11287523

•

Gallstones, the choledochoduodenal junction and initiation of acute pancreatitis: are two stones the culprits rather than one stone? Author(s): Arendt T, Monig H, Stuber E, Katsoulis S, Folsch UR. Source: Medical Hypotheses. 2000 April; 54(4): 570-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10859640

•

Gastric colonisation, intestinal permeability and septic morbidity in acute pancreatitis. Author(s): McNaught CE, Woodcock NP, Mitchell CJ, Rowley G, Johnstone D, MacFie J. Source: Pancreatology : Official Journal of the International Association of Pancreatology (Iap). [et Al.]. 2002; 2(5): 463-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12378114

•

Gastric intramucosal pH predicts death in severe acute pancreatitis. Author(s): Bonham MJ, Abu-Zidan FM, Simovic MO, Windsor JA. Source: The British Journal of Surgery. 1997 December; 84(12): 1670-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9448612

•

Gastric tonometry in assessing splanchnic tissue perfusion in acute pancreatitis. Author(s): Juvonen PO, Alhava EM, Takala JA. Source: Scandinavian Journal of Gastroenterology. 2000 March; 35(3): 318-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10766328

•

Gastrointestinal bleeding due to acute pancreatitis. Author(s): Verger P, Gruau M, Dhunnoo K, Blais J. Source: Endoscopy. 1998 September; 30(7): S87. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9826163

Studies

47

•

Gastrointestinal case of the day. Pseudoaneurysm of the left gastric artery as a complication of acute pancreatitis. Author(s): Smith RE, Fontanez-Garcia D, Plavsic BM. Source: Radiographics : a Review Publication of the Radiological Society of North America, Inc. 1999 September-October; 19(5): 1390-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10489192

•

Gastrointestinal disorders of the critically ill. Shock and acute pancreatitis. Author(s): Isenmann R, Henne-Bruns D, Adler G. Source: Best Practice & Research. Clinical Gastroenterology. 2003 June; 17(3): 345-55. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12763500

•

Gastrointestinal dysmotility in patients with acute pancreatitis. Author(s): Wang X, Gong Z, Wu K, Wang B, Yuang Y. Source: Journal of Gastroenterology and Hepatology. 2003 January; 18(1): 57-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12519225

•

Gastrointestinal mucosal lesions in patients with acute pancreatitis. Author(s): Lin CK, Wang ZS, Lai KH, Lo GH, Hsu PI. Source: Zhonghua Yi Xue Za Zhi (Taipei). 2002 June; 65(6): 275-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12201568

•

Gatifloxacin-induced hepatotoxicity and acute pancreatitis. Author(s): Cheung O, Chopra K, Yu T, Nalesnik MA, Amin S, Shakil AO. Source: Annals of Internal Medicine. 2004 January 6; 140(1): 73-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14706991

•

Glutamine-supplemented total parenteral nutrition reduces blood mononuclear cell interleukin-8 release in severe acute pancreatitis. Author(s): de Beaux AC, O'Riordain MG, Ross JA, Jodozi L, Carter DC, Fearon KC. Source: Nutrition (Burbank, Los Angeles County, Calif.). 1998 March; 14(3): 261-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9583368

•

Guidelines for the management of acute pancreatitis. Author(s): Toouli J, Brooke-Smith M, Bassi C, Carr-Locke D, Telford J, Freeny P, Imrie C, Tandon R; Working Party of the Program Commitee of the Bangkok World Congress of Gastroenterology 2002. Source: Journal of Gastroenterology and Hepatology. 2002 February; 17 Suppl: S15-39. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12000591

48

Acute Pancreatitis

•

Guidelines for treatment of acute pancreatitis. Author(s): Andrulli A, Perri F, Annese V. Source: Gut. 1999 April; 44(4): 579-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10366292

•

Guidelines for treatment of severe acute pancreatitis. Author(s): Wu XN. Source: Hepatobiliary Pancreat Dis Int. 2002 August; 1(3): 446-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14607725

•

Gut barrier dysfunction in experimental acute pancreatitis. Author(s): Andersson R, Wang XD. Source: Ann Acad Med Singapore. 1999 January; 28(1): 141-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10374040

•

Gut barrier dysfunction in patients with acute pancreatitis. Author(s): Ammori BJ. Source: Journal of Hepato-Biliary-Pancreatic Surgery. 2002; 9(4): 411-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12483261

•

Gut permeability in patients with acute pancreatitis. Author(s): Juvonen PO, Alhava EM, Takala JA. Source: Scandinavian Journal of Gastroenterology. 2000 December; 35(12): 1314-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11199373

•

Haemobilia causing acute pancreatitis after percutaneous liver biopsy: diagnosis by magnetic resonance cholangiopancreatography. Author(s): Asselah T, Condat B, Sibert A, Rivet P, Lebray P, Bernuau J, Benhamou JP, Erlinger S, Marcellin P, Valla D. Source: European Journal of Gastroenterology & Hepatology. 2001 July; 13(7): 877-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11474321

•

Has blood glucose level measured on admission to hospital in a patient with acute pancreatitis any prognostic value? Author(s): Lankisch PG, Blum T, Bruns A, Droge M, Brinkmann G, Struckmann K, Nauck M, Maisonneuve P, Lowenfels AB. Source: Pancreatology : Official Journal of the International Association of Pancreatology (Iap). [et Al.]. 2001; 1(3): 224-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12120199

Studies

49

•

Hepatitis A and acute pancreatitis. Author(s): Sood A, Midha V. Source: J Assoc Physicians India. 1999 July; 47(7): 736-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10778600

•

Hepatobiliary and pancreatic: a woman with recurrent idiopathic acute pancreatitis. Intraductal papillary mucinous tumor of the pancreas. Author(s): Mosca S, Bottino V, Molino C. Source: Journal of Gastroenterology and Hepatology. 2001 September; 16(9): 1070, 1075. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11595076

•

Hereditary pancreatitis--a rare differential diagnosis in patients with menstruationassociated recurrent acute pancreatitis: a case report. Author(s): Heinig J, Greb RR, Kiesel L, Bass S, Simon P. Source: Gynecological Endocrinology : the Official Journal of the International Society of Gynecological Endocrinology. 2004 January; 18(1): 47-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15106365

•

Hiatal hernia with pancreatic volvulus: a rare cause of acute pancreatitis. Author(s): Chevallier P, Peten E, Pellegrino C, Souci J, Motamedi JP, Padovani B. Source: Ajr. American Journal of Roentgenology. 2001 August; 177(2): 373-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11461866

•

High dose octreotide in the management of acute pancreatitis. Author(s): Karakoyunlar O, Sivrel E, Tanir N, Denecli AG. Source: Hepatogastroenterology. 1999 May-June; 46(27): 1968-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10430379

•

High early mortality rate from acute pancreatitis in Scotland, 1984-95. Author(s): Woodcock S, Siriwardena A. Source: The British Journal of Surgery. 2000 March; 87(3): 379-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10718974

•

High signal peripancreatic fat on fat-suppressed spoiled gradient echo imaging in acute pancreatitis: preliminary evaluation of the prognostic significance. Author(s): Martin DR, Karabulut N, Yang M, McFadden DW. Source: Journal of Magnetic Resonance Imaging : Jmri. 2003 July; 18(1): 49-58. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12815639

50

Acute Pancreatitis

•

High, not low, amylase and lipase levels indicate severe acute pancreatitis! Author(s): Lankisch PG, Petersen M, Gottesleben F. Source: Zeitschrift Fur Gastroenterologie. 1994 April; 32(4): 213-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7517087

•

HLA-DR expression in acute pancreatitis. Author(s): Richter A, Nebe T, Wendl K, Schuster K, Klaebisch G, Quintel M, Lorenz D, Post S, Trede M. Source: The European Journal of Surgery = Acta Chirurgica. 1999 October; 165(10): 94751. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10574102

•

How hemolysis causes acute pancreatitis. Author(s): Saruc M, Ozden N, Yuceyar H. Source: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2002 December; 8(12): Le51-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12546022

•

How we do it: Acute pancreatitis. Author(s): Horton KM. Source: Critical Reviews in Computed Tomography. 2003; 44(2): 63-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12757312

•

Human leukocyte antigen-DR expression on peripheral monocytes as a predictive marker of sepsis during acute pancreatitis. Author(s): Satoh A, Miura T, Satoh K, Masamune A, Yamagiwa T, Sakai Y, Shibuya K, Takeda K, Kaku M, Shimosegawa T. Source: Pancreas. 2002 October; 25(3): 245-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12370535

•

Hydronephrosis associated with acute pancreatitis. Author(s): Takeyama Y, Ueda T, Hori Y, Takase K, Fukumoto S, Kuroda Y. Source: Pancreas. 2001 August; 23(2): 218-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11484926

•

Hypertriglyceridemia, acute pancreatitis, and diabetic ketoacidosis possibly associated with mirtazapine therapy: a case report. Author(s): Chen JL, Spinowitz N, Karwa M. Source: Pharmacotherapy. 2003 July; 23(7): 940-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12885107

Studies

51

•

Hypertriglyceridemia-induced acute pancreatitis--treatment with heparin and insulin. Author(s): Monga A, Arora A, Makkar RP, Gupta AK. Source: Indian J Gastroenterol. 2003 May-June; 22(3): 102-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12839385

•

Hypocalcemia in patients with acute pancreatitis: a putative role for systemic endotoxin exposure. Author(s): Ammori BJ, Barclay GR, Larvin M, McMahon MJ. Source: Pancreas. 2003 April; 26(3): 213-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12657944

•

Hypocaloric jejunal feeding is better than total parenteral nutrition in acute pancreatitis: results of a randomized comparative study. Author(s): Abou-Assi S, Craig K, O'Keefe SJ. Source: The American Journal of Gastroenterology. 2002 September; 97(9): 2255-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12358242

•

Hypothermia and acute pancreatitis: myth or reality? Author(s): Stiff RE, Morris-Stiff GJ, Torkington J. Source: Journal of the Royal Society of Medicine. 2003 May; 96(5): 228-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12724432

•

IAP guidelines in acute pancreatitis. Author(s): Sarr MG. Source: Digestive Surgery. 2003; 20(1): 1-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12846213

•

Idiopathic acute pancreatitis. Author(s): Kim HJ, Kim MH, Bae JS, Lee SS, Seo DW, Lee SK. Source: Journal of Clinical Gastroenterology. 2003 September; 37(3): 238-50. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12960724

•

Imaging changes of the pancreas and the occasion of refeeding in patients with acute pancreatitis. Author(s): Qin RY, Qiu FZ. Source: Hepatobiliary Pancreat Dis Int. 2002 May; 1(2): 290-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14612287

•

Immune function early in acute pancreatitis. Author(s): Wyllie JH, Myint F. Source: The British Journal of Surgery. 1996 October; 83(10): 1480-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8944482

52

Acute Pancreatitis

•

Immune function in patients with acute pancreatitis. Author(s): Uehara S, Gothoh K, Handa H, Tomita H, Tomita Y. Source: Journal of Gastroenterology and Hepatology. 2003 April; 18(4): 363-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12653883

•

Incidence, etiology, and impact of Fever in patients with acute pancreatitis. Author(s): Bohidar NP, Garg PK, Khanna S, Tandon RK. Source: Pancreatology : Official Journal of the International Association of Pancreatology (Iap). [et Al.]. 2003; 3(1): 9-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12649559

•

Increased nitric oxide excretion in patients with severe acute pancreatitis: evidence of an endotoxin mediated inflammatory response? Author(s): Rahman SH, Ammori BJ, Larvin M, McMahon MJ. Source: Gut. 2003 February; 52(2): 270-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12524412

•

Indications for surgery in severe acute pancreatitis. Author(s): McFadden DW, Reber HA. Source: International Journal of Pancreatology : Official Journal of the International Association of Pancreatology. 1994 April; 15(2): 83-90. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8071574

•

Infected necrosis complicating acute pancreatitis: experience with 131 cases. Author(s): Bhansali SK, Shah SC, Desai SB, Sunawala JD. Source: Indian J Gastroenterol. 2003 January-February; 22(1): 7-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12617444

•

Infectious causes of acute pancreatitis. Author(s): Parenti DM, Steinberg W, Kang P. Source: Pancreas. 1996 November; 13(4): 356-71. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8899796

•

Influence of etiology on the course and outcome of acute pancreatitis. Author(s): Uhl W, Isenmann R, Curti G, Vogel R, Beger HG, Buchler MW. Source: Pancreas. 1996 November; 13(4): 335-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8899793

Studies

53

•

Influence of severe underlying pathology and hypovolemic shock on the development of acute pancreatitis in children. Author(s): Berney T, Belli D, Bugmann P, Beghetti M, Morel P, LeCoultre C. Source: Journal of Pediatric Surgery. 1996 September; 31(9): 1256-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8887096

•

Influence of somatostatin in the evolution of acute pancreatitis. A prospective randomized study. Author(s): Luengo L, Vicente V, Gris F, Coronas JM, Escuder J, Ramon Gomez J, Castellote JM. Source: International Journal of Pancreatology : Official Journal of the International Association of Pancreatology. 1994 April; 15(2): 139-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7915294

•

Interleukin 18 levels reflect the severity of acute pancreatitis. Author(s): Endo S, Inoue Y, Fujino Y, Wakabayashi G, Inada K, Sato S. Source: Res Commun Mol Pathol Pharmacol. 2001; 110(5-6): 285-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12889520

•

Interleukin-6 is a useful marker for early prediction of the severity of acute pancreatitis. Author(s): Inagaki T, Hoshino M, Hayakawa T, Ohara H, Yamada T, Yamada H, Iida M, Nakazawa T, Ogasawara T, Uchida A, Hasegawa C, Miyaji M, Takeuchi T. Source: Pancreas. 1997 January; 14(1): 1-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8981500

•

Intestinal hypoperfusion contributes to gut barrier failure in severe acute pancreatitis. Author(s): Rahman SH, Ammori BJ, Holmfield J, Larvin M, McMahon MJ. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2003 January; 7(1): 26-35; Discussion 35-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12559182

•

Intrahepatic hemorrhage and subcapsular hematoma developing in acute pancreatitis. Author(s): Lin CK, Chen CH, Yeh CH, Lin SL, Tsang YM, Sheu JC. Source: Hepatogastroenterology. 2003 March-April; 50(50): 571-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12749275

•

Intramural duodenal hematoma and acute pancreatitis. Author(s): Bodnar Z, Varvolgyi C. Source: Endoscopy. 2003 August; 35(8): 708; Author Reply 708. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12929071

54

Acute Pancreatitis

•

Intravenous n-acetylcysteine, ascorbic acid and selenium-based anti-oxidant therapy in severe acute pancreatitis. Author(s): Virlos IT, Mason J, Schofield D, McCloy RF, Eddleston JM, Siriwardena AK. Source: Scandinavian Journal of Gastroenterology. 2003 December; 38(12): 1262-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14750647

•

Is site of necrosis in acute pancreatitis a predictor of outcome? Author(s): Blazeby JM, Cooper MJ. Source: Lancet. 1996 October 19; 348(9034): 1044. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8874449

•

Jejunal feeding in necrotising acute pancreatitis--a retrospective study. Author(s): Hamvas J, Schwab R, Pap A. Source: Acta Chir Hung. 1999; 38(2): 177-85. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10596325

•

Jejunal perforation mimicking acute pancreatitis in a patient with systemic lupus erythematosus: case report. Author(s): Doyle GJ, Pugash RA, Clark JA, Mustard R. Source: Canadian Association of Radiologists Journal = Journal L'association Canadienne Des Radiologistes. 1999 June; 50(3): 159-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10405646

•

Kallikrein-kinin system in acute pancreatitis: potential of B(2)-bradykinin antagonists and kallikrein inhibitors. Author(s): Griesbacher T. Source: Pharmacology. 2000 April; 60(3): 113-20. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10754447

•

Ketorolac tromethamine-induced acute pancreatitis. Author(s): Goyal SB, Goyal RS. Source: Archives of Internal Medicine. 1998 February 23; 158(4): 411. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9487239

•

Laboratory diagnostic tests in acute pancreatitis. Author(s): Smotkin J, Tenner S. Source: Journal of Clinical Gastroenterology. 2002 April; 34(4): 459-62. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11907364

Studies

55

•

Lamivudine-induced acute pancreatitis in a patient with decompensated Hbv-related chronic liver disease. Author(s): Soylu AR, Dokmeci G, Tezel A, Cakir B, Umit H, Karahan N, Amuca H. Source: Journal of Clinical Gastroenterology. 2004 February; 38(2): 134. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14745288

•

Laparoscopic management of severe acute pancreatitis. Author(s): Zhou ZG, Zheng YC, Shu Y, Hu WM, Tian BL, Li QS, Zhang ZD. Source: Pancreas. 2003 October; 27(3): E46-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14508140

•

Laparoscopic treatment of secondary infected pancreatic collections after an acute pancreatitis: two cases. Author(s): el Yassini AE, Hoebeke Y, Keuleneer RD. Source: Acta Chir Belg. 1996 September-October; 96(5): 226-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8950385

•

Laparoscopic treatment of severe acute pancreatitis. Author(s): Kjossev KT, Losanoff JE. Source: Surgical Endoscopy. 2001 October; 15(10): 1239-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11727121

•

Late mortality in patients with severe acute pancreatitis. Author(s): Senapati PS, Ammori BJ. Source: The British Journal of Surgery. 2002 April; 89(4): 491; Author Reply 491. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11952601

•

Late mortality in patients with severe acute pancreatitis. Author(s): Gloor B, Muller CA, Worni M, Martignoni ME, Uhl W, Buchler MW. Source: The British Journal of Surgery. 2001 July; 88(7): 975-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11442530

•

Leptin modulates the inflammatory response in acute pancreatitis. Author(s): Konturek PC, Jaworek J, Maniatoglou A, Bonior J, Meixner H, Konturek SJ, Hahn EG. Source: Digestion. 2002; 65(3): 149-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12138320

56

Acute Pancreatitis

•

Letter 1: Randomized clinical trial of specific lactobacillus and fibre supplement to early enteral nutrition in patients with acute pancreatitis (Br J Surg 2002; 89: 11031107). Author(s): Weale R, Edwards A. Source: The British Journal of Surgery. 2003 January; 90(1): 122-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12520591

•

Letter 2: Randomized clinical trial of specific lactobacillus and fibre supplement to early enteral nutrition in patients with acute pancreatitis (Br J Surg 2002; 89: 11031107). Author(s): Rahman SH, Catton JA, McMahon MJ. Source: The British Journal of Surgery. 2003 January; 90(1): 123. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12520593

•

Levels of leukocyte proteases in plasma and peritoneal exudate in severe, acute pancreatitis. Author(s): Bergenfeldt M, Berling R, Ohlsson K. Source: Scandinavian Journal of Gastroenterology. 1994 April; 29(4): 371-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8047815

•

Levels of the chemokines growth-related oncogene alpha and epithelial neutrophilactivating protein 78 are raised in patients with severe acute pancreatitis (Br J Surg 2002; 89: 566-72). Author(s): Makhija R, Kingsnorth AN. Source: The British Journal of Surgery. 2002 September; 89(9): 1194. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12190691

•

Levels of the chemokines growth-related oncogene alpha and epithelial neutrophilactivating protein 78 are raised in patients with severe acute pancreatitis. Author(s): Shokuhi S, Bhatia M, Christmas S, Sutton R, Neoptolemos JP, Slavin J. Source: The British Journal of Surgery. 2002 May; 89(5): 566-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11972545

•

Lexipafant and acute pancreatitis: a critical appraisal of the clinical trials. Author(s): Abu-Zidan FM, Windsor JA. Source: The European Journal of Surgery = Acta Chirurgica. 2002; 168(4): 215-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12440758

•

Liver damages during experimental acute pancreatitis. Author(s): Mozzhelin ME, Vengerovskii AI, Sukhodolo IV, Saratikov AS. Source: Bulletin of Experimental Biology and Medicine. 2001 July; 132(1): 647-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11687843

Studies

57

•

Local renin-angiotensin system in the pancreas: the significance in acute pancreatitis. Author(s): Lai PB. Source: Jop [electronic Resource] : Journal of the Pancreas. 2001 January; 2(1): 13-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11862017

•

Local renin-angiotensin system in the pancreas: the significance of changes by chronic hypoxia and acute pancreatitis. Author(s): Leung PS. Source: Jop [electronic Resource] : Journal of the Pancreas. 2001 January; 2(1): 3-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11862015

•

Long-term health-related quality of life in survivors of severe acute pancreatitis. Author(s): Halonen KI, Pettila V, Leppaniemi AK, Kemppainen EA, Puolakkainen PA, Haapiainen RK. Source: Intensive Care Medicine. 2003 May; 29(5): 782-6. Epub 2003 April 09. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12684744

•

Long-term results of endoscopic management of pancreas divisum with recurrent acute pancreatitis. Author(s): Heyries L, Barthet M, Delvasto C, Zamora C, Bernard JP, Sahel J. Source: Gastrointestinal Endoscopy. 2002 March; 55(3): 376-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11868012

•

Lung injury in acute pancreatitis: mechanisms, prevention, and therapy. Author(s): Shields CJ, Winter DC, Redmond HP. Source: Current Opinion in Critical Care. 2002 April; 8(2): 158-63. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12386518

•

Macrophage migration inhibitory factor is a critical mediator of severe acute pancreatitis. Author(s): Sakai Y, Masamune A, Satoh A, Nishihira J, Yamagiwa T, Shimosegawa T. Source: Gastroenterology. 2003 March; 124(3): 725-36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12612911

•

Magnetic resonance imaging of acute pancreatitis: the pancreatogram. Author(s): Gosset J, Deviere J, Matos C. Source: Jop [electronic Resource] : Journal of the Pancreas. 2004 January; 5(1): 48-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14730123

58

Acute Pancreatitis

•

Malignant pheochromocytoma masquerading as acute pancreatitis--a rare but potentially lethal occurrence. Author(s): Perrier NA, van Heerden JA, Wilson DJ, Warner MA. Source: Mayo Clinic Proceedings. 1994 April; 69(4): 366-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7513373

•

Management of acute pancreatitis. Author(s): O'Reilly DA, Kingsnorth AN. Source: Bmj (Clinical Research Ed.). 2004 April 24; 328(7446): 968-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15105303

•

Management of infected necrosis secondary to acute pancreatitis: a balanced role for minimal access techniques. Author(s): Carter R. Source: Pancreatology : Official Journal of the International Association of Pancreatology (Iap). [et Al.]. 2003; 3(2): 133-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12774803

•

Management of infection in acute pancreatitis. Author(s): Hartwig W, Werner J, Uhl W, Buchler MW. Source: Journal of Hepato-Biliary-Pancreatic Surgery. 2002; 9(4): 423-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12483263

•

Management of severe acute pancreatitis. Author(s): Yousaf M, McCallion K, Diamond T. Source: The British Journal of Surgery. 2003 April; 90(4): 407-20. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12673741

•

Management of sterile necrosis in acute pancreatitis: is surgery a necessity? Author(s): Collawn C, Barkin JS. Source: The American Journal of Gastroenterology. 1996 November; 91(11): 2443-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8931442

•

Matrix metalloproteinase-1 and cytokines in patients with acute pancreatitis. Author(s): Nakae H, Endo S, Inoue Y, Fujino Y, Wakabayashi G, Inada K, Sato S. Source: Pancreas. 2003 March; 26(2): 134-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12604910

Studies

59

•

Microcirculatory dysfunction in acute pancreatitis. A new concept of pathogenesis involving vasomotion-associated arteriolar constriction and dilation. Author(s): Vollmar B, Menger MD. Source: Pancreatology : Official Journal of the International Association of Pancreatology (Iap). [et Al.]. 2003; 3(3): 181-90. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12817573

•

Minimal-access approaches to complications of acute pancreatitis and benign neoplasms of the pancreas. Author(s): Kellogg TA, Horvath KD. Source: Surgical Endoscopy. 2003 November; 17(11): 1692-704. Epub 2003 September 10. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12958685

•

Minute pancreatic carcinoma with initial symptom of acute pancreatitis. Author(s): Imamura M, Asahi S, Yamauchi H, Tadokoro K, Suzuki H. Source: Journal of Hepato-Biliary-Pancreatic Surgery. 2002; 9(5): 632-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12541052

•

Mirtazapine: another drug responsible for drug-induced acute pancreatitis? A letter of warning. Author(s): Lankisch PG, Werner HM. Source: Pancreas. 2003 March; 26(2): 211. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12604923

•

Modern phase-specific management of acute pancreatitis. Author(s): Werner J, Uhl W, Hartwig W, Hackert T, Muller C, Strobel O, Buchler MW. Source: Digestive Diseases (Basel, Switzerland). 2003; 21(1): 38-45. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12837999

•

Natural history of organ failure in acute pancreatitis. Author(s): McKay CJ, Buter A. Source: Pancreatology : Official Journal of the International Association of Pancreatology (Iap). [et Al.]. 2003; 3(2): 111-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12748419

•

Necrotic stenosis of the right colon secondary to acute pancreatitis. Author(s): Chartrand-Lefebvre C, Clermont RJ, Heppell J, Bernard EJ, Prosmanne O. Source: Canadian Journal of Surgery. Journal Canadien De Chirurgie. 1994 April; 37(2): 140-2. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8156467

60

Acute Pancreatitis

•

Necrotizing acute pancreatitis induced by Salmonella typhimurium. Author(s): Blank A, Maybody M, Isom-Batz G, Roslin M, Dillon EH. Source: Digestive Diseases and Sciences. 2003 August; 48(8): 1472-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12924638

•

Neopterin in acute pancreatitis. Author(s): Uomo G, Spada OA, Manes G, Feola B, Misso S, Cavallera A, Rabitti PG. Source: Scandinavian Journal of Gastroenterology. 1996 October; 31(10): 1032-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8898426

•

New-onset QT prolongation and torsades de pointes accompanied by left ventricular dysfunction secondary to acute pancreatitis. Author(s): Mofrad PS, Rashid H, Tracy CM. Source: Pacing and Clinical Electrophysiology : Pace. 2003 August; 26(8): 1765-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12877713

•

No parallel between the biochemical course of acute pancreatitis and morphologic findings. Author(s): Lankisch PG, Haseloff M, Becher R. Source: Pancreas. 1994 March; 9(2): 240-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8190726

•

Non-occlusive mesenteric ischemia and its associated intestinal gangrene in acute pancreatitis. Author(s): Hirota M, Inoue K, Kimura Y, Mizumoto T, Kuwata K, Ohmuraya M, Ishiko T, Beppu T, Ogawa M. Source: Pancreatology : Official Journal of the International Association of Pancreatology (Iap). [et Al.]. 2003; 3(4): 316-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12890994

•

Novel therapeutic targets for acute pancreatitis and associated multiple organ dysfunction syndrome. Author(s): Bhatia M. Source: Current Drug Targets. Inflammation and Allergy. 2002 December; 1(4): 343-51. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14561181

•

Nutritional support in acute pancreatitis. Author(s): Avgerinos C, Delis S, Rizos S, Dervenis C. Source: Digestive Diseases (Basel, Switzerland). 2003; 21(3): 214-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14571094

Studies

61

•

Nutritional support in acute pancreatitis. Author(s): McClave SA. Source: Nestle Nutr Workshop Ser Clin Perform Programme. 2003; (8): 207-15; Discussion 215-21. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12968456

•

Obesity and treatment of diabetes with glyburide may both be risk factors for acute pancreatitis. Author(s): Blomgren KB, Sundstrom A, Steineck G, Wiholm BE. Source: Diabetes Care. 2002 February; 25(2): 298-302. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11815499

•

Olanzapine-induced acute pancreatitis. Author(s): Doucette DE, Grenier JP, Robertson PS. Source: The Annals of Pharmacotherapy. 2000 October; 34(10): 1128-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11054978

•

Onset time of complications in patients with severe acute pancreatitis receiving nonoperative therapy. Author(s): Gong ZY, Tang YQ. Source: Hepatobiliary Pancreat Dis Int. 2002 February; 1(1): 143-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14607645

•

Operative timing and indications for patients with severe acute pancreatitis: report of 172 cases. Author(s): Sun B, Jiang HC, Xun J. Source: Hepatobiliary Pancreat Dis Int. 2002 February; 1(1): 129-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14607641

•

Optimising outcomes in acute pancreatitis. Author(s): Norton ID, Clain JE. Source: Drugs. 2001; 61(11): 1581-91. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11577795

•

Organ failure associated with severe acute pancreatitis. Author(s): Zhu AJ, Shi JS, Sun XJ. Source: World Journal of Gastroenterology : Wjg. 2003 November; 9(11): 2570-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14606099

62

Acute Pancreatitis

•

Outcome analysis of patients with acute pancreatitis by using an artificial neural network. Author(s): Keogan MT, Lo JY, Freed KS, Raptopoulos V, Blake S, Kamel IR, Weisinger K, Rosen MP, Nelson RC. Source: Academic Radiology. 2002 April; 9(4): 410-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11942655

•

Outcome and quality of life of patients with acute pancreatitis requiring intensive care. Author(s): Soran A, Chelluri L, Lee KK, Tisherman SA. Source: The Journal of Surgical Research. 2000 June 1; 91(1): 89-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10816356

•

Outcome of necrosectomy in acute pancreatitis: the case for continued vigilance. Author(s): Beattie GC, Mason J, Swan D, Madhavan KK, Siriwardena AK. Source: Scandinavian Journal of Gastroenterology. 2002 December; 37(12): 1449-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12523596

•

Outcome of open necrosectomy in acute pancreatitis. Author(s): Bassi C, Butturini G, Falconi M, Salvia R, Frigerio I, Pederzoli P. Source: Pancreatology : Official Journal of the International Association of Pancreatology (Iap). [et Al.]. 2003; 3(2): 128-32. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12748421

•

Patent accessory pancreatic duct prevents acute pancreatitis. Author(s): Kamisawa T, Yoshiike M, Egawa N, Nakajima H. Source: The American Journal of Gastroenterology. 2003 December; 98(12): 2807-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14687842

•

Perforation of a gastrojejunal anastomosis due to acute pancreatitis revealed by helical computed tomography. Author(s): Pinto A, Scaglione M, Romano L. Source: Acta Radiologica (Stockholm, Sweden : 1987). 2003 November; 44(6): 572-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14616199

•

Plasma endothelin and nitric oxide levels in patients with acute pancreatitis. Author(s): Zeng XH, Zhu SQ, Zhang XM, Luo WJ, Li SW. Source: Hepatobiliary Pancreat Dis Int. 2002 February; 1(1): 140-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14607644

Studies

63

•

Portal vein erosion and acute abdominal hemorrhage as a complication of acute pancreatitis. Author(s): Ko HS, Anders M, Diehl S, Dominguez E, Lohr M, Duber C. Source: Abdominal Imaging. 2003 September-October; 28(5): 700-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14628880

•

Predictive value of complement activation fragments C3a and sC5b-9 for development of severe disease in patients with acute pancreatitis. Author(s): Gloor B, Stahel PF, Muller CA, Schmidt OI, Buchler MW, Uhl W. Source: Scandinavian Journal of Gastroenterology. 2003 October; 38(10): 1078-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14621284

•

Primary human immunodeficiency virus infection presenting as acute pancreatitis. Author(s): Tyner R, Turett G. Source: Southern Medical Journal. 2004 April; 97(4): 393-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15108835

•

Prognostic value of CT in the early assessment of patients with acute pancreatitis. Author(s): Casas JD, Diaz R, Valderas G, Mariscal A, Cuadras P. Source: Ajr. American Journal of Roentgenology. 2004 March; 182(3): 569-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14975947

•

Prophylactic antibiotic treatment in patients with predicted severe acute pancreatitis: a placebo-controlled, double-blind trial. Author(s): Isenmann R, Runzi M, Kron M, Kahl S, Kraus D, Jung N, Maier L, Malfertheiner P, Goebell H, Beger HG; German Antibiotics in Severe Acute Pancreatitis Study Group. Source: Gastroenterology. 2004 April; 126(4): 997-1004. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15057739

•

Prophylactic antibiotic use in severe acute pancreatitis: hemlock, help, or hype? Author(s): Brown A. Source: Gastroenterology. 2004 April; 126(4): 1195-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15057759

•

Prospective multicentre survey on acute pancreatitis in Italy (ProInf-AISP): results on 1005 patients. Author(s): Cavallini G, Frulloni L, Bassi C, Gabbrielli A, Castoldi L, Costamagna G, De Rai P, Di Carlo V, Falconi M, Pezzilli R, Uomo G; ProInf-AISP Study Group. Source: Dig Liver Dis. 2004 March; 36(3): 205-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15046191

64

Acute Pancreatitis

•

Red blood cells deformability and oxidative stress in acute pancreatitis. Author(s): Chmiel B, Grabowska Bochenek R, Piskorska D, Skorupa A, Cierpka L, Kusmierski S. Source: Clinical Hemorheology and Microcirculation. 2002; 27(3-4): 155-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12454371

•

Redifferentiation and apoptosis of pancreatic cells during acute pancreatitis. Author(s): Iovanna JL. Source: International Journal of Pancreatology : Official Journal of the International Association of Pancreatology. 1996 October; 20(2): 77-84. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8968862

•

Relapses of biliary acute pancreatitis in patients with previous attack of biliary pancreatitis and gallbladder in situ. Author(s): Billi P, Barakat B, D'Imperio N, Pezzilli R. Source: Dig Liver Dis. 2003 September; 35(9): 653-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14563188

•

Results of treating severe acute pancreatitis with gabexate is associated with neutrophil apoptosis activity. Author(s): Chiu DF, Chen JC, Chen HM, Ng CJ, Shyr MH, Chen MF. Source: Hepatogastroenterology. 2003 March-April; 50(50): 553-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12749271

•

Risk factors influencing mortality of patients with severe acute pancreatitis within 24 hours after admission. Author(s): Zhu AJ, Shi JS, Sun XJ. Source: Hepatobiliary Pancreat Dis Int. 2003 August; 2(3): 453-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14599959

•

Risk of acute pancreatitis in users of azathioprine: a population-based case-control study. Author(s): Floyd A, Pedersen L, Nielsen GL, Thorlacius-Ussing O, Sorensen HT. Source: The American Journal of Gastroenterology. 2003 June; 98(6): 1305-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12818274

•

Risk of acute pancreatitis in users of finasteride: a population-based case-control study. Author(s): Floyd A, Pedersen L, Nielsen GL, Thorlacius-Ussing O, Sorensen HT. Source: Journal of Clinical Gastroenterology. 2004 March; 38(3): 276-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15128076

Studies

65

•

Role of cytokines and oxidative stress in the pathophysiology of acute pancreatitis: therapeutical implications. Author(s): Gomez-Cambronero LG, Sabater L, Pereda J, Cassinello N, Camps B, Vina J, Sastre J. Source: Current Drug Targets. Inflammation and Allergy. 2002 December; 1(4): 393-403. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14561185

•

Role of oxygen free radicals in patients with acute pancreatitis. Author(s): Park BK, Chung JB, Lee JH, Suh JH, Park SW, Song SY, Kim H, Kim KH, Kang JK. Source: World Journal of Gastroenterology : Wjg. 2003 October; 9(10): 2266-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14562390

•

Role of the gut in the course of severe acute pancreatitis. Author(s): Ammori BJ. Source: Pancreas. 2003 March; 26(2): 122-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12604908

•

Serum alpha 2-macroglobulin-trypsin complex and early recognition of severe acute pancreatitis after endoscopic retrograde pancreatography. Author(s): Nakae Y, Hayakawa T, Kondo T, Shibata T, Kitagawa M, Sakai Y, Sobajima H, Ishiguro H, Tanikawa M. Source: Journal of Gastroenterology and Hepatology. 1994 May-June; 9(3): 272-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7519897

•

Serum complex of trypsin 2 and alpha 1 antitrypsin as diagnostic and prognostic marker of acute pancreatitis: clinical study in consecutive patients. Author(s): Hedstrom J, Sainio V, Kemppainen E, Haapiainen R, Kivilaakso E, Schroder T, Leinonen J, Stenman UH. Source: Bmj (Clinical Research Ed.). 1996 August 10; 313(7053): 333-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8760740

•

Severe acute pancreatitis associated with acute hepatitis A: a case report. Author(s): Batra Y, Chakravarty S, Bhatt G. Source: Trop Gastroenterol. 2003 January-March; 24(1): 27-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12974212

•

Severe acute pancreatitis due to hepatitis A virus infection in a patient of acute viral hepatitis. Author(s): Khanna S, Vij JC. Source: Trop Gastroenterol. 2003 January-March; 24(1): 25-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12974211

66

Acute Pancreatitis

•

Should enteral feeding be the standard of care for acute pancreatitis? Author(s): Alsolaiman MM, Green JA, Barkin JS. Source: The American Journal of Gastroenterology. 2003 November; 98(11): 2565-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14638366

•

Spontaneous resolution of a pancreatic-colonic fistula after acute pancreatitis. Author(s): Green BT, Mitchell RM, Branch MS. Source: The American Journal of Gastroenterology. 2003 December; 98(12): 2809-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14687844

•

State-of-the-art imaging of acute pancreatitis. Author(s): Mortele KJ, Banks PA, Silverman SG. Source: Jbr-Btr. 2003 July-August; 86(4): 193-208. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14527059

•

Surgical treatment of severe acute pancreatitis: timing of operation is crucial for survival. Author(s): Gotzinger P, Wamser P, Exner R, Schwanzer E, Jakesz R, Fugger R, Sautner T. Source: Surgical Infections. 2003 Summer; 4(2): 205-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12906721

•

Systemic lupus erythematosus as a cause and prognostic factor of acute pancreatitis. Author(s): Pascual-Ramos V, Duarte-Rojo A, Villa AR, Hernandez-Cruz B, AlarconSegovia D, Alcocer-Varela J, Robles-Diaz G. Source: The Journal of Rheumatology. 2004 April; 31(4): 707-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15088295

•

Systemic lupus erythematosus-related acute pancreatitis: a case report. Author(s): Fan HC, Cheng SN, Hua YM, Chu CH, Juan CJ, Lee MY, Hung CH. Source: J Microbiol Immunol Infect. 2003 September; 36(3): 212-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14582568

•

Technetium-99m hexamethylpropylene amine oxime leucocyte scintigraphy in the early course of mild acute pancreatitis following endoscopic retrograde cholangiopancreatography. Author(s): Mortensen JC, Jensen JJ, Thorsgaard N. Source: European Journal of Nuclear Medicine. 1996 November; 23(11): 1460-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8854842

Studies

67

•

The ascites to serum amylase ratio identifies two distinct populations in acute pancreatitis with ascites. Author(s): Haas LS, Gates LK Jr. Source: Pancreatology : Official Journal of the International Association of Pancreatology (Iap). [et Al.]. 2002; 2(2): 100-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12123088

•

The biochemical detection of biliary etiology of acute pancreatitis on admission: a revisit in the modern era of biliary imaging. Author(s): Ammori BJ, Boreham B, Lewis P, Roberts SA. Source: Pancreas. 2003 March; 26(2): E32-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12604925

•

The early increase in intestinal permeability and systemic endotoxin exposure in patients with severe acute pancreatitis is not associated with systemic bacterial translocation: molecular investigation of microbial DNA in the blood. Author(s): Ammori BJ, Fitzgerald P, Hawkey P, McMahon MJ. Source: Pancreas. 2003 January; 26(1): 18-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12499912

•

The soluble interleukin-2 receptor, peripheral blood, and reticulocyte fractions in acute pancreatitis. Author(s): Salomone T, Boni P, Serra C, Morselli-Labate AM, Di Gioia AL, Romboli M, Guariento A. Source: International Journal of Pancreatology : Official Journal of the International Association of Pancreatology. 1996 December; 20(3): 197-203. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9013281

•

The usefulness of laboratory tests in the early assessment of severity of acute pancreatitis. Author(s): Rettally CA, Skarda S, Garza MA, Schenker S. Source: Critical Reviews in Clinical Laboratory Sciences. 2003 April; 40(2): 117-49. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12755453

•

The William Nelson ECG quiz: acute pancreatitis. Author(s): Nelson W. Source: Cardiovasc J S Afr. 2002 March-April; 13(2): 77, 84. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12166358

68

Acute Pancreatitis

•

Therapeutic efficacy of high-dose vitamin C on acute pancreatitis and its potential mechanisms. Author(s): Du WD, Yuan ZR, Sun J, Tang JX, Cheng AQ, Shen DM, Huang CJ, Song XH, Yu XF, Zheng SB. Source: World Journal of Gastroenterology : Wjg. 2003 November; 9(11): 2565-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14606098

•

Thrombotic microangiopathy in acute pancreatitis. Author(s): Bong JJ, Ammori BJ, McMahon MJ, Kumar A, Turney JH, Norfolk DR. Source: Pancreas. 2002 July; 25(1): 107-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12131780

•

Trypsinogen-2 and trypsinogen activation peptide (TAP) in urine of patients with acute pancreatitis. Author(s): Lempinen M, Stenman UH, Finne P, Puolakkainen P, Haapiainen R, Kemppainen E. Source: The Journal of Surgical Research. 2003 May 15; 111(2): 267-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12850473

•

Ultrasonographic splanchnic arterial flow measurement in severe acute pancreatitis. Author(s): Sakagami J, Kataoka K, Sogame Y, Usui N, Mitsuyoshi M. Source: Pancreas. 2002 May; 24(4): 357-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11961488

•

Ultrathin cutting needle biopsy histology in the tissue diagnosis of acute pancreatitis-experimental study and application in a human case. Author(s): He ZJ, Alho H, Harmoinen A, Sand J, Nordback I. Source: International Journal of Surgical Investigation. 2000; 1(5): 441-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11341600

•

Understanding the care of patients with acute pancreatitis. Author(s): Hughes E. Source: Nursing Standard : Official Newspaper of the Royal College of Nursing. 2004 January 14-20; 18(18): 45-52; Quiz 54-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14768233

•

Unraveling the mystery of acute pancreatitis. Author(s): Cole L. Source: Dimensions of Critical Care Nursing : Dccn. 2002 May-June; 21(3): 86-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12042691

Studies

69

•

Unraveling the mystery of acute pancreatitis. Author(s): Cole L. Source: Nursing. 2001 December; 31(12): 58-63; Quiz 64. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11921720

•

Urinary trypsinogen activation peptide is more accurate than hematocrit in determining severity in patients with acute pancreatitis: a prospective study. Author(s): Khan Z, Vlodov J, Horovitz J, Jose RM, Iswara K, Smotkin J, Brown A, Tenner S. Source: The American Journal of Gastroenterology. 2002 August; 97(8): 1973-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12190163

•

Use of antioxidants to treat pain in patients with acute pancreatitis. Author(s): Ladero JM. Source: Rev Esp Enferm Dig. 2000 June; 92(6): 371-4. English, Spanish. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10985096

•

Use of endoscopic naso-pancreatic drainage in the treatment of severe acute pancreatitis. Author(s): Quan ZF, Wang ZM, Li WQ, Li JS. Source: World Journal of Gastroenterology : Wjg. 2003 April; 9(4): 868-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12679951

•

Useful markers for predicting severity and monitoring progression of acute pancreatitis. Author(s): Werner J, Hartwig W, Uhl W, Muller C, Buchler MW. Source: Pancreatology : Official Journal of the International Association of Pancreatology (Iap). [et Al.]. 2003; 3(2): 115-27. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12748420

•

Usefulness of endoscopic ultrasonography in patients with "idiopathic" acute pancreatitis. Author(s): Frossard JL, Sosa-Valencia L, Amouyal G, Marty O, Hadengue A, Amouyal P. Source: The American Journal of Medicine. 2000 August 15; 109(3): 196-200. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10974181

•

Valproate-associated acute pancreatitis in a child with neuronal ceroid lipofuscinosis. Author(s): Talwar D. Source: Journal of Child Neurology. 1994 January; 9(1): 36-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8151078

70

Acute Pancreatitis

•

Value of early blood Th-1 cytokine determination in predicting severity of acute pancreatitis. Author(s): Heresbach D, Letourneur JP, Bahon I, Pagenault M, Guillou YM, Dyard F, Fauchet R, Malledant Y, Bretagne JF, Gosselin M. Source: Scandinavian Journal of Gastroenterology. 1998 May; 33(5): 554-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9648999

•

Variations in implementation of current national guidelines for the treatment of acute pancreatitis: implications for acute surgical service provision. Author(s): Barnard J, Siriwardena AK. Source: Annals of the Royal College of Surgeons of England. 2002 March; 84(2): 79-81. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11995768

•

Varicella infection as a cause of acute pancreatitis in an immunocompetent child. Author(s): Torre JA, Martin JJ, Garcia CB, Polo ER. Source: The Pediatric Infectious Disease Journal. 2000 December; 19(12): 1218-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11144392

•

Vascular complications in acute pancreatitis assessed by color duplex ultrasonography. Author(s): Dorffel T, Wruck T, Ruckert RI, Romaniuk P, Dorffel Q, Wermke W. Source: Pancreas. 2000 August; 21(2): 126-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10975705

•

Vitamin C status in patients with acute pancreatitis. Author(s): Scott P, Bruce C, Schofield D, Shiel N, Braganza JM, McCloy RF. Source: The British Journal of Surgery. 1993 June; 80(6): 750-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8330166

•

Von Hippel-Lindau disease complicated by acute pancreatitis and Evan's syndrome. Author(s): Tenner S, Roston A, Lichtenstein D, Sica G, Carr-Locke D, Banks PA. Source: International Journal of Pancreatology : Official Journal of the International Association of Pancreatology. 1995 December; 18(3): 271-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8708400

•

Wandering spleen presenting as acute pancreatitis in pregnancy. Author(s): Gilman RS, Thomas RL. Source: Obstetrics and Gynecology. 2003 May; 101(5 Pt 2): 1100-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12738115

Studies

71

•

Wegener's granulomatosis with onset of acute pancreatitis and rapid progress. A case report. Author(s): Matsubayashi H, Seki T, Niki S, Mizumura Y, Taguchi Y, Moriyasu F, Go K. Source: Pancreatology : Official Journal of the International Association of Pancreatology (Iap). [et Al.]. 2001; 1(3): 263-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12120205

•

Wernicke's encephalopathy: a complication of acute pancreatitis? Author(s): Lee YD, Lee SO, Lee ST. Source: Hosp Med. 2003 June; 64(6): 372-3. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12833836

•

What is the best biochemical test to diagnose acute pancreatitis? A prospective clinical study. Author(s): Sternby B, O'Brien JF, Zinsmeister AR, DiMagno EP. Source: Mayo Clinic Proceedings. 1996 December; 71(12): 1138-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8945483

•

When should radiologists intervene in management of pancreatic pseudocysts and other complications of acute pancreatitis? Author(s): Wittich GR, vanSonnenberg E. Source: Ajr. American Journal of Roentgenology. 1996 January; 166(1): 211. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8571881

•

Which etiology causes the most severe acute pancreatitis? Author(s): Lankisch PG, Assmus C, Pflichthofer D, Struckmann K, Lehnick D. Source: International Journal of Pancreatology : Official Journal of the International Association of Pancreatology. 1999 October; 26(2): 55-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10597400

•

Why clinical trials might succeed in acute pancreatitis when they failed in septic shock. Author(s): Frossard JL, Morel P, Pastor CM. Source: Jop [electronic Resource] : Journal of the Pancreas. 2003 January; 4(1): 11-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12555010

73

CHAPTER 2. NUTRITION AND ACUTE PANCREATITIS Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and acute pancreatitis.

Finding Nutrition Studies on Acute Pancreatitis 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 “acute pancreatitis” (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.

74

Acute Pancreatitis

The following information is typical of that found when using the “Full IBIDS Database” to search for “acute pancreatitis” (or a synonym): •

Animal model of acute pancreatitis induced by synthetic prooxidant. Author(s): Medical University, Gdansk (Poland) I.N.R.C.A. and Biancalana Mazera Foundation, Ancona (Italy) Ancona University, (Italy) Source: Sledzinski, Z. Stanek, A. Wajda, Z. Wozniak, M. Brunelli, A. Scutti, G. Bertoil, E. Lezoche, E. Polish-Journal-of-Environmental-Studies (Poland). (1998). volume 7(6) page 373.

Additional physician-oriented references include: •

Absence of endogenous interleukin-6 enhances the inflammatory response during acute pancreatitis induced by cerulein in mice. Author(s): Institute of Pharmacology, School of Medicine, University of Messina, Italy. [email protected] Source: Cuzzocrea, S Mazzon, E Dugo, L Centorrino, T Ciccolo, A McDonald, M C de Sarro, A Caputi, A P Thiemermann, C Cytokine. 2002 June 7; 18(5): 274-85 1043-4666

•

Acute pancreatitis after morphine administration. Source: Famularo, G Pozzessere, C Polchi, S De Simone, C Ital-J-Gastroenterol-Hepatol. 1999 Aug-September; 31(6): 522-3 1125-8055

•

Acute pancreatitis in a multi-ethnic population. Author(s): Department of Surgery, Perak College of Medicine, Malaysia. [email protected] Source: Kandasami, P Harunarashid, H Kaur, H Singapore-Med-J. 2002 June; 43(6): 2848 0037-5675

•

Acute pancreatitis secondary to isotretinoin-induced hyperlipidemia. Author(s): St. Anthony Hospital, 608 NW 9th Street, Suite 4100, Oklahoma City, OK 73102, USA. Source: Jamshidi, Mohammad Obermeyer, Robert J Govindaraj, Satish Garcia, Armand Ghani, Abdul J-Okla-State-Med-Assoc. 2002 February; 95(2): 79-80 0030-1876

•

Acute pancreatitis. Hillbrow Hospital experience. Source: D'Egidio, A S-Afr-J-Surg. 1988 December; 26(4): 163-5 0038-2361

•

Acute pancreatitis-induced hypomagnesemia. Author(s): Department of Internal Medicine, Medical School, University of Ioannina, GR-451 10 Ioannina, Greece. Source: Liamis, G Gianoutsos, C Elisaf, M Pancreatology. 2001; 1(1): 74-6 1424-3903

•

Caerulein-induced acute pancreatitis in rats: changes in glycoprotein-composition of subcellular membrane systems in acinar cells. Author(s): Department of Internal Medicine, Philipps-University Marburg, Federal Republic of Germany. Source: Willemer, S Bialek, R Kohler, H Adler, G Histochemistry. 1990; 95(1): 87-96 03015564

•

CFTR gene mutations in patients suffering from acute pancreatitis. Author(s): Department of Human Genetics, Medical University, Lublin, Poland. Source: Kostuch, M Rudzki, S Semczuk, A Kulczycki, L Med-Sci-Monit. 2002 September; 8(9): BR369-72 1234-1010

Nutrition

75

•

Changes of plasma levels of gastrointestinal peptides over the course of acute pancreatitis. Any significance for the pathophysiology and treatment of acute pancreatitis? Author(s): 1st Department of Propedeutic Medicine, University of Athens, Medical School, Athens, Greece. Source: Nikou, G C Giamarellos Bourboulis, E J Toumpanakis, C Arnaoutis, T P Kitsou, E Kyriaki, D Katsilambros, N Hepatogastroenterology. 2002 May-June; 49(45): 706-8 0172-6390

•

Conservative treatment of acute pancreatitis: the use of somatostatin. Author(s): 2nd Department of Internal Medicine-Propaedeutic, Athens University, Evangelismos Hospital, Greece. Source: Ladas, S D Raptis, S A Hepatogastroenterology. 1992 October; 39(5): 466-9 01726390

•

Early acinar cell changes in caerulein-induced interstitial acute pancreatitis in the rat. Author(s): Department of Pathology, University of Turku, Finland. Source: Gronroos, J M Aho, H J Hietaranta, A J Nevalainen, T J Exp-Pathol. 1991; 41(1): 21-30 0232-1513

•

Early jejunal nutrition and changes in the immunological parameters of patients with acute pancreatitis. Author(s): Second Department of Surgery, University of Debrecen, Debrecen, Moricz Zs. str. 22., 4004 Debrecen, Hungary. [email protected] Source: Hallay, J Kovacs, G Szatmari, K Bako, A Szentkereszty, Z Lakos, G Sipka, S Sapy, P Hepatogastroenterology. 2001 Sep-October; 48(41): 1488-92 0172-6390

•

Effect of different regimens of gut decontamination on bacterial translocation and mortality in experimental acute pancreatitis. Author(s): Department of Surgery, University of Cincinnati, School of Medicine, Ohio, USA. Source: Gianotti, L Munda, R Gennari, R Pyles, R Alexander, J W Eur-J-Surg. 1995 February; 161(2): 85-92 1102-4151

•

Effect of platelet-activating factor antagonists (BN-52021, WEB-2170, and BB-882) on bacterial translocation in acute pancreatitis. Author(s): Department of Gastroenterology, Sao Paulo University Medical School, Rua Maria Jesus de Simoes, 48 Lauzanne Paulista, 02469-010 Sao Paulo SP, Brazil. [email protected] Source: de Souza, L J Sampietre, S N Assis, R S Knowles, C H Leite, K R Jancar, S Monteiro Cunha, J E Machado, M C J-Gastrointest-Surg. 2001 Jul-August; 5(4): 364-70 1091-255X

•

Effects of short-term administration of the CCK receptor antagonist, KSG-504, on regeneration of pancreatic acinar cells in acute pancreatitis in rats. Author(s): Department of Internal Medicine, Shiga University of Medical Science, Japan. Source: Okumura, Y Inoue, H Fujiyama, Y Bamba, T J-Gastroenterol. 1995 August; 30(4): 493-9 0944-1174

•

Effects of Tetrandrine and QYT on ICAM-1 and SOD gene expression in pancreas and liver of rats with acute pancreatitis. Author(s): Department of Pathophysiology, Medical College of Tongji University, Shanghai 200331, China. [email protected] Source: Li, Y Y Li, X L Yang, C X Zhong, H Yao, H Zhu, L World-J-Gastroenterol. 2003 January; 9(1): 155-9 1007-9327

76

Acute Pancreatitis

•

Evidence for extraluminal trypsinogen activation in three different models of acute pancreatitis. Author(s): Department of Surgery, Massachusetts General Hospital, Boston 02114. Source: Foitzik, T Lewandrowski, K B Fernandez del Castillo, C Rattner, D W Warshaw, A L Surgery. 1994 June; 115(6): 698-702 0039-6060

•

Exocrine pancreatic disease in the dog and cat. 1. Acute pancreatitis. Source: Pidgeon, G. Companion-Anim-Pract. Santa Barbara, Calif. : Veterinary Practice Publishing Co. March 1987. volume 1 (1) page 67, 70-71. 0894-9794

•

Feeding a cat with acute pancreatitis. Author(s): University of Florida, Gainesville, FL. Source: Hill, R. North-American-Veterinary-Conference (USA). (1996). volume 10 page 320-321. cats animal nutrition pancreatitis

•

Gallium-67 scintigraphy in acute pancreatitis. Author(s): Mubarak Al-Kabeer Hospital, Ministry of Public Health, Kuwait. Source: al Suhaili, A R Wafai, I Bahar, R Nawaz, K Nema, T A Eriksson, S Higazi, E Abdel Dayem, H M Eur-J-Nucl-Med. 1988; 14(1): 8-11 0340-6997

•

Histoprotective effect of antihypoxant olifen during experimental acute pancreatitis. Author(s): I. I. Dzhanelidze St. Petersburg Institute of Ambulance Service. Source: Tolstoi, A D Dzhurko, B I Vashetko, R V Medvedev, Y V Gol'tsov, V R DvoiNovember, V G Zakharova, E V Bull-Exp-Biol-Med. 2001 April; 131(4): 312-4 00074888

•

Induction of heat shock proteins fails to produce protection against trypsin-induced acute pancreatitis in rats. Author(s): First Department of Medicine, University of Szeged, Hungary. [email protected] Source: Rakonczay, Z Jr Takacs, T Ivanyi, B Mandi, Y Papai, G Boros, I Varga, I Jost, K Lonovics, J Clin-Exp-Med. 2002 July; 2(2): 89-97 1591-8890

•

Influence of somatostatin on acute pancreatitis in rats. Author(s): Department of Surgery, Hopital de la Timone, Marseille, France. Source: Berthet, B Guillou, N Brioche, M I Choux, R Viret, P Ledoray, V Billardon, M Assadourian, R Eur-J-Surg. 1998 October; 164(10): 785-90 1102-4151

•

Nitric oxide, heparin and procaine treatment in experimental ceruleine-induced acute pancreatitis in rats. Author(s): 2nd Department of General, Gastroenterological and Endocrine Surgery, University Medical School, Gdansk, Poland. Source: Dobosz, M Wajda, Z Hac, S Mysliwska, J Bryl, E Mionskowska, L Roszkiewicz, A Mysliwski, A Arch-Immunol-Ther-Exp-(Warsz). 1999; 47(3): 155-60 0004-069X

•

Nutrition in patients with acute pancreatitis. Author(s): Department of Surgery, Academic Hospital Maastricht, NL-6202 Maastricht, The Netherlands. [email protected] Source: Dejong, C H Greve, J W Soeters, P B Curr-Opin-Crit-Care. 2001 August; 7(4): 251-6 1070-5295

•

Nutritional management of patients with feeding-induced pain: acute pancreatitis. Author(s): Cleveland Clinic Foundation, OH, USA. Source: Seidner, D L Fish, J A Semin-Gastrointest-Dis. 1998 October; 9(4): 200-9 10495118

Nutrition

77

•

Oxidative stress in acute pancreatitis. Author(s): Department of Surgery, Otto-von-Guericke-University of Magdeburg, Germany. [email protected] Source: Schulz, H U Niederau, C Klonowski Stumpe, H Halangk, W Luthen, R Lippert, H Hepatogastroenterology. 1999 Sep-October; 46(29): 2736-50 0172-6390

•

Pancreatic head mass: how can we treat it? Acute pancreatitis: conservative treatment. Author(s): Internal Medicine Department, 3rd Division, Cardarelli Hospital. Napoli, Italy. [email protected] Source: Uomo, G JOPage 2000 September; 1(3 Suppl): 130-7 1590-8577

•

Pathogenesis of acute pancreatitis. Author(s): Department of Surgery, Charles A. Dana Research Laboratories, Boston, Massachusetts. Source: Steer, M L Meldolesi, J Annu-Rev-Med. 1988; 3995-105 0066-4219

•

Possible role of cholecystokinin in the development of acute pancreatitis in rats. Source: Shinya, H Fujimura, M Nippon-Geka-Hokan. 1989 January 1; 58(1): 3-17 00039152

•

Protecting effects of intravenous insoluble glycogen treatment on the experimental necrotizing acute pancreatitis of dogs. Author(s): 3rd Department of Internal Medicine, University Medical School of Debrecen. Source: Sipka, S Sapy, P Bot, G Furka, I Miko, I Arkossy, P Dauda, G Szappanos, M Kovacs, J Lakos, G Szegedi, G Hepatogastroenterology. 1997 Jan-February; 44(13): 12732 0172-6390

•

Secondary pancreatic involvement by diffuse large B-cell lymphoma presenting as acute pancreatitis: treatment and outcome. Author(s): Department of Gastroenterology and Hepatology, Henry Mondor University Hospital, Creteil, France. Source: Bernardeau, M Auroux, J Cavicchi, M Haioun, C Tsakiris, L Delchier, J C Pancreatology. 2002; 2(4): 427-30 1424-3903

•

Severe acute pancreatitis: treatment with somatostatin. Author(s): Intensive Care Unit, Hospital General Universitari Vall d'Hebron, Barcelona, Spain. Source: Planas, M Perez, A Iglesia, R Porta, I Masclans, J R Bermejo, B Intensive-CareMed. 1998 January; 24(1): 37-9 0342-4642

•

Somatostatin and octreotide in acute pancreatitis: the never-ending story. Author(s): Department of Surgical and Gastroenterological Sciences, University of Verona, Italy. Source: Cavallini, G Frulloni, L Dig-Liver-Dis. 2001 March; 33(2): 192-201

•

Somatostatin prevents acute pancreatitis after pancreatic duct sphincter hydrostatic balloon dilation in patients with idiopathic recurrent pancreatitis. Author(s): Gastroenterology Department, Hospital General del Oeste, M.S.A.S. Los Magallanes, Catia, Caracas, Venezuela. Source: Guelrud, M Mendoza, S Viera, L Gelrud, D Gastrointest-Endosc. 1991 JanFebruary; 37(1): 44-7 0016-5107

•

The effect of fat-rich diet and chronic ethanol ingestion on ascitic fluid and plasma enzyme activities in acute pancreatitis in rats. Source: Ramo, O J Jalovaara, P Makela, A Schroder, T Acta-Chir-Scand. 1987 March; 153(3): 203-7 0001-5482

78

Acute Pancreatitis

•

The influence of nifedipine (calcium channel blocker) and Bay-K-8644 (calcium channel agonist) on the development of experimental acute pancreatitis. Author(s): Dept. of Gastroenterology, Medical University of Lublin. Source: Slomka, M Celinski, K Wargocki, J Kleinrok, Z Czerny, K Cichoz Lach, H AnnUniv-Mariae-Curie-Sklodowska-[Med]. 2001; 56: 29-34 0066-2240

•

The role of oxygen-derived free radicals in two models of experimental acute pancreatitis: effects of catalase, superoxide dismutase, dimethylsulfoxide, and allopurinol. Author(s): Department of Surgery, Beth Israel Hospital, Boston. Source: Steer, M L Rutledge, P L Powers, R E Saluja, M Saluja, A K Klin-Wochenschr. 1991 December 15; 69(21-23): 1012-7 0023-2173

•

The role of prostaglandins in acute pancreatitis. Source: Glazer, G Gilliland, E L Aldridge, M A Surg-Annu. 1987; 19175-203 0081-9638

•

Thyroid function in acute pancreatitis. Author(s): Department of Digestive Medicine, Costa del Sol Hospital, Marbella, Malaga, Spain. Source: De Sola, C Redondo, M Pallares, F Redondo, E Hortas, M L Morell, M Rev-EspEnferm-Dig. 1998 January; 90(1): 15-22 1130-0108

•

Time course of malonic dialdehyde and alpha-tocopherol in rat pancreas during the first hours of acute pancreatitis. Author(s): Institute of Molecular Biology and Biophysics, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk. Source: Prokop'eva, N V Gulyaeva, L F Kolosova, N G Bull-Exp-Biol-Med. 2000 May; 129(5): 452-4 0007-4888

•

Timing of tumor necrosis factor antagonism is critical in determining outcome in murine lethal acute pancreatitis. Author(s): Department of Surgery, University of South Florida, Tampa 33612, USA. Source: Norman, J G Fink, G W Messina, J Carter, G Franz, M G Surgery. 1996 September; 120(3): 515-21 0039-6060

•

Use of a synthetic protease inhibitor for the treatment of L-asparaginase-induced acute pancreatitis complicated by disseminated intravascular coagulation. Author(s): First Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan. Source: Murakawa, M Okamura, T Shibuya, T Harada, M Otsuka, T Niho, Y AnnHematol. 1992 May; 64(5): 249-52 0939-5555

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

•

The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov

Nutrition

79

•

The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov

•

The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/

•

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/

•

Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/

•

Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/

•

Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/

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

•

Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html

•

Google: http://directory.google.com/Top/Health/Nutrition/

•

Healthnotes: http://www.healthnotes.com/

•

Open Directory Project: http://dmoz.org/Health/Nutrition/

•

Yahoo.com: http://dir.yahoo.com/Health/Nutrition/

•

WebMDHealth: http://my.webmd.com/nutrition

•

WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html

The following is a specific Web list relating to acute pancreatitis; 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: •

Food and Diet Beef Source: Healthnotes, Inc.; www.healthnotes.com Kiwi Source: Healthnotes, Inc.; www.healthnotes.com

81

CHAPTER 3. ALTERNATIVE MEDICINE AND ACUTE PANCREATITIS Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to acute pancreatitis. 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 acute pancreatitis 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 “acute pancreatitis” (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 acute pancreatitis: •

A randomized double-blind study using CaNa2EDTA, a phospholipase A2 inhibitor, in the management of human acute pancreatitis. Author(s): Tykka HT, Vaittinen EJ, Mahlberg KL, Railo JE, Pantzar PJ, Sarna S, Tallberg T. Source: Scandinavian Journal of Gastroenterology. 1985 January; 20(1): 5-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3922048

•

Acute pancreatitis associated with chemotherapy for germ cell tumors in two patients. Author(s): Socinski MA, Garnick MB. Source: Annals of Internal Medicine. 1988 April; 108(4): 567-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2450502

82

Acute Pancreatitis

•

Acute pancreatitis causing death in a child on the ketogenic diet. Author(s): Stewart WA, Gordon K, Camfield P. Source: Journal of Child Neurology. 2001 September; 16(9): 682. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11575609

•

Acute pancreatitis induced by diffuse pancreatic invasion of adult T-cell leukemia/lymphoma cells. Author(s): Mori A, Kikuchi Y, Motoori S, Watanabe J, Shinozaki M, Eguchi M. Source: Digestive Diseases and Sciences. 2003 October; 48(10): 1979-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14627344

•

Alterations in intestinal function in acute pancreatitis in an experimental model. Author(s): Wang XD, Wang Q, Andersson R, Ihse I. Source: The British Journal of Surgery. 1996 November; 83(11): 1537-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9026331

•

An observational study of severe hypertriglyceridemia, hypertriglyceridemic acute pancreatitis, and failure of triglyceride-lowering therapy when estrogens are given to women with and without familial hypertriglyceridemia. Author(s): Goldenberg NM, Wang P, Glueck CJ. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 2003 June; 332(1-2): 11-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12763274

•

Cerulein-induced acute pancreatitis in the rat is significantly ameliorated by treatment with MEK1/2 inhibitors U0126 and PD98059. Author(s): Clemons AP, Holstein DM, Galli A, Saunders C. Source: Pancreas. 2002 October; 25(3): 251-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12370536

•

Cholecystokinin cleavage to cholecystokinin-octapeptide in vivo and in vitro: accelerated cleavage in acute pancreatitis. Author(s): Springer CJ, Calam J. Source: Gastroenterology. 1988 July; 95(1): 143-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2453390

•

Controlled trial of high-dose octreotide in treatment of acute pancreatitis. Evidence of improvement in disease severity. Author(s): Beechey-Newman N. Source: Digestive Diseases and Sciences. 1993 April; 38(4): 644-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8462363

Alternative Medicine 83

•

Cytostatics in the treatment of chronic and acute pancreatitis. Author(s): Popiela T, Turczynowski W, Zajac A. Source: Hepatogastroenterology. 1980 October; 27(5): 390-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7009361

•

Effect of Qingyitang on activity of intracellular Ca2+-Mg2+-ATPase in rats with acute pancreatitis. Author(s): Qiu Y, Li YY, Li SG, Song BG, Zhao GF. Source: World Journal of Gastroenterology : Wjg. 2004 January; 10(1): 100-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14695778

•

Effects of green tea catechins (Polyphenon 100) on cerulein-induced acute pancreatitis in rats. Author(s): Takabayashi F, Harada N. Source: Pancreas. 1997 April; 14(3): 276-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9094158

•

Effects of Tetrandrine and QYT on ICAM-1 and SOD gene expression in pancreas and liver of rats with acute pancreatitis. Author(s): Li YY, Li XL, Yang CX, Zhong H, Yao H, Zhu L. Source: World Journal of Gastroenterology : Wjg. 2003 January; 9(1): 155-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12508373

•

Emblica officinalis: a novel therapy for acute pancreatitis--an experimental study. Author(s): Thorat SP, Rege NN, Naik AS, Thatte UM, Joshi A, Panicker KN, Bapat RD, Dahanukar SA. Source: Hpb Surg. 1995; 9(1): 25-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8857450

•

Foreign serum-induced pancreatitis in mice. I. A new model of acute pancreatitis. Author(s): Janigan DT, Nevalainen TJ, MacAulay MA, Vethamany VG. Source: Laboratory Investigation; a Journal of Technical Methods and Pathology. 1975 December; 33(6): 591-607. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1202281

•

Formalized therapeutic guideline for hyperlipidemic severe acute pancreatitis. Author(s): Mao EQ, Tang YQ, Zhang SD. Source: World Journal of Gastroenterology : Wjg. 2003 November; 9(11): 2622-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14606112

•

Guidelines for treatment of severe acute pancreatitis. Author(s): Wu XN.

84

Acute Pancreatitis

Source: Hepatobiliary Pancreat Dis Int. 2002 August; 1(3): 446-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14607725 •

High dose octreotide in the management of acute pancreatitis. Author(s): Karakoyunlar O, Sivrel E, Tanir N, Denecli AG. Source: Hepatogastroenterology. 1999 May-June; 46(27): 1968-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10430379

•

Hyperbaric oxygen therapy in the treatment of refractory peripancreatic abscess associated with severe acute pancreatitis. Author(s): Izawa K, Tsunoda T, Ura K, Yamaguchi T, Ito T, Kanematsu T, Tsuchiya R. Source: Gastroenterol Jpn. 1993 April; 28(2): 284-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8486216

•

Hyperbaric oxygen, allopurinol, and diet-induced acute pancreatitis. Author(s): Degertekin H, Ertan A, Yater RD, Van Meter K, Akdamar K. Source: Annals of Internal Medicine. 1985 September; 103(3): 474-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4026099

•

Letter 1: Randomized clinical trial of specific lactobacillus and fibre supplement to early enteral nutrition in patients with acute pancreatitis (Br J Surg 2002; 89: 11031107). Author(s): Weale R, Edwards A. Source: The British Journal of Surgery. 2003 January; 90(1): 122-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12520591

•

Mechanisms of Chinese herb emodin and somatostatin analogs on pancreatic regeneration in acute pancreatitis in rats. Author(s): Gong Z, Yuan Y, Lou K, Tu S, Zhai Z, Xu J. Source: Pancreas. 2002 August; 25(2): 154-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12142738

•

Pancreatic microvascular permeability in caerulein-induced acute pancreatitis. Author(s): Sweiry JH, Mann GE. Source: The American Journal of Physiology. 1991 October; 261(4 Pt 1): G685-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1928354

•

Pathological events in experimental acute pancreatitis prevented by the bradykinin antagonist, Hoe 140. Author(s): Griesbacher T, Tiran B, Lembeck F.

Alternative Medicine 85

Source: British Journal of Pharmacology. 1993 February; 108(2): 405-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8448591 •

Patient with gemfibrozil-controlled hypertriglyceridemia that developed acute pancreatitis after starting ketogenic diet. Author(s): Buse GJ, Riley KD, Dress CM, Neumaster TD. Source: Current Surgery. 2004 March-April; 61(2): 224-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15051269

•

Phospholipase A2 inhibitors and their possible clinical use in the treatment of acute pancreatitis. Author(s): Tykka H, Mahlberg K, Pantzar P, Tallberg T. Source: Scandinavian Journal of Gastroenterology. 1980; 15(5): 519-28. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6777862

•

Phospholipase activity in pancreatic exudate in experimental acute pancreatitis. Author(s): Gjone E, Ofstad E, Marton PF, Amundsen E. Source: Scandinavian Journal of Gastroenterology. 1967; 2(3): 181-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4963682

•

Protective effect of a microtubule stabilizer taxol on caerulein-induced acute pancreatitis in rat. Author(s): Ueda T, Takeyama Y, Kaneda K, Adachi M, Ohyanagi H, Saitoh Y. Source: The Journal of Clinical Investigation. 1992 January; 89(1): 234-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1370296

•

Protective effects of rhubarb on experimental severe acute pancreatitis. Author(s): Zhao YQ, Liu XH, Ito T, Qian JM. Source: World Journal of Gastroenterology : Wjg. 2004 April 1; 10(7): 1005-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15052683

•

Secondary pancreatic involvement by diffuse large B-cell lymphoma presenting as acute pancreatitis: treatment and outcome. Author(s): Bernardeau M, Auroux J, Cavicchi M, Haioun C, Tsakiris L, Delchier JC. Source: Pancreatology : Official Journal of the International Association of Pancreatology (Iap). [et Al.]. 2002; 2(4): 427-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12138234

•

The effect of combination therapy of hyperbaric oxygen, meropenem, and selective nitric oxide synthase inhibitor in experimental acute pancreatitis. Author(s): Isik AT, Mas MR, Comert B, Yasar M, Korkmaz A, Akay C, Deveci S, Tasci I, Mas N, Ates Y, Kocar IH.

86

Acute Pancreatitis

Source: Pancreas. 2004 January; 28(1): 53-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14707730 •

The effects of free oxygen radical scavenger and platelet-activating factor antagonist agents in experimental acute pancreatitis. Author(s): Soybir G, Koksoy F, Ekiz F, Yalcin O, Fincan K, Haklar G, Yuksel M. Source: Pancreas. 1999 August; 19(2): 143-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10438161

•

The effects of green tea catechins (Polyphenon) on DL-ethionine-induced acute pancreatitis. Author(s): Takabayashi F, Harada N, Hara Y. Source: Pancreas. 1995 August; 11(2): 127-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7479668

•

Therapeutic efficacy of high-dose vitamin C on acute pancreatitis and its potential mechanisms. Author(s): Du WD, Yuan ZR, Sun J, Tang JX, Cheng AQ, Shen DM, Huang CJ, Song XH, Yu XF, Zheng SB. Source: World Journal of Gastroenterology : Wjg. 2003 November; 9(11): 2565-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14606098

•

Treatment of acute pancreatitis with liyi tang--a report of 50 cases. Author(s): Chen Q, Lu J. Source: J Tradit Chin Med. 1997 December; 17(4): 250-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10437205

•

Use of a synthetic protease inhibitor for the treatment of L-asparaginase-induced acute pancreatitis complicated by disseminated intravascular coagulation. Author(s): Murakawa M, Okamura T, Shibuya T, Harada M, Otsuka T, Niho Y. Source: Annals of Hematology. 1992 May; 64(5): 249-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1623061

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/

•

AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats

•

Chinese Medicine: http://www.newcenturynutrition.com/

•

drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html

Alternative Medicine 87

•

Family Village: http://www.familyvillage.wisc.edu/med_altn.htm

•

Google: http://directory.google.com/Top/Health/Alternative/

•

Healthnotes: http://www.healthnotes.com/

•

MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine

•

Open Directory Project: http://dmoz.org/Health/Alternative/

•

HealthGate: http://www.tnp.com/

•

WebMDHealth: http://my.webmd.com/drugs_and_herbs

•

WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html

•

Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/

The following is a specific Web list relating to acute pancreatitis; 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 Pancreatic Insufficiency Source: Healthnotes, Inc.; www.healthnotes.com Pancreatitis 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.

89

CHAPTER 4. DISSERTATIONS ON ACUTE PANCREATITIS Overview In this chapter, we will give you a bibliography on recent dissertations relating to acute pancreatitis. 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 “acute pancreatitis” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on acute pancreatitis, we have not necessarily excluded non-medical dissertations in this bibliography.

Dissertations on Acute Pancreatitis 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 acute pancreatitis. 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: •

The role of cyclooxygenase-2 (COX-2) in acute pancreatitis by Ethridge, Richard Thomas; PhD from The University of Texas Graduate Sch. of Biomedical Sci. at Galveston, 2003, 108 pages http://wwwlib.umi.com/dissertations/fullcit/3083540

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.

91

CHAPTER 5. PATENTS ON ACUTE PANCREATITIS 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.8 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 “acute pancreatitis” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on acute pancreatitis, we have not necessarily excluded nonmedical patents in this bibliography.

Patents on Acute Pancreatitis By performing a patent search focusing on acute pancreatitis, 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. 8Adapted

from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.

92

Acute Pancreatitis

The following is an example of the type of information that you can expect to obtain from a patent search on acute pancreatitis: •

Bradykinin-antagonists for the treatment of acute pancreatitis Inventor(s): Griesbacher; Thomas (Hitzendorf, AT), Lembeck; Fred (Graz, AT) Assignee(s): Hoechst Aktiengesellschaft (frankfurt AM Main, De) Patent Number: 5,670,619 Date filed: April 22, 1994 Abstract: The invention relates to the use of bradykinin-antagonists of the formulaR.sup.1 -A-B-C-E-F-G-J-K-R.sup.2wherein R.sup.1 represents hydrogen, C.sub.1 -C.sub.4 -alkanoyl which can be substituted by mercapto, hydroxyphenyl, (4benzoyl)phenoxy or represents (4-benzoyl)benzoyl-Lys; A represents D-Arg or D-Lys or stands for a direct bond; B represents Arg which can be substituted by NO.sub.2 or toluol-4-sulfonyl or represents Lys which can be substituted by toluol-4-sulfonyl or CO-NH--C.sub.6 H.sub.5, or stands for a direct bond; C represents Hyp-Pro-Gly, Pro-HypGly, Pro-Pro-Gly or dehydroPro-Hyp-Gly; E represents Thi, Phe, Leu or Cha; F represents Ser or Cys; G represents D-Tic, D-Phe or D-Hyp substituted by C.sub.1 C.sub.4 -alkoxy; J represents Tic, Aoc or Oic; K represents Arg or Ahx or stands for a direct bond; R.sup.2 is hydroxy or amino; and the physiologically tolerable salts thereof for the treatments of acute pancreatitis, to pharmaceutical agents containing them and to the use thereof for the preparation of appropriate pharmaceutical compositions. Excerpt(s): The invention relates to the use of bradykinin-antagonists or the physiologically tolerated salts thereof for the treatments of acute pancreatitis, to pharmaceutical agents containing them and to the use thereof for the preparation of appropriate pharmaceutical compositions. Bradykinin has long been thought to participate in acute pancreatitis. In 1989 however, Berg et. al. have defeated this hypothesis. Berg et al. have demonstrated (The Journal of Pharmacology and Experimental Therapeutics, Vol. 251, No. 2 (1989) p. 731-734) that hypotension caused by development of acute pancreatitis in rats was not influenced by D-Arg.sup.0 Hyp.sup.3 -Thi.sup.5.8 -D-Phe.sup.7 -BK (D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Phe-ThiArg). and their physiologically tolerable salts. Web site: http://www.delphion.com/details?pn=US05670619__

•

Interleukin-1 receptor antagonist decreases severity of acute pancreatitis Inventor(s): Norman, Jr.; James G. (Tampa, FL) Assignee(s): University of South Florida (tampa, Fl) Patent Number: 5,508,262 Date filed: December 15, 1993 Abstract: A method for treating acute pancreatitis comprising administering an effective amount of Interleukin-1 receptor antagonist (IL-1ra) or a pharmaceutically acceptable salt thereof to a person afflicted with that condition. Excerpt(s): The present invention relates to a method for treating acute pancreatitis. Acute pancreatitis is a common clinical problem which remains evasive of specific therapy.sup.1 Each year more than 15,000 admissions to U.S. hospitals are caused by

Patents 93

acute pancreatitis. It is most often caused by alcoholism or biliary tract disease. Less commonly, it is associated with hyperlipemia, hyperparathyroidism, abdominal trauma, vasculitis or uremia. The average length of hospitalization for the disease is 12.4 days, with a significant number of patients staying much longer because of associated complications. With more recent understanding of the complex mechanisms of tissue and cellular injury associated with inflammatory processes, such as sepsis,.sup.5 it is reasonable to assume that many of these inflammatory processes are not specific to sepsis syndromes alone. Several authors have suggested that much of the intrinsic pancreatic damage seen in acute pancreatitis is due to the release of toxic substances from macrophages and other white blood cells which migrate into the damaged gland.sup.6,7,8,9,10,11,12 These substances are known as cytokines and are now well known as mediators of inflammation and tissue injury. Web site: http://www.delphion.com/details?pn=US05508262__ •

Method of diagnosis and severity-assessment of pancreatic disease Inventor(s): Austen; Brian M. (London, GB2), Hermon-Taylor; John (London, GB2) Assignee(s): Bioscience International, Inc. (boston, Ma) Patent Number: 4,948,723 Date filed: July 28, 1987 Abstract: Pancreatic disease can be diagnosed by assaying a patient's body fluid, e.g. serum or urine, for the activation peptides of pancreatic zymogens specifically cleaved by proteolysis during activation, (PAP) e.g. peptides including the sequence D.sub.4 K having the lysine as the carboxy terminus. When PAP is assayed for, the test provides a means for distinguishing necrotising acute pancreatitis from oedematous acute pancreatitis, provides for diagnosis of chronic pancreatitis in exacerbation, and permits monitoring of the severity progress of the disease. Also described are antibodies having specificity for the pancreatic activation peptides, as well as such peptides and antibodies which are labelled with revealing agents and/or immobilized on solid supports, and their use in diagnostic test kits. Excerpt(s): The present invention relates generally to the diagnosis of pancreatic disease. More particularly, the present invention relates to trypsinogen activation peptides and their use in diagnosing pancreatitis. Acute and chronic pancreatitis are human diseases which have shown a significant increase in frequency in recent years [1]. Acute pancreatitis presents as an abdominal emergency, whereas chronic pancreatitis in general involves the differential diagnosis of chronic or intermittent abdominal pain. The exocrine pancreas produces and stores a range of digestive enzymes, including amylase and lipase, biosynthesised in active form, and others including trypsinogens, chymotrypsinogens, proelastases, procarboxypeptidases, and prophospholipases A2, synthesised as inactive proenzymes or zymogens. Zymogen activation normally occurs following secretion of pancreatic juice into the duodenal lumen, and involves the specific catalytic conversion of trypsinogen to active trypsin by duodenal enteropeptidase (E.C. 3.4.21.9). This removes from trypsinogen an amino-terminal oligopeptide containing the sequence tetra-L-aspartyl-L-lysine, an event followed by tryptic activation of the other proenzymes in a cascade of proteolytic cleavage. Activation peptides of pancreatic zymogens released in the course of this physiological process are thought to be degraded by duodenal oligopeptidases. Web site: http://www.delphion.com/details?pn=US04948723__

94

•

Acute Pancreatitis

Method of treating acute pancreatitis with isometheptene Inventor(s): DeNovellis; Michelangelo (Bologna, IT), Labriola; Ernesto (Bologna, IT), Marlettini; Maria G. (Bologna, IT), Salomone; Teresa (Bologna, IT), Tomassetti; Paola (Bologna, IT) Assignee(s): Knoll AG (de) Patent Number: 4,522,827 Date filed: July 2, 1982 Abstract: A method of relieving the symptoms of acute pancreatitis comprising administering Isometheptene to a person afflicted with that condition. Excerpt(s): This invention relates to a method for relieving symptoms of acute pancreatitis in mammals. More particularly, the invention concerns a method for treating persons afflicted with acute pancreatitis by administering to such a person a sufficient amount of Isometheptene to effectively relieve symptoms of that disease. Acute pancreatitis causes pathologic changes in the pancreas ranging from a mild edematous process to an overwhelming necrotizing lesion which may be lifethreatening. While its symptoms are variable it is principally characterized by epigastric pain radiating to either the upper quadrant or directly through to the back. The typical pain is gnawing, of sudden onset, of exceeding severity, unremitting, and sometimes colicky in character. It is not relieved by vomiting and is little affected by morphine, for example. Patients with this condition are also commonly found to have persistent high amylase in the blood and urine and frequently develop shock due to circulating vasoactive substances or retroperitoneal hemorrhage. A standard rationale in treating this condition is to set the gland to rest, such as by restricting the intake of food, administering fluids, and maintaining electrolyte balance. Treatment involving the use of various drug compositions has also been attempted previously, including the use of specific drugs which are known to inhibit gastric and/or pancreatic secretions such as Aprotinin, but none of these treatments appears to exhibit any proven overall benefit. Web site: http://www.delphion.com/details?pn=US04522827__

•

Method of using IL-11 for inflammation associated with acute pancreatitis Inventor(s): Keith; James (Andover, MA), Schendel; Paul (Wayland, MA) Assignee(s): Genetics Institute, Inc. (cambridge, Ma) Patent Number: 6,274,135 Date filed: June 22, 1999 Abstract: Provided by the present invention are methods of treating a variety of disorders including AIDS, arthritis (rheumatoid arthritis, osteoarthritis, spondyloarthropathies), antibiotic induced diarrheal diseases (Closbidium difficile), multiple sclerosis, osteoporosis, gingivitis, peptic ulcer disease, esophagitis, diabetes, retinitis, uveitis, reperfusion injury after myocardial infarction (MI) or cerebral vascular accident (CVA), aphthous ulcers (oral), atherosclerosis (plaque rupture), prevention of tumor metastases, asthma, preeclampsia, acute pancreatitis, psoriasis, infertility and allergic disorders such as rhinitis, conjunctivitis, and urticaria. Excerpt(s): The present invention relates generally to methods of treating disorders such as AIDS, arthritis (rheumatoid arthritis, osteoarthritis, spondyloarthropathies), antibiotic induced diarrheal diseases (Clostridium difficile), multiple sclerosis, osteoporosis,

Patents 95

gingivitis, peptic ulcer disease, esophagitis, diabetes, retinitis, uveitis, reperfusion injury after myocardial infarction (MI), cerebral vascular accident (CVA), aphthous ulcers (oral), atherosclerosis (plaque rupture), prevention of tumor metastases, asthma, preeclampsia, acute pancreatitis, psoriasis, infertility and allergic disorders such as rhinitis, conjunctivitis, and urticaria. Inflammatory responses include a broad range of host reaction to a variety of insults, such as injury, infection, or rejection. It is the over production 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 (Clostridium difficile), multiple sclerosis, osteoporosis, gingivitis, peptic ulcer disease, esophagitis, diabetes, retinitis, uveitis, reperfusion injury after myocardial infarction (MI), cerebral vascular accident (CVA), aphthous ulcers (oral), atherosclerosis (plaque rupture), tumor metastases, asthma, preeclampsia, acute pancreatitis, psoriasis, infertility and allergic disorders such as rhinitis, conjunctivitis, and urticaria. These disorders and their symptoms are briefly summarized below. According to the methods of the present invention, IL-11 is administered to modulate the hosts' over reaction to insult thereby treating the following disorders. Web site: http://www.delphion.com/details?pn=US06274135__ •

Monoclonal antibodies against type I phospholipase A.sub.2 as a diagnostic and antiinflammatory therapeutic agent Inventor(s): Hubner-Parajsz; Christa (Tutzing, DE), Scheuer; Werner (Penzberg, DE), Tibes; Ulrich (Frankfurt, DE) Assignee(s): Boehringer Mannheim Gmbh (mannheim, De) Patent Number: 5,767,249 Date filed: August 8, 1995 Abstract: The invention provides for monoclonal antibodies which specifically bind to type I phospholipase A.sub.2 for use as a diagnostic agent and as an anti-inflammatory therapeutic agent, which is particularly suitable for application in acute pancreatitis. The invention further provides for pharmaceutical compositions including the antibodies of the invention. The invention also provides for a method for treating subjects suffering from inflammatory symptoms and for detecting the activity of type I phospholipase A.sub.2 in a sample. Excerpt(s): The invention concerns the use of monoclonal antibodies against type I phospholipase A.sub.2 for the production of an anti-inflammatory therapeutic agent which is particularly suitable for application in acute pancreatitis. There is neither a causal nor symptomatic therapy for acute pancreatitis (The Merck Manual of Diagnosis and Therapy 15 (1987), pages 763-767). The pathogenetic basis of acute pancreatitis is autolysis of the pancreas. Phospholipase A.sub.2 has been attributed a decisive function in this process. It has a lysing action on the cell membrane and liberates arachidonic acid from the membrane phospholipids in this process. The metabolites of arachidonic acid (prostaglandins and leukotrienes) are an important component of the inflammatory reaction. Phospholipase A.sub.2 occurs in two forms. The phospholipase A.sub.2 designated type I is mainly found in pancreatic tissue and plays an important role in acute pancreatitis. In contrast type II phospholipase A.sub.2 occurs in many different tissues. Web site: http://www.delphion.com/details?pn=US05767249__

96

•

Acute Pancreatitis

Pancreas elastase 1-specific antibody, a process for obtaining it, and a test kit containing such antibody Inventor(s): Scheefers; Hans (Wettenberg, DE), Scheefers-Borchel; Ursula (Wettenberg, DE), Sziegoleit; Andreas (Langgons, DE) Assignee(s): Schebo Tech Medizinisch-biologische Forschungsgesellschaft Mbh (wettenberg, De) Patent Number: 5,622,837 Date filed: June 1, 1995 Abstract: A process is described for obtaining highly specific pancreas elastase 1 antibodies which react both with bodily fluids and with stools. Such an antibody is obtainable by immunizing with an antigen having the amino acid sequence Thr-MetVal-Ala-Gly-Gly-Asp-Ile-Arg (SEQ ID NO:1) or immunologically active partial peptides thereof. A test kit containing such antibodies is suitable for the diagnosis and course monitoring of chronic and acute pancreatitis as well as mucoviscidosis in bodily fluids and/or in stools. Excerpt(s): This invention relates to a highly sensitive and selective anti-elastase 1 antibody, a process for its manufacture, and a highly sensitive diagnostic test kit containing said antibody. Instances of inflammatory diseases of the pancreas are constantly increasing in industrial countries (W. Rosch, Deutsches Arzteblatt 84: C-397398, 1987). These diseases usually have an intermittent course and can finally lead to complete loss of the gland. Acute episodes are recognizable by severe abdominal pain and nausea, but intermediate phases are usually experienced by the patient as free from pain. They evolve only with uncharacteristic digestive complaints, so that they are hard to recognize. Consideration is therefore to be given to a chronic pancreatic disease in all digestive disorders. Determination of the serum amylase level has hitherto usually been made in laboratory diagnoses of pancreatitis. However, an elevation in serum amylase also occurs in other intra-abdominal inflammations, e.g., in intestinal perforation, mumps or renal failure. Moreover, an elevation in the serum amylase level may also be observed following the administration of morphines. Another laboratory diagnostic possibility consists of determining the ratio of amylase to creatinine clearance, which ratio increases in acute pancreatitis. Unfortunately, amylase values elevated in acute pancreatitis normalize very rapidly, so that normal values are already found 48 hours after the onset of the disease in one-third of the patients (J. A. Eckfeldt et al., Arch. Pathol. Lab. Med. 109:316-319, 1985). Web site: http://www.delphion.com/details?pn=US05622837__

•

Protein associated with acute pancreatitis agents for the screening of acute pancreatitis Inventor(s): Dagorn; Jean-Charles (Marseille, FR), Iovanna; Juan-Lucio (Marseille, FR), Volker; Keim (Heddesheim, FR) Assignee(s): Institut National DE LA Sante ET DE LA Recherche Medicale (paris Cedex, Fr) Patent Number: 5,436,169 Date filed: December 19, 1991

Patents 97

Abstract: The invention relates to the family of the protein (PAP) associated with acute pancreatitis in man and in the rat. It also relates to the nucleotide fragments coding for the above proteins.Also included in the framework of the invention are antibodies which recognize the PAP and which are capable of being used for the purpose of diagnosing pancreatitis.The invention also relates to the production of the PAP, in particular by genetic engineering. Excerpt(s): The present invention relates to proteins associated with acute pancreatitis and agents for the diagnosis of this disease. Acute pancreatitis is an inflammatory disease of the pancreas which, pathologically speaking, extends from the simple edematous form to the complete hemorrhagic necrosis of the gland. Necrohemorrhagic hepatitis is a very serious disease since, depending on the authors, its mortality is estimated to vary from 30 to 70%. In certain cases it is very difficult to establish the diagnosis of acute pancreatitis with certainty (Sarner, M. et al, Gastroenterol. (1984), 13: 865-870). This diagnosis is based in particular on clinical examination (acute abdominal pain), on the determination of a certain number of substances in the plasma or in the peritoneal fluid (Bradley, J. et al., Br. J. Surg. (1981), 68: 245-246; and Dubick, M. et al., Dig. Dis. Sci. (1987), 32: 305-312). The analytical determinations employed include those for amylase, lipase, trypsin, elastase, ribonuclease, phospholipase A2,.alpha.-2 macroglobulin, calcium, LDH, protease inhibitors and others. However, none of them has proved to be specific, practical or above all, discriminating. Hence, it is usually considered sufficient to determine amylasemia. Recently, ultrasonography and computerized tomography have appeared to be able to facilitate the diagnosis of pancreatitis without, however, decisive progress being made (Silverstein, W. et al., Am. J. Roentgenol., (1981), 137: 497-502). In 1984, Keim et al. published (Digestion, (1984), 29: 242-249) results of the consequences of cannulation of the pancreatic duct and the induction of pancreatitis on the protein composition of the pancreatic juice in the rat, this animal being used as an experimental model. After the operation of cannulation (1 to 2 days later), the authors observed a fall in the level of amylase in the pancreatic juice followed, 3 to 4 days after the operation, by a return to the normal amylase level. Web site: http://www.delphion.com/details?pn=US05436169__

Patent Applications on Acute Pancreatitis As of December 2000, U.S. patent applications are open to public viewing.9 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 acute pancreatitis: •

AGENT FOR PREVENTING AND/OR TREATING MULTIPLE ORGAN FAILURE Inventor(s): ARISAWA, HIROHIKO; (TOCHIGI, JP), HIGASHIO, KANJI; (SAITAMA, JP), MASUNAGA, HIROAKI; (TOCHIGI, JP), OGAWA, HIROMI; (TOCHIGI, JP) Correspondence: Testa Hurwitz & Thbeault; High Street Tower; 125 High Street; Boston; MA; 02110 Patent Application Number: 20010051146 Date filed: August 27, 1999

9

This has been a common practice outside the United States prior to December 2000.

98

Acute Pancreatitis

Abstract: The present invention is to provide an agent for preventing and/or treating multiple organ failure comprising Tumor cytotoxic factor-II (TCF-II) or Hepatocyte growth factor (HGF) as an effective ingredient.The agent of the present invention will be useful for preventing and/or treating the development from burn, disseminated intravascular coagulation (DIC), circulatory failure, hemorrhagic shock, infectious disease, acute pancreatitis, ischemic disorder, hepatorenal syndrome, gastrointestinal hemorrhage, nutritional metabolic failure, terminal cancer, acquired immunodeficiency syndrome (AIDS), deterioration of systemic conditions due to radiation affection and cachexia etc. to multiple organ failure. Excerpt(s): The present invention relates to a novel agent for preventing and/or treating multiple organ failure. Development from burn, disseminated intravascular coagulation (DIC), circulatory failure, hemorrhagic shock, infectious disease, acute pancreatitis, ischemic disorder, hepatorenal syndrome, gastrointestial hemorrhage, nutritional metabolic failure, terminal cancer, acquired immunodeficiency syndrome (AIDS), deterioration of systemic conditions due to radiation affection and cachexia etc. to multiple organ failure can be prevented or treated by the present invention. Onset or exacerbation of multiple organ failure can be classified into the following 3 categories with respect to mechanism: (1) Parallel induction of several organ disorders due to the same factor; (2) Induction of a specific organ dysfunction due to disorder of an organ; and (3) Participation of an iatrogenic factor. Excessive insults due to severe trauma or major surgeries, infectious diseases, shock etc. directly or through various kinds of mediator participate in the onset or deterioration of multiple organ failure by mechanism (1). In the case of multiple organ failure accompanied with organ disorder due to trauma or primary hepatic insufficiency, participation of mechanism (2) through organ correlation mechanism will largely contribute to the onset or deterioration thereof. By mechanism (3), medical care carried out during intensive care or care to correspond with an organ disorder may result in the other organ disorder. In patients, these 3 mechanisms participate to the development or deterioration of disorder in a complexed manner. The prognosis of patients of multiple organ failure is generally very poor and, in fact, the survival rate is low as 20-30% in spite of a wide variety of corresponding treatment. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Method of detecting procarboxypeptidase A and carboxypeptidase A levels in biological fluids Inventor(s): Gilvarg, Charles; (Princeton, NJ) Correspondence: Licata & Tyrrell P.C.; 66 E. Main Street; Marlton; NJ; 08053; US Patent Application Number: 20010055785 Date filed: June 12, 2001 Abstract: Methods of enhancing sensitivity and specificity of an assay measuring enzymatic activity in a sample by measuring enzymatic activity in the sample in the presence and absence of a specific inhibitor of the enzymatic activity are provided. Methods of measuring carboxypeptidase A levels and total carboxypeptidase A levels, wherein procarboxypeptidase A is converted to carboxypeptidase A by addition of clostripain, in a biological fluid with a carboxypeptidase A substrate, specificity of which is enhanced by addition of a carboxypeptidase A specific inhibitor are also provided. In addition, methods of diagnosing acute pancreatitis by measurement of

Patents 99

carboxypeptidase A levels and pancreatic cancer by measurement of total carboxypeptidase A levels are also provided. Excerpt(s): This application is a continuation of U.S. patent application Ser. No. 09/402,405 filed Oct. 4, 1999, which is the U.S. National Phase of PCT Application PCT/US98/06615 filed Apr. 10, 1998, which claims the benefit of priority from U.S. Provisional Application Serial Nos. 60/055,495 filed Aug. 12, 1997 and 60/041,835 filed Apr. 10, 1997. Determination of altered enzyme levels by measurement of enzyme activity in biological samples is used routinely by clinicians to assist in the diagnosis of a multitude of diseases or conditions wherein physical symptoms alone may not be definitive. However, the usefulness of such assays is dependent upon the specificity of the enzyme to the disease or condition and the sensitivity and selectivity of the enzymatic assay. For example, acute pancreatitis is defined clinically as a discrete episode of symptoms caused by intrapancreatic activation of digestive enzymes. The cause of this activation is unknown; however, premature activation of zymogen to active enzymes within the pancreas results in autodigestion and inflammation of the pancreas. Symptoms include a steady, dull or boring pain in the epigastrium or left upper abdominal quadrant which is poorly localized and reaches peak intensity within fifteen minutes to one hour. The incidence of acute pancreatitis is difficult to ascertain as uniform diagnostic criteria and effort have not been applied. However, there is an urgency in accurately diagnosing acute pancreatitis to exclude other acute conditions that require different, usually surgical, management such as perforated peptic ulcer, acute cholangitis, appendicitis and mesenteric infarction. In contrast, pancreatitis is best treated through a "hands off" approach of eliminating food intake and increasing hydration. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

METHODS AND COMPOSITIONS FOR THE TREATMENT OF PANCREATITIS Inventor(s): AOKI, KEI ROGER; (COTO DE CAZA, CA), SACHS, GEORGE; (ENCINO, CA) Correspondence: Allergan Inc; 2525 Dupont Drive; Irvine; CA; 92612 Patent Application Number: 20010018049 Date filed: April 8, 1999 Abstract: Methods and compositions for the treatment of acute pancreatitis in a mammal. Particular compositions comprise a binding element, a translocation element, and a therapeutic element able to prevent accumulation of digestive enzymes within the pancreas. Excerpt(s): The present invention includes methods and compositions for the treatment of acute pancreatitis. In a preferred embodiment the invention concerns the use of agents to reduce or prevent the secretion of pancreatic digestive enzymes within the pancreas. Such agents are targeted to pancreatic cells, and serve to prevent the exocytotic fusion of vesicles containing these enzymes with the plasma membrane. The invention is also concerned with methods of treating a mammal suffering from pancreatitis through the administration of such agents. Pancreatitis is a serious medical condition involving an inflammation of the pancreas. In acute or chronic pancreatitis the inflammation manifests itself in the release and activation of pancreatic enzymes within the organ itself, leading to autodigestion. In many cases of acute pancreatitis, the condition can lead to death. In normal mammals, the pancreas, a large gland similar in

100

Acute Pancreatitis

structure to the salivary gland, is responsible for the production and secretion of digestive enzymes, which digest ingested food, and bicarbonate for the neutralization of the acidic chyme produced in the stomach. The pancreas contains acinar cells, responsible for enzyme production, and ductal cells, which secrete large amounts of sodium bicarbonate solution. The combined secretion product is termed "pancreatic juice"; this liquid flows through the pancreatic duct past the sphincter of Oddi into the duodenum. The secretion of pancreatic juice is stimulated by the presence of chyme in the upper portions of the small intestine, and the precise composition of pancreatic juice appears to be influenced by the types of compounds (carbohydrate, lipid, protein, and/or nucleic acid) in the chyme. 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 acute pancreatitis, 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 “acute pancreatitis” (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 acute pancreatitis. You can also use this procedure to view pending patent applications concerning acute pancreatitis. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.

101

CHAPTER 6. BOOKS ON ACUTE PANCREATITIS Overview This chapter provides bibliographic book references relating to acute pancreatitis. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on acute pancreatitis 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 “acute pancreatitis” (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 acute pancreatitis: •

ABC of Liver, Pancreas and Gall Bladder Source: London, UK: BMJ Publishing Group. 2001. 54 p. Contact: Available from BMJ Publishing Group. BMA Books, BMA House, Tavistock Square, London WCIH 9JR. Fax 44 (0)20 7383 6402. E-mail: [email protected]. Website: www.bmjbooks.com. PRICE: Contact publisher for price. ISBN: 0727915312. Summary: Diseases of the liver, pancreas, and biliary system affect a substantial proportion of the world's population and involve doctors and health care workers across many disciplines. Many of these disease produce great misery and distress and are economically important requiring much time off work. This atlas of the liver, pancreas and gallbladder provides an overview of these diseases and enable the busy clinician to keep abreast of advances in diagnosis and management of not only the common but also the rarer, but none the less important, conditions. The atlas includes

102

Acute Pancreatitis

fourteen chapters: investigation of liver and biliary disease, gallstone disease, acute hepatitis, chronic viral hepatitis, other causes of parenchymal liver disease, portal hypertension and ascites, portal hypertension and encephalopathy, liver tumors, liver abscesses and hydatid disease, acute pancreatitis, chronic pancreatitis, pancreatic tumors, liver and pancreatic trauma, and transplantation of the liver and pancreas. Each chapter covers the symptoms, diagnosis, etiology, natural course, and treatment of the disease under consideration. Each chapter is illustrated with full-color diagrams, charts, and clinical photographs. A subject index concludes the book. •

Hepatobiliary and Pancreatic Disease: The Team Approach to Management Source: Boston, MA: Little, Brown and Company. 1995. 493 p. Contact: Available from Lippincott-Raven Publishers. 12107 Insurance Way, Hagerstown, MD 21740. (800) 777-2295. Fax (301) 824-7390. E-mail: [email protected]. Website: http://www.lrpub.com. PRICE: $99.95. ISBN: 0316709158. Summary: In this book, the editors identify 42 hepatobiliary and pancreatic problems that require a team approach to management. For each of the 42 chapters, a surgeon, gastroenterologist, or radiologist is the lead author, and physicians from different specialties are coauthors. The authors discuss etiology, pathogenesis, and diagnosis, but focus on patient management and results. The chapters cover hepatitis, hepatic failure, cirrhosis, portal hypertension, primary biliary cirrhosis, Budd-Chiari syndrome, noninflammatory cysts, hepatic abscesses, hydatid disease, hemobilia, hepatic trauma, benign hepatic tumors, hepatocellular carcinoma, hepatic metastases, biliary atresia, biliary cysts, gallbladder stones, choledocholithiasis, hepatolithiasis, acute cholecystitis, acute cholangitis, biliary parasites, sclerosing cholangitis, benign strictures, motility disorders, gallbladder cancer, cholangiocarcinoma, acute pancreatitis, gallstone pancreatitis, pseudocysts, pancreatic abscesses, pancreatic necrosis, pancreatic hemorrhage, pancreas divisum, chronic pancreatitis, pancreatic fistulas, pancreatic trauma, islet cell tumors, cystic neoplasms, ampullary carcinoma, and pancreatic cancer. Each chapter includes numerous black-and-white photographs, and a subject index concludes the volume.

•

Gastroenterology and Hepatology: The Comprehensive Visual Reference. Volume 8: Pancreas Source: Philadelphia, PA: Current Medicine. 1998. [200 p.]. Contact: Available from Current Medicine. 400 Market Street, Suite 700, Philadelphia, PA 19106. (800) 427-1796 or (215) 574-2266. Fax (215) 574-2270. E-mail: [email protected]. Website: current-medicine.com. PRICE: $125.00 plus shipping and handling. ISBN: 0443078629. Summary: This atlas is one in an 8-volume collection of images that pictorially displays the gastrointestinal tract, liver, biliary tree, and pancreas in health and disease, both in children and adults. This volume includes 10 chapters on the pancreas. Topics covered include neurohormonal control of the pancreas, pathogenesis of pancreatic diseases, acute pancreatitis, chronic pancreatitis, surgery for chronic pancreatitis, developmental anomalies of the pancreas, pancreatic cancer, the rationale and application of radioligand imaging in gastroenterology, cystic fibrosis, and hereditary pancreatitis. The format of the atlas is visual images supported by relatively brief text. Tables, charts, diagrams, and photomicrographs are used extensively. A subject index concludes the volume.

Books

•

103

Evidence Based Gastroenterology and Hepatology Source: London, UK: BMJ Publishing Group. 1999. 557 p. Contact: Available from BMJ Publishing Group. BMA Books, BMA House, Tavistock Square, London WCIH 9JR. Fax 44 (0)20 7383 6402. E-mail: [email protected]. Website: www.bmjbooks.com. PRICE: Contact publisher for price. ISBN: 0727911821. Summary: This book emphasizes the approaches of evidence based medicine in gastroenterology (the study of the gastrointestinal tract and gastrointestinal diseases) and hepatology (the study of the liver and liver diseases). The authors use clinical epidemiology to present the strongest and most current evidence for interventions for the major diseases of the gastrointestinal tract and liver. Thirty chapters are included: an introduction to evidence based gastroenterology and hepatology; gastroesophageal reflux disease (GERD); ulcer disease and Helicobacter pylori; ulcer disease and nonsteroidal antiinflammatory drugs; treatment options for non-variceal gastrointestinal hemorrhage; the diagnosis and treatment of functional dyspepsia (indigestion); the diagnosis, treatment, and prognosis of celiac disease (gluten intolerance); the treatment of Crohn's disease; the diagnosis, prognosis, and treatment of ulcerative colitis (UC); pouchitis after restorative proctocolectomy; metabolic bone disease in gastrointestinal disorders; colorectal cancer in UC and the role of surveillance; population based screening and surveillance for colorectal cancer; irritable bowel syndrome (IBS); the surgical treatment of gallstone disease; the prognosis and treatment of acute pancreatitis; hepatitis C; hepatitis B; the screening and treatment of alcoholic liver disease; hemochromatosis and Wilson disease; primary biliary cirrhosis (PBC); autoimmune hepatitis; primary sclerosing cholangitis (PSC); the prevention and treatment of portal hypertensive bleeding; ascites, hepatorenal syndrome, and spontaneous bacterial peritonitis; hepatic encephalopathy; hepatocellular carcinoma; fulminant hepatic failure; the prevention and treatment of rejection after liver transplantation; and the prevention and treatment of infection after liver transplantation. Each chapter features the grading of recommendations and levels of evidence used by the authors to note the research basis on which their clinical guidelines are formed. Chapters conclude with extensive reference lists; the text concludes with a subject index. A glossary of acronyms is also provided.

•

Clinical Practice of Gastroenterology. Volume Two Source: Philadelphia, PA: Current Medicine. 1999. 861 p. Contact: Available from W.B. Saunders Company. Order Fulfillment, 6277 Sea Harbor Drive, Orlando, FL 32887. (800) 545-2522. Fax (800) 874-6418 or (407) 352-3445. Website: www.wbsaunders.com. PRICE: $235.00 plus shipping and handling. ISBN: 0443065209 (two volume set); 0443065217 (volume 1); 0443065225 (volume 2). Summary: This lengthy textbook brings practitioners up to date on the complexities of gastroenterology practice, focusing on the essentials of patient care. This second volume includes 113 chapters in five sections: liver, gallbladder and biliary tract, pancreas, pediatric gastroenterology, and special topics. Specific topics include hepatic (liver) structure and function, jaundice, viral hepatitis, alcoholic liver injury, liver tumors, parasitic diseases of the liver, Wilson's disease, hemochromatosis, the pregnancy patient with liver disease, portal hypertension, hepatic encephalopathy, fulminant hepatic failure, liver transplantation, the anatomy of the gallbladder and biliary tract, gallstones, laparoscopic cholecystectomy (gallbladder removal), cholecystitis (gallbladder infection), primary sclerosing cholangitis, biliary obstruction, pancreatic anatomy and physiology, acute pancreatitis, pancreatic fistulas and ascites (fluid accumulation),

104

Acute Pancreatitis

chronic pancreatitis, cancer of the pancreas, endoscopic retrograde cholangiopancreatography, esophageal atresia, gastroesophageal reflux in infants and children, achalasia and esophageal motility disorders, caustic and foreign body ingestion, vomiting, chronic abdominal pain, gastritis and peptic ulcer disease in children, malabsorption syndromes in children, inflammatory bowel disease in children and adolescents, acute appendicitis, cystic fibrosis, constipation and fecal soiling (incontinence), hepatitis in children, liver transplantation in children, failure to thrive, pediatric AIDS, the gastrointestinal manifestations of AIDS, the evaluation and management of acute upper gastrointestinal bleeding, principles of endoscopy, eating disorders, nutritional assessment, enteral and parenteral nutrition, gastrointestinal diseases in the elderly and in pregnancy, nosocomial infections, and the psychosocial aspects of gastroenterology (doctor patient interactions). The chapters include figures, algorithms, charts, graphs, radiographs, endoscopic pictures, intraoperative photographs, photomicrographs, tables, and extensive references. The volume concludes with a detailed subject index and a section of color plates.

Chapters on Acute Pancreatitis In order to find chapters that specifically relate to acute pancreatitis, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and acute pancreatitis 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 “acute pancreatitis” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on acute pancreatitis: •

Acute Pancreatitis: Prognosis and Treatment Source: in McDonald, J.W.D.; Burroughs, A.K.; Feagan, B.G., eds. Evidence Based Gastroenterology and Hepatology. London, UK: BMJ Publishing Group. 1999. p. 271293. Contact: Available from BMJ Publishing Group. BMA Books, BMA House, Tavistock Square, London WCIH 9JR. Fax 44 (0)20 7383 6402. E-mail: [email protected]. Website: www.bmjbooks.com. PRICE: Contact publisher for price. Summary: This chapter on the prognosis and treatment of acute pancreatitis is from a book that emphasizes the approaches of evidence based medicine in gastroenterology (the study of the gastrointestinal tract and gastrointestinal diseases) and hepatology (the study of the liver and liver diseases). The authors of this chapter review the evidence available from the literature that examines the use of various prognostic instruments and the medical, surgical, and endoscopic treatment options available for acute pancreatitis. Most patients with acute pancreatitis will have a mild form and ultimately follow a benign clinical course, but up to 20 percent will develop severe pancreatitis with all its inherent morbidity (illness) and risk of mortality (death). Medical management remains the mainstay of treatment for patients with acute pancreatitis. Early reduction in the systemic response to pancreatitis might be achieved with drug therapy, but this has not been proven to be effective with the medications presently available. Antibiotic prophylaxis is likely to become part of the standard therapy for those with necrotizing pancreatitis. While total parenteral nutrition (TPN) is of little

Books

105

benefit for those with severe pancreatitis, early enteral feeding shows promise and should become the standard method of nutritional supplementation in these patients. The role of peritoneal lavage (washing out of the organ or peritoneal cavity) remains controversial and the patient population that may benefit from this intervention is not well defined. The surgical approach still remains controversial but, based on the evidence available, widespread necrosectomy (removal of the dead tissue) and lavage, or necrosectomy and open management probably results in a better overall outcome than the conventional surgical approach. 10 tables. 123 references.

107

CHAPTER 7. PERIODICALS AND NEWS ON ACUTE PANCREATITIS Overview In this chapter, we suggest a number of news sources and present various periodicals that cover acute pancreatitis.

News Services and Press Releases One of the simplest ways of tracking press releases on acute pancreatitis 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 “acute pancreatitis” (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 acute pancreatitis. 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 “acute pancreatitis” (or synonyms). The following was recently listed in this archive for acute pancreatitis: •

Antibiotic prophylaxis in severe acute pancreatitis may not improve outcomes Source: Reuters Industry Breifing Date: April 07, 2004

108

Acute Pancreatitis

•

Cimetidine ineffective for acute pancreatitis Source: Reuters Industry Breifing Date: July 23, 2002

•

Serum IL-10 and IL-11 concentrations reflect acute pancreatitis severity Source: Reuters Medical News Date: December 24, 1999

•

AIDS does not increase severity of acute pancreatitis Source: Reuters Medical News Date: March 18, 1999

•

Extracorporeal Membrane Oxygenation Efficacious For ARDS Linked To Acute Pancreatitis Source: Reuters Medical News Date: April 28, 1998

•

New Dipstick Test Effective For Acute Pancreatitis Screening In The ED Source: Reuters Medical News Date: June 19, 1997

•

Urinary Test Strip May Help Diagnose Acute Pancreatitis Source: Reuters Medical News Date: March 20, 1996

•

Octreotide Shows Promise In The Treatment Of Acute Pancreatitis Source: Reuters Medical News Date: August 14, 1995 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 “acute pancreatitis” (or synonyms) into the search box, and click on “Search News.” As this service

Periodicals and News

109

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 “acute pancreatitis” (or synonyms). If you know the name of a company that is relevant to acute pancreatitis, 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/. 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 “acute pancreatitis” (or synonyms).

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 “acute pancreatitis” (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 acute pancreatitis: •

Following Endoscopic Therapy. Pancreatitis Patients Report Pain Relief Source: Gastroenterology and Endoscopy News. 51(10): 1, 41. 2000. Contact: Available from McMahon Publishing Group. 545 West 45th Street, 8th Floor, New York, NY 10036. (212) 957-5300. Website: www.mcmahonmed.com. Summary: This news article reports on a retrospective study that has demonstrated that endoscopic therapy can have significant long term benefits on patients with chronic pancreatitis (inflammation of the pancreas), and that the technique offers similar success rates to those of surgery, while being minimally invasive for the patient. The study revealed that more than 60 percent of patients with chronic pancreatitis or unexplained abdominal pain resulting from pancreatic sphincter dysfunction reported a greater than 50 percent decrease in their pain 16 months after endoscopic therapy. Complications of endoscopic pancreatic sphincterotomy (EPS) included pancreatitis (9 percent of patients), bleeding (4 percent of patients), and early stent occlusion (blockage) in 9 percent of patients. There were no deaths related to the procedure and no patient developed severe acute pancreatitis. The study results need to be evaluated further in a prospective fashion. The article includes the comments of one expert who cautions that

110

Acute Pancreatitis

the role of endoscopic therapy in pancreatic disease has always been controversial, especially because pancreatitis is a 'dreaded complication' of endoscopic therapy to the pancreas. •

Pancreatitis: Painful Attacks Should Not Be Ignored Source: Mayo Clinic Health Letter. 17(10): 4-5. October 1999. 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 newsletter article from the Mayo Clinic reviews the problem of pancreatitis attacks, stressing that acute pancreatitis warrants immediate medical care to avoid complications that can be fatal. Acute pancreatitis attacks consist of a sudden pain in the upper abdomen that seems to go straight through to the back and that does not ease up. The author briefly reviews the physiology and functions of the pancreas, including production of the hormones insulin and glucagon, which help regulate metabolism; and production of pancreatic juices and enzymes that are delivered to the upper part of the small intestine (duodenum) to help digest fats, proteins, and carbohydrates. Inflammation of the pancreas disrupts these functions. Acute pancreatitis comes on suddenly when digestive juices from the pancreas escape the ducts leading to the small intestine and instead enter pancreas tissue itself, causing potentially severe damage. Acute pancreatitis is usually caused by either gallstones leaving the gallbladder and obstructing the pancreatic duct, or by excessive alcohol use. Most attacks of pancreatitis range from mild to moderate and may last only a couple of days. Treatment often involves a hospital stay and no food or drink by mouth (in order to rest the pancreas). By comparison, chronic pancreatitis (progressive inflammation and damage to the pancreas) is sometimes difficult to detect early. Most of the time it is caused by excessive alcohol use over many years. Treatment for chronic pancreatitis focuses on pain management and preventing attacks by avoiding alcohol, following a careful diet, and working closely with a health care provider. 1 figure.

Academic Periodicals covering Acute Pancreatitis Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to acute pancreatitis. In addition to these sources, you can search for articles covering acute pancreatitis 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.”

111

APPENDICES

113

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 Institute10: •

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/

10

These publications are typically written by one or more of the various NIH Institutes.

114

Acute Pancreatitis

•

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/

•

National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/

•

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

•

National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm

•

National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm

•

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

•

National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm

•

Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp

•

National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/

•

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

Physician Resources

115

NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.11 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:12 •

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

11

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). 12 See http://www.nlm.nih.gov/databases/databases.html.

116

Acute Pancreatitis

•

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 NLM Gateway13 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.14 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “acute pancreatitis” (or synonyms) into the search box and click “Search.” The results 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 17984 99 947 41 332 19403

HSTAT15 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.16 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.17 Simply search by “acute pancreatitis” (or synonyms) at the following Web site: http://text.nlm.nih.gov.

13

Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.

14

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). 15 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 16 17

The HSTAT URL is http://hstat.nlm.nih.gov/.

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.

Physician Resources

117

Coffee Break: Tutorials for Biologists18 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.19 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.20 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/.

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/.

18 Adapted 19

from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html.

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. 20 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.

119

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 acute pancreatitis 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 acute pancreatitis. 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 acute pancreatitis. 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 “acute pancreatitis”:

120

Acute Pancreatitis

Cancer http://www.nlm.nih.gov/medlineplus/cancer.html Digestive Diseases http://www.nlm.nih.gov/medlineplus/digestivediseases.html Laboratory Tests http://www.nlm.nih.gov/medlineplus/laboratorytests.html Pancreatic Diseases http://www.nlm.nih.gov/medlineplus/pancreaticdiseases.html Ulcerative Colitis http://www.nlm.nih.gov/medlineplus/ulcerativecolitis.html 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 acute pancreatitis. 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: •

Acute Pancreatitis Source: Wexford, PA: National Pancreas Foundation. 200x. [4 p.]. Contact: Available from National Pancreas Foundation. P.O. Box 935, Wexford, PA 15090-0935. (866) 726-2737. Website: www.pancreasfoundation.org. PRICE: Single copy free. Summary: This brochure provides basic information about acute pancreatitis, a sudden inflammation of the pancreas that is usually associated with severe upper abdominal pain. The most common cause of acute pancreatitis is gallstones. Other causes include alcohol abuse, hereditary conditions, trauma, medications, infections, electrolyte abnormalities, high lipid levels, and hormonal abnormalities. The brochure reviews these causes, then discusses the clinical signs of acute pancreatitis, diagnostic tests used to confirm the condition, and treatment options. Treatment for acute pancreatitis depends on the severity of the condition. Sometimes the patient needs hospitalization with administration of intravenous fluids to help restore blood volume. Antibiotics are often prescribed if infection occurs and pain medications are often used to provide relief. Surgery is sometimes needed when complications such as infection, cysts, or bleeding occur. Patients usually recover fully form acute pancreatitis and do not experience recurrence if the cause is removed. 1 figure.

Patient Resources

121

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 “acute pancreatitis” (or synonyms). The following was recently posted: •

ACR Appropriateness Criteria™ for acute pancreatitis Source: American College of Radiology - Medical Specialty Society; 1998 (revised 2001); 5 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3257&nbr=2483&a mp;string=acute+AND+pancreatitis

•

Treatment of acute pancreatitis Source: Society for Surgery of the Alimentary Tract, Inc - Medical Specialty Society; 1996 (revised 2000 Jan); 3 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2166&nbr=1392&a mp;string=acute+AND+pancreatitis 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 acute pancreatitis. 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. 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/

•

WebMDHealth: http://my.webmd.com/health_topics

122

Acute Pancreatitis

Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to acute pancreatitis. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with acute pancreatitis. 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 acute pancreatitis. 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 “acute pancreatitis” (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 “acute pancreatitis”. 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 “acute pancreatitis” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months.

Patient Resources

123

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 “acute pancreatitis” (or a synonym) into the search box, and click “Submit Query.”

125

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.21

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

21

Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.

126

Acute Pancreatitis

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)22: •

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)

•

Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm

•

California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html

•

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

•

California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html

•

California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/

•

California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/

•

California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/

•

California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html

•

California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/

•

Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/

•

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/

22

Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.

Finding Medical Libraries

127

•

Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml

•

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

•

Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html

•

Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm

•

Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp

•

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

•

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

•

Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/

•

Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/

•

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

•

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/

128

Acute Pancreatitis

•

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

•

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

•

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/

Finding Medical Libraries

129

•

Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm

•

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/

130

Acute Pancreatitis

•

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

131

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 acute pancreatitis: •

Basic Guidelines for Acute Pancreatitis Acute pancreatitis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000287.htm

•

Signs & Symptoms for Acute Pancreatitis Abdomen, swollen Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003122.htm Abdominal fullness, gaseous Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003124.htm Abdominal indigestion Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003260.htm Abdominal pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003120.htm

132

Acute Pancreatitis

Anxiety Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003211.htm Fever Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003090.htm Hiccups Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003068.htm Indigestion Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003260.htm Jaundice Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003243.htm Low blood pressure Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003083.htm Nausea Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003117.htm Skin rash or lesion Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003220.htm Swelling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003103.htm Vomiting Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003117.htm •

Diagnostics and Tests for Acute Pancreatitis Abdominal CT scan Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003789.htm Abdominal MRI Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003796.htm Abdominal ultrasound Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003777.htm ALT Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003473.htm AST Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003472.htm Blood pressure Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003398.htm Calcium (ionized) Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003486.htm

Online Glossaries 133

CBC Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003642.htm CEA Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003574.htm CT Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003330.htm Cysts Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003240.htm Fecal fat Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003588.htm Glucagon Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003716.htm Glucose test Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003482.htm Heart rate Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003399.htm LDH Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003471.htm LDH isoenzymes Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003499.htm MRI Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003335.htm Serum amylase Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003464.htm Serum calcium Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003477.htm Serum lipase Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003465.htm Serum magnesium - test Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003487.htm Trypsinogen Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003560.htm Ultrasound Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003336.htm

134

Acute Pancreatitis

Urine amylase Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003607.htm WBC count Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003643.htm •

Nutrition for Acute Pancreatitis Fat Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002468.htm

•

Background Topics for Acute Pancreatitis Alcohol abuse Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001944.htm Alcohol use Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001944.htm Analgesics Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002123.htm Bile Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002237.htm Chronic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002312.htm Endoscopic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002360.htm Hemorrhagic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002373.htm Immunizations - general overview Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002024.htm Intravenous Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002383.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

Online Glossaries 135

•

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

137

ACUTE PANCREATITIS DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 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 Pain: Sensation of discomfort, distress, or agony in the abdominal region. [NIH] Abscess: A localized, circumscribed collection of pus. [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] Acetaminophen: Analgesic antipyretic derivative of acetanilide. It has weak antiinflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage. [NIH] 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] Acne: A disorder of the skin marked by inflammation of oil glands and hair glands. [NIH] Acne Vulgaris: A chronic disorder of the pilosebaceous apparatus associated with an increase in sebum secretion. It is characterized by open comedones (blackheads), closed comedones (whiteheads), and pustular nodules. The cause is unknown, but heredity and age are predisposing factors. [NIH] Acquired Immunodeficiency Syndrome: An acquired defect of cellular immunity associated with infection by the human immunodeficiency virus (HIV), a CD4-positive Tlymphocyte count under 200 cells/microliter or less than 14% of total lymphocytes, and increased susceptibility to opportunistic infections and malignant neoplasms. Clinical manifestations also include emaciation (wasting) and dementia. These elements reflect criteria for AIDS as defined by the CDC in 1993. [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] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [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] Adenocarcinoma: A malignant epithelial tumor with a glandular organization. [NIH]

138

Acute Pancreatitis

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] Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [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] Adverse Effect: An unwanted side effect of treatment. [NIH] Afferent: Concerned with the transmission of neural impulse toward the central part of the nervous system. [NIH] Afferent Loop Syndrome: A complication of gastrojejunostomy, caused by acute or chronic obstruction of the afferent loop due to hernia, intussusception, kinking, volvulus, etc. It is characterized by pain and vomiting of bile-stained fluid and includes acute afferent loop obstruction. [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] Affinity Chromatography: In affinity chromatography, a ligand attached to a column binds specifically to the molecule to be purified. [NIH] 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]

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] 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] Aldehydes: Organic compounds containing a carbonyl group in the form -CHO. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH]

Dictionary 139

Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU] Alkaline: Having the reactions of an alkali. [EU] 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] Allergen: An antigenic substance capable of producing immediate-type hypersensitivity (allergy). [EU] Allopurinol: A xanthine oxidase inhibitor that decreases uric acid production. [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] 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] 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] Ameliorated: 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 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] 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] 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] Amylase: An enzyme that helps the body digest starches. [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

140

Acute Pancreatitis

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] Anabolic: Relating to, characterized by, or promoting anabolism. [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] 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] 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 shows no spasmogenic activity though it contains some chemotactic ability. [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] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [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] Anginal: Pertaining to or characteristic of angina. [EU] Angiotensinogen: An alpha-globulin of which a fragment of 14 amino acids is converted by renin to angiotensin I, the inactive precursor of angiotensin II. It is a member of the serpin superfamily. [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] Anionic: Pertaining to or containing an anion. [EU] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Anomalies: Birth defects; abnormalities. [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] 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]

Dictionary 141

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] Anticholinergics: Medicines that calm muscle spasms in the intestine. Examples are dicyclomine (dy-SY-kloh-meen) (Bentyl) and hyoscyamine (HY-oh-SY-uh-meen) (Levsin). [NIH]

Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Anticonvulsant: An agent that prevents or relieves convulsions. [EU] Antidiabetic: An agent that prevents or alleviates diabetes. [EU] 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] Anti-inflammatory: Having to do with reducing 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] 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] Antispasmodic: An agent that relieves spasm. [EU] Anuria: Inability to form or excrete urine. [NIH] Anus: The opening of the rectum to the outside of the body. [NIH] Apolipoproteins: The protein components of lipoproteins which remain after the lipids to which the proteins are bound have been removed. They play an important role in lipid transport and metabolism. [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] Appendicitis: Acute inflammation of the vermiform appendix. [NIH] Aqueous: Having to do with water. [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

142

Acute Pancreatitis

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] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arteriography: A procedure to x-ray arteries. The arteries can be seen because of an injection of a dye that outlines the vessels on an x-ray. [NIH] Arteriolar: Pertaining to or resembling arterioles. [EU] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] 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] Arteriovenous: Both arterial and venous; pertaining to or affecting an artery and a vein. [EU] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Articular: Of or pertaining to a joint. [EU] Ascites: Accumulation or retention of free fluid within the peritoneal cavity. [NIH] Ascitic Fluid: The serous fluid which accumulates in the peritoneal cavity in ascites. [NIH] Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant. [NIH] Asparaginase: A hydrolase enzyme that converts L-asparagine and water to L-aspartate and NH3. EC 3.5.1.1. [NIH] Aspartate: A synthetic amino acid. [NIH] Aspartic Acid: One of the non-essential amino acids commonly occurring in the L-form. It is found in animals and plants, especially in sugar cane and sugar beets. It may be a neurotransmitter. [NIH] Aspiration: The act of inhaling. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Asymptomatic: Having no signs or symptoms of disease. [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] 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] 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

Dictionary 143

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] Autolysis: The spontaneous disintegration of tissues or cells by the action of their own autogenous enzymes. [NIH] Autosuggestion: Suggestion coming from the subject himself. [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 Physiology: Physiological processes and activities of bacteria. [NIH] Bacterial Translocation: The passage of viable bacteria from the gastrointestinal tract to extra-intestinal sites, such as the mesenteric lymph node complex, liver, spleen, kidney, and blood. Factors that promote bacterial translocation include overgrowth with gram-negative enteric bacilli, impaired host immune defenses, and injury to the intestinal mucosa resulting in increased intestinal permeability. These mechanisms can act in concert to promote synergistically the systemic spread of indigenous translocating bacteria to cause lethal sepsis. [NIH] Bactericidal: Substance lethal to bacteria; substance capable of killing bacteria. [NIH] Balloon dilation: A treatment for benign prostatic hyperplasia or prostate enlargement. A tiny balloon is inflated inside the urethra to make it wider so urine can flow more freely from the bladder. [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] 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] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]

Benign prostatic hyperplasia: A benign (noncancerous) condition in which an overgrowth of prostate tissue pushes against the urethra and the bladder, blocking the flow of urine. Also called benign prostatic hypertrophy or BPH. [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] 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

144

Acute Pancreatitis

digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones. [NIH] Bile duct: A tube through which bile passes in and out of the liver. [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 Atresia: Atresia of the biliary tract, most commonly of the extrahepatic bile ducts. [NIH]

Biliary Tract: The gallbladder and its ducts. [NIH] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [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] Bladder: The organ that stores urine. [NIH] Bloating: Fullness or swelling in the abdomen that often occurs after meals. [NIH] Blood Cell Count: A count of the number of leukocytes and erythrocytes per unit volume in a sample of venous blood. A complete blood count (CBC) also includes measurement of the hemoglobin, hematocrit, and erythrocyte indices. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Coagulation Factors: Endogenous substances, usually proteins, that are involved in the blood coagulation process. [NIH] Blood Glucose: Glucose in blood. [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] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blood Volume: Volume of circulating blood. It is the sum of the plasma volume and erythrocyte volume. [NIH] Blot: To transfer DNA, RNA, or proteins to an immobilizing matrix such as nitrocellulose. [NIH]

Body Fluids: Liquid components of living organisms. [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

Dictionary 145

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] 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] 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] Bronchoconstriction: Diminution of the caliber of a bronchus physiologically or as a result of pharmacological intervention. [NIH] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [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] Caerulein: A specific decapeptide obtained from the skin of Hila caerulea, an Australian amphibian. Caerulein is similar in action and composition to cholecystokinin. It stimulates gastric, biliary, and pancreatic secretion and certain smooth muscle. It is used in paralytic ileus and as diagnostic aid in pancreatic malfunction. [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] 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] 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] 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] Carboxy: Cannabinoid. [NIH]

146

Acute Pancreatitis

Carcinogenic: Producing carcinoma. [EU] Carcinogens: Substances that increase the risk of neoplasms in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included. [NIH] Carcinoid: A type of tumor usually found in the gastrointestinal system (most often in the appendix), and sometimes in the lungs or other sites. Carcinoid tumors are usually benign. [NIH]

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] 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] Caspases: A family of intracellular cysteine endopeptidases. They play a key role in inflammation and mammalian apoptosis. They are specific for aspartic acid at the P1 position. They are divided into two classes based on the lengths of their N-terminal prodomains. Caspases-1,-2,-4,-5,-8, and -10 have long prodomains and -3,-6,-7,-9 have short prodomains. EC 3.4.22.-. [NIH] Catabolism: Any destructive metabolic process by which organisms convert substances into excreted compounds. [EU] 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] Catheter: A flexible tube used to deliver fluids into or withdraw fluids from the body. [NIH] Causal: Pertaining to a cause; directed against a cause. [EU] Caustic: An escharotic or corrosive agent. Called also cauterant. [EU] Cefamandole: Semisynthetic wide-spectrum cephalosporin with prolonged action, probably due to beta-lactamase resistance. It is used also as the nafate. [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 Cycle: The complex series of phenomena, occurring between the end of one cell division and the end of the next, by which cellular material is divided between daughter cells. [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]

Dictionary 147

Cell Division: The fission of a cell. [NIH] Cell Lineage: The developmental history of cells as traced from the first division of the original cell or cells in the embryo. [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] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [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] Cephalothin: A cephalosporin antibiotic. [NIH] Cerebral: Of or pertaining of the cerebrum or the 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] Ceroid: A naturally occurring lipid pigment with histochemical characteristics similar to lipofuscin. It accumulates in various tissues in certain experimental and pathological conditions. [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] Chemical Warfare: Tactical warfare using incendiary mixtures, smokes, or irritant, burning, or asphyxiating gases. [NIH] Chemical Warfare Agents: Chemicals that are used to cause the disturbance, disease, or death of humans during war. [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] 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] Chemotherapy: Treatment with anticancer drugs. [NIH] Cholangiography: Radiographic examination of the bile ducts. [NIH] Cholangitis: Inflammation of a bile duct. [NIH] Cholecystectomy: Surgical removal of the gallbladder. [NIH] Cholecystitis: Inflammation of the gallbladder. [NIH] Cholecystokinin: A 33-amino acid peptide secreted by the upper intestinal mucosa and also found in the central nervous system. It causes gallbladder contraction, release of pancreatic exocrine (or digestive) enzymes, and affects other gastrointestinal functions. Cholecystokinin may be the mediator of satiety. [NIH]

148

Acute Pancreatitis

Choledocholithiasis: Gallstones in the bile ducts. [NIH] Cholelithiasis: Presence or formation of gallstones. [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] 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] Choroid: The thin, highly vascular membrane covering most of the posterior of the eye between the retina and sclera. [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] 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 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] Chyme: A thick liquid made of partially digested food and stomach juices. This liquid is made in the stomach and moves into the small intestine for further digestion. [NIH] Chymotrypsin: A serine endopeptidase secreted by the pancreas as its zymogen, chymotrypsinogen and carried in the pancreatic juice to the duodenum where it is activated by trypsin. It selectively cleaves aromatic amino acids on the carboxyl side. [NIH] Cirrhosis: A type of chronic, progressive liver disease. [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 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] 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] 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] 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]

Dictionary 149

Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Colitis: Inflammation of the colon. [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] Colon: The long, coiled, tubelike organ that removes water from digested food. The remaining material, solid waste called stool, moves through the colon to the rectum and leaves the body through the anus. [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] Combination Therapy: Association of 3 drugs to treat AIDS (AZT + DDC or DDI + protease inhibitor). [NIH] Common Bile Duct: The largest biliary duct. It is formed by the junction of the cystic duct and the hepatic duct. [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] Complement Activation: The sequential activation of serum components C1 through C9,

150

Acute Pancreatitis

initiated by an erythrocyte-antibody complex or by microbial polysaccharides and properdin, and producing an inflammatory response. [NIH] 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, 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] 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] Computerized 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 computerized axial tomography (CAT) scan and computed tomography (CT scan). [NIH] Confusion: A mental state characterized by bewilderment, emotional disturbance, lack of clear thinking, and perceptual disorientation. [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 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]

Dictionary 151

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] 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] Consultation: A deliberation between two or more physicians concerning the diagnosis and the proper method of treatment in a case. [NIH] 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 medium: A substance that is introduced into or around a structure and, because of the difference in absorption of x-rays by the contrast medium and the surrounding tissues, allows radiographic visualization of the structure. [EU] 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] 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] 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] Cornea: The transparent part of the eye that covers the iris and the pupil and allows light to enter the inside. [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 Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [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 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]

152

Acute Pancreatitis

Creatinine: A compound that is excreted from the body in urine. Creatinine levels are measured to monitor kidney function. [NIH] Creatinine clearance: A test that measures how efficiently the kidneys remove creatinine and other wastes from the blood. Low creatinine clearance indicates impaired kidney function. [NIH] Critical Care: Health care provided to a critically ill patient during a medical emergency or crisis. [NIH] Crossing-over: The exchange of corresponding segments between chromatids of homologous chromosomes during meiosia, forming a chiasma. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Cutaneous: Having to do with the skin. [NIH] Cyanosis: A bluish or purplish discoloration of the skin and mucous membranes due to an increase in the amount of deoxygenated hemoglobin in the blood or a structural defect in the hemoglobin molecule. [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] Cyst: A sac or capsule filled with fluid. [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 process. This group of enzymes is inactivated by sulfhydryl reagents. EC 3.4.22. [NIH] Cystic Duct: The tube that carries bile from the gallbladder into the common bile duct and the small intestine. [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]

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] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [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] Cytotoxic: Cell-killing. [NIH] Decarboxylation: The removal of a carboxyl group, usually in the form of carbon dioxide, from a chemical compound. [NIH] Decontamination: The removal of contaminating material, such as radioactive materials, biological materials, or chemical warfare agents, from a person or object. [NIH]

Dictionary 153

Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [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] 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] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diabetic Ketoacidosis: Complication of diabetes resulting from severe insulin deficiency coupled with an absolute or relative increase in glucagon concentration. The metabolic acidosis is caused by the breakdown of adipose stores and resulting increased levels of free fatty acids. Glucagon accelerates the oxidation of the free fatty acids producing excess ketone bodies (ketosis). [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Dialyzer: A part of the hemodialysis machine. (See hemodialysis under dialysis.) The dialyzer has two sections separated by a membrane. One section holds dialysate. The other holds the patient's blood. [NIH] Diarrhea: Passage of excessively liquid or excessively frequent stools. [NIH] Diastolic: Of or pertaining to the diastole. [EU] Dicyclomine: A muscarinic antagonist used as an antispasmodic and in urinary incontinence. It has little effect on glandular secretion or the cardiovascular system. It does have some local anesthetic properties and is used in gastrointestinal, biliary, and urinary tract spasms. [NIH] Dietary Fats: Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados. [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] 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]

154

Acute Pancreatitis

Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Discrete: Made up of separate parts or characterized by lesions which do not become blended; not running together; separate. [NIH] 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] Disinfectant: An agent that disinfects; applied particularly to agents used on inanimate objects. [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 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] Double-blind: Pertaining to a clinical trial or other experiment in which neither the subject nor the person administering treatment knows which treatment any particular subject is receiving. [EU] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Duct: A tube through which body fluids pass. [NIH] Duodenum: The first part of the small intestine. [NIH] Dyspepsia: Impaired digestion, especially after eating. [NIH] Dyspnea: Difficult or labored breathing. [NIH] Eating Disorders: A group of disorders characterized by physiological and psychological disturbances in appetite or food intake. [NIH] Eclampsia: Onset of convulsions or coma in a previously diagnosed pre-eclamptic patient. [NIH]

Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [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] Elastic: Susceptible of resisting and recovering from stretching, compression or distortion applied by a force. [EU] Elastin: The protein that gives flexibility to tissues. [NIH] Electrocoagulation: Electrosurgical procedures used to treat hemorrhage (e.g., bleeding

Dictionary 155

ulcers) and to ablate tumors, mucosal lesions, and refractory arrhythmias. [NIH] 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] Emaciation: Clinical manifestation of excessive leanness usually caused by disease or a lack of nutrition. [NIH] Embolus: Bit of foreign matter which enters the blood stream at one point and is carried until it is lodged or impacted in an artery and obstructs it. It may be a blood clot, an air bubble, fat or other tissue, or clumps of bacteria. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Emodin: Purgative anthraquinone found in several plants, especially Rhamnus frangula. It was formerly used as a laxative, but is now used mainly as tool in toxicity studies. [NIH] Encephalopathy: A disorder of the brain that can be caused by disease, injury, drugs, or chemicals. [NIH] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [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 for visualization of the ampulla of Vater. [NIH] Endoscopic retrograde cholangiopancreatography: ERCP. A procedure to x-ray the pancreatic duct, hepatic duct, common bile duct, duodenal papilla, and gallbladder. In this procedure, a thin, lighted tube (endoscope) is passed through the mouth and down into the first part of the small intestine (duodenum). A smaller tube (catheter) is then inserted through the endoscope into the bile and pancreatic ducts. A dye is injected through the catheter into the ducts, and an x-ray is taken. [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-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [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] 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]

156

Acute Pancreatitis

Enteropeptidase: A specialized proteolytic enzyme secreted by intestinal cells. It converts trypsinogen into its active form trypsin by removing the N-terminal peptide. EC 3.4.21.9. [NIH]

Environmental Exposure: The exposure to potentially harmful chemical, physical, or 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] Epigastric: Having to do with the upper middle area of the abdomen. [NIH] 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] Erythrocyte Volume: Volume of circulating erythrocytes. It is usually measured by radioisotope dilution technique. [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] Esophageal: Having to do with the esophagus, the muscular tube through which food passes from the throat to the stomach. [NIH] Esophageal Atresia: Congenital failure of the full esophageal lumen to develop that commonly occurs with tracheoesophageal fistula. Symptoms include excessive salivation, gagging, cyanosis, and dyspnea. [NIH] Esophageal Motility Disorders: Disorders affecting the motor function of the upper or lower esophageal sphincters, the esophageal body, or a combination of these parts. The failure of the sphincters to maintain a tonic pressure may result in the impeding of the passage of food, regurgitation of food, or reflux of gastric acid into the esophagus. [NIH] Esophagitis: Inflammation, acute or chronic, of the esophagus caused by bacteria, chemicals, or trauma. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]

Estrogens: A class of sex hormones associated with the development and maintenance of secondary female sex characteristics and control of the cyclical changes in the reproductive

Dictionary 157

cycle. They are also required for pregnancy maintenance and have an anabolic effect on protein metabolism and water retention. [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] Ethionine: 2-Amino-4-(ethylthio)butyric acid. An antimetabolite and methionine antagonist that interferes with amino acid incorporation into proteins and with cellular ATP utilization. It also produces liver neoplasms. [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] Excrete: To get rid of waste from the body. [NIH] Exhaustion: The feeling of weariness of mind and body. [NIH] 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] Extensor: A muscle whose contraction tends to straighten a limb; the antagonist of a flexor. [NIH]

Extracellular: Outside a cell or cells. [EU] Extravasation: A discharge or escape, as of blood, from a vessel into the tissues. [EU] Exudate: Material, such as fluid, cells, or cellular debris, which has escaped from blood vessels and has been deposited in tissues or on tissue surfaces, usually as a result of inflammation. An exudate, in contrast to a transudate, is characterized by a high content of protein, cells, or solid materials derived from cells. [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] Failure to Thrive: A condition in which an infant or child's weight gain and growth are far below usual levels for age. [NIH] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatty acids: A major component of fats that are used by the body for energy and tissue development. [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] Fibrin: A protein derived from fibrinogen in the presence of thrombin, which forms part of the blood clot. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH]

158

Acute Pancreatitis

Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Finasteride: An orally active testosterone 5-alpha-reductase inhibitor. It is used as a surgical alternative for treatment of benign prostatic hyperplasia. [NIH] Fine-needle aspiration: The removal of tissue or fluid with a needle for examination under a microscope. Also called needle biopsy. [NIH] Fistula: Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body. [NIH] Fixation: 1. The act or operation of holding, suturing, or fastening in a fixed position. 2. The condition of being held in a fixed position. 3. In psychiatry, a term with two related but distinct meanings : (1) arrest of development at a particular stage, which like regression (return to an earlier stage), if temporary is a normal reaction to setbacks and difficulties but if protracted or frequent is a cause of developmental failures and emotional problems, and (2) a close and suffocating attachment to another person, especially a childhood figure, such as one's mother or father. Both meanings are derived from psychoanalytic theory and refer to 'fixation' of libidinal energy either in a specific erogenous zone, hence fixation at the oral, anal, or phallic stage, or in a specific object, hence mother or father fixation. 4. The use of a fixative (q.v.) to preserve histological or cytological specimens. 5. In chemistry, the process whereby a substance is removed from the gaseous or solution phase and localized, as in carbon dioxide fixation or nitrogen fixation. 6. In ophthalmology, direction of the gaze so that the visual image of the object falls on the fovea centralis. 7. In film processing, the chemical removal of all undeveloped salts of the film emulsion, leaving only the developed silver to form a permanent image. [EU] 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] Fold: A plication or doubling of various parts of the body. [NIH] Foramen: A natural hole of perforation, especially one in a bone. [NIH] Forearm: The part between the elbow and the wrist. [NIH] 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 Radicals: Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated. [NIH] Fulminant Hepatic Failure: Liver failure that occurs suddenly in a previously healthy person. The most common causes of FHF are acute hepatitis, acetaminophen overdose, and liver damage from prescription drugs. [NIH] Gabexate: A serine proteinase inhibitor used therapeutically in the treatment of pancreatitis, disseminated intravascular coagulation (DIC), and as a regional anticoagulant for hemodialysis. The drug inhibits the hydrolytic effects of thrombin, plasmin, and kallikrein,

Dictionary 159

but not of chymotrypsin and aprotinin. [NIH] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gangrene: Death and putrefaction of tissue usually due to a loss of blood supply. [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 Juices: Liquids produced in the stomach to help break down food and kill bacteria. [NIH]

Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]

Gastritis: Inflammation of the stomach. [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 Hemorrhage: Bleeding in the gastrointestinal tract. [NIH] Gastrointestinal Hormones: Hormones secreted by the gastrointestinal mucosa that affect the timing or the quality of secretion of digestive enzymes, and regulate the motor activity of the digestive system organs. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gastrostomy: Creation of an artificial external opening into the stomach for nutritional support or gastrointestinal compression. [NIH] Gemfibrozil: A lipid-regulating agent that lowers elevated serum lipids primarily by decreasing serum triglycerides with a variable reduction in total cholesterol. These decreases occur primarily in the VLDL fraction and less frequently in the LDL fraction. Gemfibrozil increases HDL subfractions HDL2 and HDL3 as well as apolipoproteins A-I and A-II. Its mechanism of action has not been definitely established. [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 Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Therapy: The introduction of new genes into cells for the purpose of treating disease

160

Acute Pancreatitis

by restoring or adding gene expression. Techniques include insertion of retroviral vectors, transfection, homologous recombination, and injection of new genes into the nuclei of single cell embryos. The entire gene therapy process may consist of multiple steps. The new genes may be introduced into proliferating cells in vivo (e.g., bone marrow) or in vitro (e.g., fibroblast cultures) and the modified cells transferred to the site where the gene expression is required. Gene therapy may be particularly useful for treating enzyme deficiency diseases, hemoglobinopathies, and leukemias and may also prove useful in restoring drug sensitivity, particularly for leukemia. [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 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 testing: Analyzing DNA to look for a genetic alteration that may indicate an increased risk for developing a specific disease or disorder. [NIH] Genital: Pertaining to the genitalia. [EU] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Germ cell tumors: Tumors that begin in the cells that give rise to sperm or eggs. They can occur virtually anywhere in the body and can be either benign or malignant. [NIH] Gingivitis: Inflammation of the gingivae. Gingivitis associated with bony changes is referred to as periodontitis. Called also oulitis and ulitis. [EU] 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] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]

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] Glutathione Peroxidase: An enzyme catalyzing the oxidation of 2 moles of glutathione in the presence of hydrogen peroxide to yield oxidized glutathione and water. EC 1.11.1.9. [NIH]

Gluten: The protein of wheat and other grains which gives to the dough its tough elastic

Dictionary 161

character. [EU] Glyburide: An antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide. [NIH] 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] Glycodeoxycholic Acid: A bile salt formed in the liver by conjugation of deoxycholate with glycine, usually as the sodium salt. It acts as a detergent to solubilize fats for absorption and is itself absorbed. It is used as a cholagogue and choleretic. [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] Glycoside: Any compound that contains a carbohydrate molecule (sugar), particularly any such natural product in plants, convertible, by hydrolytic cleavage, into sugar and a nonsugar component (aglycone), and named specifically for the sugar contained, as glucoside (glucose), pentoside (pentose), fructoside (fructose) etc. [EU] 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]

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-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] Granule: A small pill made from sucrose. [EU] Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [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] Habitual: Of the nature of a habit; according to habit; established by or repeated by force of habit, customary. [EU]

162

Acute Pancreatitis

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] Heartburn: Substernal pain or burning sensation, usually associated with regurgitation of gastric juice into the esophagus. [NIH] Helix-loop-helix: Regulatory protein of cell cycle. [NIH] Hematocrit: Measurement of the volume of packed red cells in a blood specimen by centrifugation. The procedure is performed using a tube with graduated markings or with automated blood cell counters. It is used as an indicator of erythrocyte status in disease. For example, anemia shows a low hematocrit, polycythemia, high values. [NIH] Hematoma: An extravasation of blood localized in an organ, space, or tissue. [NIH] Hemlock: Any of several poisonous plants commonly called the poison hemlock (Conium maculatum and Cicuta major) and the water hemlock (Cicuta maculata). Conium maculatum is a large toxic umbelliferous plant herb, which contains the poisonous alkaloid coniine which affects the nervous system. The dried, fully grown, unripe fruit has sedative, anodyne, and antispasmodic effects. Cicuta maculata is also toxic. Its foliage contains a complex unsaturated alcohol that causes convulsions. The hemlock tree, genus Tsuga, unrelated to poison hemlock, is an evergreen coniferous tree of the pine family. [NIH] Hemobilia: Hemorrhage in or through the biliary tract, due to trauma, inflammation, cholelithiasis, vascular disease, or neoplasms. [NIH] Hemochromatosis: A disease that occurs when the body absorbs too much iron. The body stores the excess iron in the liver, pancreas, and other organs. May cause cirrhosis of the liver. Also called iron overload disease. [NIH] Hemodialysis: The use of a machine to clean wastes from the blood after the kidneys have failed. The blood travels through tubes to a dialyzer, which removes wastes and extra fluid. The cleaned blood then flows through another set of tubes back into the body. [NIH] Hemofiltration: Extracorporeal ultrafiltration technique without hemodialysis for treatment of fluid overload and electrolyte disturbances affecting renal, cardiac, or pulmonary function. [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] Hemolysis: The destruction of erythrocytes by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [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]

Dictionary 163

Hepatic Duct, Common: Predominantly extrahepatic bile duct which is formed by the junction of the right and left hepatic ducts, which are predominantly intrahepatic, and, in turn, joins the cystic duct to form the common bile duct. [NIH] Hepatic Encephalopathy: A condition that may cause loss of consciousness and coma. It is usually the result of advanced liver disease. Also called hepatic coma. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatitis, Chronic: A collective term for a clinical and pathological syndrome which has several causes and is characterized by varying degrees of hepatocellular necrosis and inflammation. Specific forms of chronic hepatitis include autoimmune hepatitis, chronic hepatitis B, chronic hepatitis C, chronic hepatitis D, indeterminate chronic viral hepatitis, cryptogenic chronic hepatitis, and drug-related chronic hepatitis. [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] Hepatology: The field of medicine concerned with the functions and disorders of the liver. [NIH]

Hepatorenal Syndrome: Renal failure in those with liver disease, usually liver cirrhosis or obstructive jaundice. Historically called Heyd disease, urohepatic syndrome, or bile nephrosis. [NIH] Hepatotoxicity: How much damage a medicine or other substance does to the liver. [NIH] Hereditary: Of, relating to, or denoting factors that can be transmitted genetically from one 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] Hernia: Protrusion of a loop or knuckle of an organ or tissue through an abnormal opening. [NIH]

Heterodimer: 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]

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] Homodimer: Protein-binding "activation domains" always combine with identical proteins. [NIH]

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]

164

Acute Pancreatitis

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] Hybridomas: Cells artificially created by fusion of activated lymphocytes with neoplastic cells. The resulting hybrid cells are cloned and produce pure or "monoclonal" antibodies or T-cell products, identical to those produced by the immunologically competent parent, and continually grow and divide as the neoplastic parent. [NIH] Hydration: Combining with water. [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 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] Hydrolases: Any member of the class of enzymes that catalyze the cleavage of the substrate and the addition of water to the resulting molecules, e.g., esterases, glycosidases (glycoside hydrolases), lipases, nucleotidases, peptidases (peptide hydrolases), and phosphatases (phosphoric monoester hydrolases). EC 3. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [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] Hyperlipidemia: An excess of lipids in the blood. [NIH] Hyperlipoproteinemia: Metabolic disease characterized by elevated plasma cholesterol and/or triglyceride levels. The inherited form is attributed to a single gene mechanism. [NIH] 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 the number of cells. [NIH] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hyperstimulation: Excessive stimulation. [EU] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels

Dictionary 165

are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hypertriglyceridemia: Condition of elevated triglyceride concentration in the blood; an inherited form occurs in familial hyperlipoproteinemia IIb and hyperlipoproteinemia type IV. It has been linked to higher risk of heart disease and arteriosclerosis. [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] Hypotension: Abnormally low blood pressure. [NIH] 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] Hypoxanthine: A purine and a reaction intermediate in the metabolism of adenosine and in the formation of nucleic acids by the salvage pathway. [NIH] Hypoxemia: Deficient oxygenation of the blood; hypoxia. [EU] Hypoxia: Reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the tissue by blood. [EU] Iatrogenic: Resulting from the activity of physicians. Originally applied to disorders induced in the patient by autosuggestion based on the physician's examination, manner, or discussion, the term is now applied to any adverse condition in a patient occurring as the result of treatment by a physician or surgeon, especially to infections acquired by the patient during the course of treatment. [EU] Idiopathic: Describes a disease of unknown cause. [NIH] Ileum: The lower end of the small intestine. [NIH] Ileus: Obstruction of the intestines. [EU] Immune response: The activity of the immune system against foreign substances (antigens). [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] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunogenic: Producing immunity; evoking an immune response. [EU] Immunology: The study of the body's immune system. [NIH] Impaction: The trapping of an object in a body passage. Examples are stones in the bile duct or hardened stool in the colon. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH]

166

Acute Pancreatitis

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] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH] Incubated: Grown in the laboratory under controlled conditions. (For instance, white blood cells can be grown in special conditions so that they attack specific cancer cells when returned to the body.) [NIH] Indigestion: Poor digestion. Symptoms include heartburn, nausea, bloating, and gas. Also called dyspepsia. [NIH] 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] 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]

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] 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]

Dictionary 167

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] Intensive Care: Advanced and highly specialized care provided to medical or surgical patients whose conditions are life-threatening and require comprehensive care and constant monitoring. It is usually administered in specially equipped units of a health care facility. [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-6: Factor that stimulates the growth and differentiation of human B-cells and is also a growth factor for hybridomas and plasmacytomas. It is produced by many different cells including T-cells, monocytes, and fibroblasts. [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] 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] Intestinal: Having to do with the intestines. [NIH] Intestinal Mucosa: The surface lining of the intestines where the cells absorb nutrients. [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] Intracellular: Inside a cell. [NIH] Intramuscular: IM. Within or into muscle. [NIH] Intraocular: Within the eye. [EU] Intraocular pressure: Pressure of the fluid inside the eye; normal IOP varies among individuals. [NIH] Intravascular: Within a vessel or vessels. [EU] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Intussusception: A rare disorder. A part of the intestines folds into another part of the intestines, causing blockage. Most common in infants. Can be treated with an operation. [NIH]

Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin

168

Acute Pancreatitis

or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]

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] Isoenzymes: One of various structurally related forms of an enzyme, each having the same mechanism but with differing chemical, physical, or immunological characteristics. [NIH] Isotretinoin: A topical dermatologic agent that is used in the treatment of acne vulgaris and several other skin diseases. The drug has teratogenic and other adverse effects. [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] 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] 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] Ketone Bodies: Chemicals that the body makes when there is not enough insulin in the blood and it must break down fat for its energy. Ketone bodies can poison and even kill body cells. When the body does not have the help of insulin, the ketones build up in the blood and then "spill" over into the urine so that the body can get rid of them. The body can also rid itself of one type of ketone, called acetone, through the lungs. This gives the breath a fruity odor. Ketones that build up in the body for a long time lead to serious illness and coma. [NIH] Ketosis: A condition of having ketone bodies build up in body tissues and fluids. The signs of ketosis are nausea, vomiting, and stomach pain. Ketosis can lead to ketoacidosis. [NIH] Kidney Failure: The inability of a kidney to excrete metabolites at normal plasma levels under conditions of normal loading, or the inability to retain electrolytes under conditions of normal intake. In the acute form (kidney failure, acute), it is marked by uremia and usually by oliguria or anuria, with hyperkalemia and pulmonary edema. The chronic form (kidney failure, chronic) is irreversible and requires hemodialysis. [NIH] Kidney Failure, Acute: A clinical syndrome characterized by a sudden decrease in glomerular filtration rate, often to values of less than 1 to 2 ml per minute. It is usually associated with oliguria (urine volumes of less than 400 ml per day) and is always associated with biochemical consequences of the reduction in glomerular filtration rate such as a rise in blood urea nitrogen (BUN) and serum creatinine concentrations. [NIH]

Dictionary 169

Kidney Failure, Chronic: An irreversible and usually progressive reduction in renal function in which both kidneys have been damaged by a variety of diseases to the extent that they are unable to adequately remove the metabolic products from the blood and regulate the body's electrolyte composition and acid-base balance. Chronic kidney failure requires hemodialysis or surgery, usually kidney transplantation. [NIH] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Lactobacillus: A genus of gram-positive, microaerophilic, rod-shaped bacteria occurring widely in nature. Its species are also part of the many normal flora of the mouth, intestinal tract, and vagina of many mammals, including humans. Pathogenicity from this genus is rare. [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] Larynx: An irregularly shaped, musculocartilaginous tubular structure, lined with mucous membrane, located at the top of the trachea and below the root of the tongue and the hyoid bone. It is the essential sphincter guarding the entrance into the trachea and functioning secondarily as the organ of voice. [NIH] Laxative: An agent that acts to promote evacuation of the bowel; a cathartic or purgative. [EU]

Leishmaniasis: A disease caused by any of a number of species of protozoa in the genus Leishmania. There are four major clinical types of this infection: cutaneous (Old and New World), diffuse cutaneous, mucocutaneous, and visceral leishmaniasis. [NIH] Lesion: An area of abnormal tissue change. [NIH] Lethal: Deadly, fatal. [EU] 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]

Leukemia: Cancer of blood-forming tissue. [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] Ligation: Application of a ligature to tie a vessel or strangulate a part. [NIH] Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC 3.1.1.3. [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]

170

Acute Pancreatitis

Lipofuscin: A naturally occurring lipid pigment with histochemical characteristics similar to ceroid. It accumulates in various normal tissues and apparently increases in quantity with age. [NIH] Lipopolysaccharide: Substance consisting of polysaccaride and lipid. [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 Cirrhosis: Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules. [NIH] Liver Neoplasms: Tumors or cancer of the liver. [NIH] Liver Transplantation: The transference of a part of or an entire liver from one human or animal to another. [NIH] Localized: Cancer which has not metastasized yet. [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]

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] Lymphocyte Count: A count of the number of lymphocytes in the blood. [NIH] Lymphocytes: White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each); those with characteristics of neither major class are called null cells. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [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] Macronutrients: Nutrients in the diet that are the key sources of energy, namely protein, fat, and carbohydrates. [NIH] Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy

Dictionary 171

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] 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] 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] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [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] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Meglumine: 1-Deoxy-1-(methylamino)-D-glucitol. A derivative of sorbitol in which the hydroxyl group in position 1 is replaced by a methylamino group. Often used in conjunction with iodinated organic compounds as contrast medium. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Membrane Lipids: Lipids, predominantly phospholipids, cholesterol and small amounts of glycolipids found in membranes including cellular and intracellular membranes. These lipids may be arranged in bilayers in the membranes with integral proteins between the layers and peripheral proteins attached to the outside. Membrane lipids are required for active transport, several enzymatic activities and membrane formation. [NIH] Menstruation: The normal physiologic discharge through the vagina of blood and mucosal tissues from the nonpregnant uterus. [NIH] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Meperidine: 1-Methyl-4-phenyl-4-piperidinecarboxylic acid ethyl ester. A narcotic analgesic that can be used for the relief of most types of moderate to severe pain, including postoperative pain and the pain of labor. Prolonged use may lead to dependence of the morphine type; withdrawal symptoms appear more rapidly than with morphine and are of shorter duration. [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] Metabolic acidosis: (met-ah-BOL-ik as-id-O-sis): A condition in which the blood is too acidic. It may be caused by severe illness or sepsis (bacteria in the bloodstream). [NIH] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from

172

Acute Pancreatitis

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] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microcirculation: The vascular network lying between the arterioles and venules; includes capillaries, metarterioles and arteriovenous anastomoses. Also, the flow of blood through this network. [NIH] Micronutrients: Essential dietary elements or organic compounds that are required in only small quantities for normal physiologic processes to occur. [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] 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] 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] 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] 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] Monocytes: Large, phagocytic mononuclear leukocytes produced in the vertebrate bone marrow and released into the blood; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles. [NIH]

Dictionary 173

Mononuclear: A cell with one nucleus. [NIH] Morphine: The principal alkaloid in opium and the prototype opiate analgesic and narcotic. Morphine has widespread effects in the central nervous system and on smooth muscle. [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] Motor Activity: The physical activity of an organism as a behavioral phenomenon. [NIH] Mucinous: Containing or resembling mucin, the main compound in mucus. [NIH] Mucocutaneous: Pertaining to or affecting the mucous membrane and the skin. [EU] Mucosa: A mucous membrane, or tunica mucosa. [EU] Mucus: The viscous secretion of mucous membranes. It contains mucin, white blood cells, water, inorganic salts, and exfoliated cells. [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] Mydriatic: 1. Dilating the pupil. 2. Any drug that dilates the pupil. [EU] Myelin: The fatty substance that covers and protects nerves. [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 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]

Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] N-acetyl: Analgesic agent. [NIH] Narcotic: 1. Pertaining to or producing narcosis. 2. An agent that produces insensibility or stupor, applied especially to the opioids, i.e. to any natural or synthetic drug that has

174

Acute Pancreatitis

morphine-like actions. [EU] Nasogastric: The process of passing a small, flexible plastic tube through the nose or mouth into the stomach or small intestine. [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] 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] Needle biopsy: The removal of tissue or fluid with a needle for examination under a microscope. Also called fine-needle aspiration. [NIH] Neoplasms: New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms. [NIH] Nephrosis: Descriptive histopathologic term for renal disease without an inflammatory component. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [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] Neurogenic: Loss of bladder control caused by damage to the nerves controlling the bladder. [NIH] Neurogenic Inflammation: Inflammation caused by an injurious stimulus of peripheral neurons and resulting in release of neuropeptides which affect vascular permeability and help initiate proinflammatory and immune reactions at the site of injury. [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] Neuropeptides: Peptides released by neurons as intercellular messengers. Many neuropeptides are also hormones released by non-neuronal cells. [NIH] Neuroretinitis: Inflammation of the optic nerve head and adjacent retina. [NIH] Neurotensin: A biologically active tridecapeptide isolated from the hypothalamus. It has been shown to induce hypotension in the rat, to stimulate contraction of guinea pig ileum and rat uterus, and to cause relaxation of rat duodenum. There is also evidence that it acts as both a peripheral and a central nervous system neurotransmitter. [NIH] Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic acid, substance P, enkephalins, endorphins, and serotonin. [EU] Neutralization: An act or process of neutralizing. [EU] 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,

Dictionary 175

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] Nifedipine: A potent vasodilator agent with calcium antagonistic action. It is a useful antianginal agent that also lowers blood pressure. The use of nifedipine as a tocolytic is being investigated. [NIH] 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] Nosocomial: Pertaining to or originating in the hospital, said of an infection not present or incubating prior to admittance to the hospital, but generally occurring 72 hours after admittance; the term is usually used to refer to patient disease, but hospital personnel may also acquire nosocomial infection. [EU] 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] Nucleotidases: A class of enzymes that catalyze the conversion of a nucleotide and water to a nucleoside and orthophosphate. EC 3.1.3.-. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [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

176

Acute Pancreatitis

results. [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 management of many pathological states including diabetes mellitus, orthostatic hypertension, hyperinsulinism, hypergastrinemia, and small bowel fistula. [NIH] Oliguria: Clinical manifestation of the urinary system consisting of a decrease in the amount of urine secreted. [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] Operon: The genetic unit consisting of a feedback system under the control of an operator gene, in which a structural gene transcribes its message in the form of mRNA upon blockade of a repressor produced by a regulator gene. Included here is the attenuator site of bacterial operons where transcription termination is regulated. [NIH] Opiate: A remedy containing or derived from opium; also any drug that induces sleep. [EU] Opium: The air-dried exudate from the unripe seed capsule of the opium poppy, Papaver somniferum, or its variant, P. album. It contains a number of alkaloids, but only a few morphine, codeine, and papaverine - have clinical significance. Opium has been used as an analgesic, antitussive, antidiarrheal, and antispasmodic. [NIH] Opportunistic Infections: An infection caused by an organism which becomes pathogenic under certain conditions, e.g., during immunosuppression. [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] 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] 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] Overdose: An accidental or deliberate dose of a medication or street drug that is in excess of what is normally used. [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]

Dictionary 177

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] Oxygenation: The process of supplying, treating, or mixing with oxygen. No:1245 oxygenation the process of supplying, treating, or mixing with oxygen. [EU] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] 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 Elastase: A protease of broad specificity, obtained from dried pancreas. Molecular weight is approximately 25,000. The enzyme breaks down elastin, the specific protein of elastic fibers, and digests other proteins such as fibrin, hemoglobin, and albumin. EC 3.4.21.36. [NIH] Pancreatic enzymes: A group of proteins secreted by the pancreas which aid in the digestion of food. [NIH] Pancreatic Fistula: Abnormal passage communicating with the pancreas. [NIH] Pancreatic Juice: The fluid containing digestive enzymes secreted by the pancreas in response to food in the duodenum. [NIH] Pancreatic Pseudocyst: Cyst-like space not lined by epithelium and contained within the pancreas. [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] Papilla: A small nipple-shaped elevation. [NIH] Papillary: Pertaining to or resembling papilla, or nipple. [EU] 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] Parasitic Diseases: Infections or infestations with parasitic organisms. They are often contracted through contact with an intermediate vector, but may occur as the result of direct exposure. [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

178

Acute Pancreatitis

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] Parathyroid hormone: A substance made by the parathyroid gland that helps the body store and use calcium. Also called parathormone, parathyrin, or PTH. [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] Particle: A tiny mass of material. [EU] 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] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]

Pelvis: The lower part of the abdomen, located between the hip bones. [NIH] Penicillin: An antibiotic drug used to treat infection. [NIH] Pepsin: An enzyme made in the stomach that breaks down proteins. [NIH] Peptic: Pertaining to pepsin or to digestion; related to the action of gastric juices. [EU] Peptic Ulcer: An ulceration of the mucous membrane of the esophagus, stomach or duodenum, caused by the action of the acid gastric juice. [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 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] 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] 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] Pericardium: The fibroserous sac surrounding the heart and the roots of the great vessels. [NIH]

Periodontitis: Inflammation of the periodontal membrane; also called periodontitis simplex.

Dictionary 179

[NIH]

Peripheral blood: Blood circulating throughout the body. [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] Peritoneal Dialysis: Dialysis fluid being introduced into and removed from the peritoneal cavity as either a continuous or an intermittent procedure. [NIH] Peritoneal Lavage: Washing out of the peritoneal cavity. The procedure is a diagnostic as well as a therapeutic technique following abdominal trauma or inflammation. [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] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] 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] 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] Phenyl: Ingredient used in cold and flu remedies. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [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] Phosphoric Monoester Hydrolases: A group of hydrolases which catalyze the hydrolysis of monophosphoric esters with the production of one mole of orthophosphate. EC 3.1.3. [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] Photocoagulation: Using a special strong beam of light (laser) to seal off bleeding blood vessels such as in the eye. The laser can also burn away blood vessels that should not have grown in the eye. This is the main treatment for diabetic retinopathy. [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] Pigment: A substance that gives color to tissue. Pigments are responsible for the color of

180

Acute Pancreatitis

skin, eyes, and hair. [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 Volume: Volume of plasma in the circulation. It is usually measured by indicator dilution techniques. [NIH] Plasmin: A product of the lysis of plasminogen (profibrinolysin) by plasminogen activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins. EC 3.4.21.7. [NIH] Plastids: Self-replicating cytoplasmic organelles of plant and algal cells that contain pigments and may synthesize and accumulate various substances. Plastids are used in phylogenetic studies. [NIH] Platelet Activating Factor: A phospholipid derivative formed by platelets, basophils, neutrophils, monocytes, and macrophages. It is a potent platelet aggregating agent and 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]

Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Pneumonia: Inflammation of the lungs. [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [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]

Dictionary 181

Polypeptide: A peptide which on hydrolysis yields more than two amino acids; called 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] Portal Hypertension: High blood pressure in the portal vein. This vein carries blood into the liver. Portal hypertension is caused by a blood clot. This is a common complication of cirrhosis. [NIH] Portal System: A system of vessels in which blood, after passing through one capillary bed, is conveyed through a second set of capillaries before it returns to the systemic circulation. It pertains especially to the hepatic portal system. [NIH] Portal Vein: A short thick vein formed by union of the superior mesenteric vein and the splenic vein. [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] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [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] Preclinical: Before a disease becomes clinically recognizable. [EU] 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] 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] Preeclampsia: A toxaemia of late pregnancy characterized by hypertension, edema, and proteinuria, when convulsions and coma are associated, it is called eclampsia. [EU] Pregnancy Maintenance: Physiological mechanisms that sustain the state of pregnancy. [NIH]

Preoperative: Preceding an operation. [EU] Primary Biliary Cirrhosis: A chronic liver disease. Slowly destroys the bile ducts in the liver. This prevents release of bile. Long-term irritation of the liver may cause scarring and cirrhosis in later stages of the disease. [NIH] Primary Sclerosing Cholangitis: Irritation, scarring, and narrowing of the bile ducts inside and outside the liver. Bile builds up in the liver and may damage its cells. Many people with this condition also have ulcerative colitis. [NIH]

182

Acute Pancreatitis

Procaine: A local anesthetic of the ester type that has a slow onset and a short duration of action. It is mainly used for infiltration anesthesia, peripheral nerve block, and spinal block. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1016). [NIH] Proctocolectomy: An operation to remove the colon and rectum. Also called coloproctectomy. [NIH] Proenzymes: 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] 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] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Prone: Having the front portion of the body downwards. [NIH] Prophylaxis: An attempt to prevent disease. [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] Prostaglandins: A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes. [NIH] 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] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] Protease Inhibitors: Compounds which inhibit or antagonize biosynthesis or actions of proteases (endopeptidases). [NIH] Protein Binding: The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific proteinbinding measures are often used as assays in diagnostic assessments. [NIH] 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

Dictionary 183

secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the 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] 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] 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] 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] Pseudocysts: A collection of enzyme-rich pancreatic fluid and tissue debris arising within areas of necrosis or an obstructed smaller duct. [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] 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 Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs. [NIH] Pulmonary Edema: An accumulation of an excessive amount of watery fluid in the lungs, may be caused by acute exposure to dangerous concentrations of irritant gasses. [NIH] 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] 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]

184

Acute Pancreatitis

Putrefaction: The process of decomposition of animal and vegetable matter by living organisms. [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] 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] Radiolabeled: Any compound that has been joined with a radioactive substance. [NIH] Radiological: Pertaining to radiodiagnostic and radiotherapeutic procedures, and interventional radiology or other planning and guiding medical radiology. [NIH] Radiologist: A doctor who specializes in creating and interpreting pictures of areas inside the body. The pictures are produced with x-rays, sound waves, or other types of energy. [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] 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] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] 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] 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] Reductase: Enzyme converting testosterone to dihydrotestosterone. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Reflux: The term used when liquid backs up into the esophagus from the stomach. [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] Regurgitation: A backward flowing, as the casting up of undigested food, or the backward

Dictionary 185

flowing of blood into the heart, or between the chambers of the heart when a valve is incompetent. [EU] 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] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [NIH] Renin: An enzyme which is secreted by the kidney and is formed from prorenin in plasma and kidney. The enzyme cleaves the Leu-Leu bond in angiotensinogen to generate angiotensin I. EC 3.4.23.15. (Formerly EC 3.4.99.19). [NIH] Renin-Angiotensin System: A system consisting of renin, angiotensin-converting enzyme, and angiotensin II. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming angiotensin I. The converting enzyme contained in the lung acts on angiotensin I in the plasma converting it to angiotensin II, the most powerful directly pressor substance known. It causes contraction of the arteriolar smooth muscle and has other indirect actions mediated through the adrenal cortex. [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] Repressor: Any of the specific allosteric protein molecules, products of regulator genes, which bind to the operator of operons and prevent RNA polymerase from proceeding into the operon to transcribe messenger RNA. [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 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] Restitution: The restoration to a normal state. [NIH] Resuscitation: The restoration to life or consciousness of one apparently dead; it includes such measures as artificial respiration and cardiac massage. [EU] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic 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] 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

186

Acute Pancreatitis

(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] Retrograde: 1. Moving backward or against the usual direction of flow. 2. Degenerating, deteriorating, or catabolic. [EU] Retroperitoneal: Having to do with the area outside or behind the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] 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] 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] Rheumatoid: Resembling rheumatism. [EU] 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] Ribonuclease: RNA-digesting enzyme. [NIH] Ribose: A pentose active in biological systems usually in its D-form. [NIH] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Rod: A reception for vision, located in the retina. [NIH] Roxithromycin: Semisynthetic derivative of erythromycin. It is concentrated by human phagocytes and is bioactive intracellularly. While the drug is active against a wide spectrum of pathogens, it is particularly effective in the treatment of respiratory and genital tract infections. [NIH] Saliva: The clear, viscous fluid secreted by the salivary glands and mucous glands of the mouth. It contains mucins, water, organic salts, and ptylin. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Salivation: 1. The secretion of saliva. 2. Ptyalism (= excessive flow of saliva). [EU] 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] 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] Secretin: A hormone made in the duodenum. Causes the stomach to make pepsin, the liver to make bile, and the pancreas to make a digestive juice. [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 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]

Dictionary 187

Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Selenium: An element with the atomic symbol Se, atomic number 34, and atomic weight 78.96. It is an essential micronutrient for mammals and other animals but is toxic in large amounts. Selenium protects intracellular structures against oxidative damage. It is an essential component of glutathione peroxidase. [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] Sensitization: 1. Administration of antigen to induce a primary immune response; priming; immunization. 2. Exposure to allergen that results in the development of hypersensitivity. 3. The coating of erythrocytes with antibody so that they are subject to lysis by complement in the presence of homologous antigen, the first stage of a complement fixation test. [EU] Sepsis: The presence of bacteria in the bloodstream. [NIH] Septic: Produced by or due to decomposition by microorganisms; putrefactive. [EU] Septicemia: Systemic disease associated with the presence and persistence of pathogenic microorganisms or their toxins in the blood. Called also blood poisoning. [EU] 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] Serous: Having to do with serum, the clear liquid part of blood. [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] 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]

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] 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]

188

Acute Pancreatitis

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] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]

Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [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] Sodium Bicarbonate: A white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions. [NIH] Sodium Channels: Cell membrane glycoproteins selective for sodium ions. Fast sodium current is associated with the action potential in neural membranes. [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] Sorbitol: A polyhydric alcohol with about half the sweetness of sucrose. Sorbitol occurs naturally and is also produced synthetically from glucose. It was formerly used as a diuretic and may still be used as a laxative and in irrigating solutions for some surgical procedures. It is also used in many manufacturing processes, as a pharmaceutical aid, and in several research applications. [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] 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] 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] Sphincter: A ringlike band of muscle fibres that constricts a passage or closes a natural orifice; called also musculus sphincter. [EU]

Dictionary 189

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] Stabilizer: A device for maintaining constant X-ray tube voltage or current. [NIH] 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] Stenosis: Narrowing or stricture of a duct or canal. [EU] 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] Sterilization: The destroying of all forms of life, especially microorganisms, by heat, chemical, or other means. [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] 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] Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are coiled together. [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] Stricture: The abnormal narrowing of a body opening. Also called stenosis. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU] Subcapsular: Situated below a capsule. [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] 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] Suction: The removal of secretions, gas or fluid from hollow or tubular organs or cavities by means of a tube and a device that acts on negative pressure. [NIH] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH]

190

Acute Pancreatitis

Superoxide Dismutase: An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC 1.15.1.1. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Supportive care: Treatment given to prevent, control, or relieve complications and side effects and to improve the comfort and quality of life of people who have cancer. [NIH] Survival Rate: The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods. [NIH] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] 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] Systemic: Affecting the entire 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. 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] Tamponade: The inserting of a tampon; a dressing is inserted firmly into a wound or body cavity, as the nose, uterus or vagina, principally for stopping hemorrhage. [NIH] Teratogenic: Tending to produce anomalies of formation, or teratism (= anomaly of formation or development : condition of a monster). [EU] Testosterone: A hormone that promotes the development and maintenance of male sex characteristics. [NIH] Tetany: 1. Hyperexcitability of nerves and muscles due to decrease in concentration of extracellular ionized calcium, which may be associated with such conditions as parathyroid hypofunction, vitamin D deficiency, and alkalosis or result from ingestion of alkaline salts; it is characterized by carpopedal spasm, muscular twitching and cramps, laryngospasm with inspiratory stridor, hyperreflexia and choreiform movements. 2. Tetanus. [EU] Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] 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.

Dictionary 191

[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] 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] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] 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] Tonic: 1. Producing and restoring the normal tone. 2. Characterized by continuous tension. 3. A term formerly used for a class of medicinal preparations believed to have the power of restoring normal tone to tissue. [EU] Tonicity: The normal state of muscular tension. [NIH] Tonometry: The standard to determine the fluid pressure inside the eye (intraocular pressure). [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] Torsades de Pointes: A ventricular tachycardia characterized by periodic twisting of the points of the QRS complexes and rates between 200 and 250 beats per minute. It may be selflimited or may progress to ventricular fibrillation. [NIH] Torsion: A twisting or rotation of a bodily part or member on its axis. [NIH] 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] 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]

192

Acute Pancreatitis

Tracheoesophageal Fistula: Abnormal communication between the esophagus and the trachea, acquired or congenital, often associated with esophageal atresia. [NIH] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] 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] Translocating: The attachment of a fragment of one chromosome to a non-homologous chromosome. [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] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] 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] Trypsin: A serine endopeptidase that is formed from trypsinogen in the pancreas. It is converted into its active form by enteropeptidase in the small intestine. It catalyzes hydrolysis of the carboxyl group of either arginine or lysine. EC 3.4.21.4. [NIH] Tube-feeding: Feeding by a tube passed into the stomach. [NIH] Tuberculosis: Any of the infectious diseases of man and other animals caused by species of Mycobacterium. [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] Tunica: A rather vague term to denote the lining coat of hollow organs, tubes, or cavities. [NIH]

Typhimurium: Microbial assay which measures his-his+ reversion by chemicals which cause base substitutions or frameshift mutations in the genome of this organism. [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] Ultrafiltration: The separation of particles from a suspension by passage through a filter with very fine pores. In ultrafiltration the separation is accomplished by convective transport; in dialysis separation relies instead upon differential diffusion. Ultrafiltration occurs naturally and is a laboratory procedure. Artificial ultrafiltration of the blood is referred to as hemofiltration or hemodiafiltration (if combined with hemodialysis). [NIH]

Dictionary 193

Ultrasonography: The visualization of deep structures of the body by recording the reflections of echoes of pulses of ultrasonic waves directed into the tissues. Use of ultrasound for imaging or diagnostic purposes employs frequencies ranging from 1.6 to 10 megahertz. [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]

Urea: A compound (CO(NH2)2), formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids. [NIH] Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [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] 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] 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] Vaccines: Suspensions of killed or attenuated microorganisms (bacteria, viruses, fungi, protozoa, or rickettsiae), antigenic proteins derived from them, or synthetic constructs, administered for the prevention, amelioration, or treatment of infectious and other diseases. [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] Valproic Acid: A fatty acid with anticonvulsant properties used in the treatment of epilepsy. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GABA levels in the brain or by altering the properties of voltage dependent sodium channels. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU]

194

Acute Pancreatitis

Vasculitis: Inflammation of a blood vessel. [NIH] Vasoactive: Exerting an effect upon the calibre of blood vessels. [EU] Vasodilatation: A state of increased calibre of the blood vessels. [EU] Vasodilator: An agent that widens blood vessels. [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] Venous: Of or pertaining to the veins. [EU] 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] Ventricular Dysfunction: A condition in which the ventricles of the heart exhibit a decreased functionality. [NIH] Ventricular fibrillation: Rapid, irregular quivering of the heart's ventricles, with no effective heartbeat. [NIH] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Villous: Of a surface, covered with villi. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Viral Hepatitis: Hepatitis caused by a virus. Five different viruses (A, B, C, D, and E) most commonly cause this form of hepatitis. Other rare viruses may also cause hepatitis. [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] Vitamin A: A substance used in cancer prevention; it belongs to the family of drugs called retinoids. [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] 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]

Withdrawal: 1. A pathological retreat from interpersonal contact and social involvement, as may occur in schizophrenia, depression, or schizoid avoidant and schizotypal personality

Dictionary 195

disorders. 2. (DSM III-R) A substance-specific organic brain syndrome that follows the cessation of use or reduction in intake of a psychoactive substance that had been regularly used to induce a state of intoxication. [EU] Xanthine: An urinary calculus. [NIH] Xanthine Oxidase: An iron-molybdenum flavoprotein containing FAD that oxidizes hypoxanthine, some other purines and pterins, and aldehydes. Deficiency of the enzyme, an autosomal recessive trait, causes xanthinuria. EC 1.1.3.22. [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] 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]

197

INDEX A Abdomen, 45, 110, 131, 137, 144, 145, 156, 167, 169, 170, 177, 178, 179, 186, 189 Abdominal Pain, 5, 93, 96, 97, 104, 109, 120, 137, 168, 171, 179, 192 Abscess, 4, 10, 27, 84, 137 Acatalasia, 137, 146 Acetaminophen, 137, 158 Acetylcholine, 137, 174, 175 Acne, 137, 168 Acne Vulgaris, 137, 168 Acquired Immunodeficiency Syndrome, 98, 137 Acute renal, 46, 137 Adaptability, 137, 146 Adaptation, 24, 137 Adenocarcinoma, 137, 163 Adenovirus, 20, 138 Adjustment, 137, 138 Adrenal Cortex, 138, 151, 164, 185 Adrenal Glands, 138, 140 Adverse Effect, 138, 168, 187 Afferent, 42, 138 Afferent Loop Syndrome, 42, 138 Affinity, 19, 21, 24, 138, 188 Affinity Chromatography, 21, 138 Agar, 138, 180 Agonist, 78, 138 Albumin, 138, 177 Aldehydes, 138, 195 Algorithms, 104, 138, 144 Alimentary, 30, 39, 53, 121, 139, 155, 178 Alkaline, 139, 145, 190 Alkaloid, 139, 162, 173 Allergen, 139, 187 Allopurinol, 78, 84, 139 Allylamine, 139 Alpha Particles, 139, 184 Alternative medicine, 108, 139 Ameliorated, 82, 139 Amine, 66, 139, 163 Amino Acid Sequence, 96, 139, 140, 157, 160 Amino Acids, 16, 139, 140, 142, 148, 156, 160, 178, 181, 183, 187, 193 Amino-terminal, 93, 139 Ammonia, 139, 193 Amplification, 24, 139

Ampulla, 9, 35, 139, 155 Amylase, 4, 6, 9, 11, 16, 50, 67, 93, 94, 96, 97, 133, 134, 139 Amyloidosis, 44, 139 Anabolic, 140, 157 Anaesthesia, 140, 166 Analgesic, 137, 140, 171, 173, 176 Analog, 14, 140, 176 Anaphylactic, 140, 180 Anaphylatoxins, 140, 149 Anaplasia, 140, 174 Anastomosis, 62, 140 Anatomical, 140, 165, 186 Anemia, 140, 162 Anesthesia, 140, 182 Anginal, 140, 175 Angiotensinogen, 140, 185 Animal model, 19, 74, 140 Anionic, 21, 140 Anions, 138, 140, 168, 190 Anomalies, 102, 140, 190 Antagonism, 78, 140 Antibiotic, 7, 31, 63, 94, 104, 107, 140, 147, 148, 156, 178, 188 Antibodies, 18, 19, 93, 95, 96, 97, 140, 141, 162, 164, 172, 180 Antibody, 19, 28, 96, 138, 141, 149, 150, 156, 162, 163, 166, 171, 172, 184, 187, 188 Anticholinergics, 9, 141 Anticoagulant, 141, 158, 182 Anticonvulsant, 141, 193 Antidiabetic, 141, 161 Antigen, 37, 50, 96, 138, 140, 141, 149, 163, 164, 166, 171, 187 Antigen-Antibody Complex, 141, 149 Anti-inflammatory, 95, 137, 141, 151, 160 Antimetabolite, 141, 157 Antioxidant, 141, 142, 177 Antispasmodic, 141, 153, 162, 176 Anuria, 141, 168 Anus, 141, 145, 149 Apolipoproteins, 141, 159 Apoptosis, 14, 15, 25, 31, 64, 141, 146 Appendicitis, 99, 104, 141 Aqueous, 141, 143, 152, 164 Arachidonic Acid, 95, 141, 169, 182 Arginine, 37, 140, 142, 175, 192 Arterial, 68, 139, 142, 164, 183, 190

198

Acute pancreatitis

Arteries, 142, 144, 151, 173, 191 Arteriography, 46, 142 Arteriolar, 22, 59, 142, 145, 185 Arterioles, 142, 144, 145, 172 Arteriosclerosis, 142, 165 Arteriovenous, 142, 172 Artery, 47, 142, 151, 155, 173, 183, 185 Articular, 142, 176 Ascites, 67, 102, 103, 142 Ascitic Fluid, 77, 142 Ascorbic Acid, 54, 142 Asparaginase, 78, 86, 142 Aspartate, 142 Aspartic Acid, 142, 146 Aspiration, 12, 142 Assay, 19, 98, 99, 142, 192 Asymptomatic, 13, 137, 142, 177 Atmospheric Pressure, 142, 164 Atrophy, 16, 142 Autodigestion, 99, 142, 177 Autoimmune disease, 10, 142, 173 Autoimmune Hepatitis, 103, 143, 163 Autolysis, 21, 95, 142, 143 Autosuggestion, 143, 165 B Bacteria, 140, 141, 143, 148, 150, 155, 156, 157, 159, 161, 162, 169, 171, 172, 187, 188, 192, 193 Bacterial Physiology, 137, 143 Bacterial Translocation, 67, 75, 143 Bactericidal, 32, 143, 157 Balloon dilation, 77, 143 Base, 24, 143, 158, 160, 168, 169, 192, 193 Basophils, 143, 161, 180 Benign, 59, 102, 104, 143, 146, 158, 160, 174 Benign prostatic hyperplasia, 143, 158 Beta-Thromboglobulin, 143, 167 Bilateral, 143, 186 Bile Acids, 143, 159 Bile Acids and Salts, 143 Bile duct, 9, 144, 147, 148, 155, 163, 165, 181 Bile Pigments, 144, 168 Biliary Atresia, 102, 144 Biliary Tract, 44, 93, 103, 144, 162, 177 Biochemical, 7, 19, 23, 25, 33, 60, 67, 71, 141, 144, 168, 176 Biopsy, 16, 48, 144, 178 Biosynthesis, 142, 144, 182, 187 Biotechnology, 27, 28, 108, 115, 144 Bladder, 101, 143, 144, 166, 173, 174, 182, 193

Bloating, 144, 166, 168, 171 Blood Cell Count, 144, 162 Blood Coagulation, 20, 144, 145, 190 Blood Coagulation Factors, 144 Blood Glucose, 48, 144, 162, 167 Blood pressure, 132, 144, 164, 165, 172, 175, 181, 188 Blood vessel, 10, 144, 146, 155, 157, 168, 170, 171, 178, 179, 188, 189, 191, 193, 194 Blood Volume, 120, 144 Blot, 15, 45, 144 Body Fluids, 144, 154, 158, 175, 188 Bone Marrow, 144, 160, 165, 170, 172 Bowel, 24, 145, 153, 166, 167, 169, 176, 179, 189, 192 Bowel Movement, 145, 153, 189 Bradykinin, 54, 84, 92, 145, 168, 175 Bronchi, 145, 191 Bronchial, 145, 163 Bronchoconstriction, 145, 180 Buccal, 145, 170 Butyric Acid, 145, 157 C Cachexia, 98, 145 Caerulein, 14, 17, 20, 74, 75, 84, 85, 145 Calcium, 10, 12, 25, 27, 78, 97, 132, 133, 145, 149, 173, 175, 178, 187, 190 Capillary, 145, 181, 194 Capillary Permeability, 145 Carbohydrate, 100, 145, 151, 161, 181 Carboxy, 93, 145 Carcinogenic, 146, 166, 182 Carcinogens, 146, 176 Carcinoid, 31, 35, 146 Carcinoma, 59, 102, 146 Cardiac, 5, 35, 139, 146, 162, 173, 185 Cardiovascular, 146, 153, 169 Case report, 27, 29, 30, 31, 34, 49, 50, 54, 65, 66, 71, 146, 148 Case series, 146, 148 Caspases, 15, 146 Catabolism, 16, 27, 146 Catalase, 78, 137, 146 Catheter, 26, 146, 155 Causal, 95, 146, 162 Caustic, 104, 146 Cefamandole, 28, 146 Celiac Disease, 103, 146 Cell Cycle, 146, 162 Cell Death, 10, 14, 15, 141, 146, 174 Cell Differentiation, 146, 187 Cell Division, 143, 146, 147, 172, 180, 187

199

Cell Lineage, 23, 147 Cell membrane, 15, 95, 147, 153, 157, 179, 188 Cell proliferation, 25, 142, 147, 187 Central Nervous System, 137, 147, 169, 173, 174, 176 Centrifugation, 147, 162 Cephalothin, 28, 147 Cerebral, 94, 95, 147, 151, 188 Cerebrum, 147 Ceroid, 69, 147, 170 Character, 94, 147, 153, 161 Chemical Warfare, 147, 152 Chemical Warfare Agents, 147, 152 Chemokines, 20, 56, 147 Chemotactic Factors, 147, 149 Chemotherapy, 81, 147 Cholangiography, 7, 147 Cholangitis, 99, 102, 147 Cholecystectomy, 7, 36, 103, 147 Cholecystitis, 102, 103, 147 Cholecystokinin, 15, 17, 24, 25, 77, 82, 145, 147 Choledocholithiasis, 38, 102, 148 Cholelithiasis, 6, 8, 148, 162 Choleretic, 148, 161 Cholesterol, 143, 148, 159, 164, 171 Chorioretinitis, 148, 185 Choroid, 148, 185, 193 Chromatin, 141, 148, 170 Chromosomal, 139, 148 Chronic Disease, 145, 148, 149 Chronic renal, 9, 148, 193 Chyme, 100, 148 Chymotrypsin, 148, 159 Cirrhosis, 102, 148, 162, 181 Clarithromycin, 29, 148 Clinical study, 35, 65, 71, 148, 151 Clinical trial, 6, 14, 56, 71, 84, 115, 148, 151, 154, 184 Cloning, 144, 148 Coagulation, 78, 86, 98, 144, 148, 158 Coenzyme, 142, 148 Cofactor, 149, 183, 190 Colitis, 120, 149, 168 Collagen, 149, 157, 164, 180 Collagen disease, 149, 164 Colon, 36, 59, 149, 165, 166, 168, 169, 182, 192 Colorectal, 103, 149 Colorectal Cancer, 103, 149 Combination Therapy, 85, 149

Common Bile Duct, 7, 149, 152, 163 Complement, 63, 140, 149, 150, 160, 187 Complement Activation, 63, 140, 149 Complementary and alternative medicine, 81, 87, 150 Complementary medicine, 81, 150 Computational Biology, 115, 150 Computed tomography, 3, 4, 5, 7, 9, 10, 12, 13, 32, 36, 39, 62, 150 Computerized axial tomography, 150 Computerized tomography, 97, 150 Confusion, 150, 193 Conjugated, 143, 150, 152 Conjugation, 150, 161 Conjunctiva, 150 Conjunctivitis, 94, 95, 150 Connective Tissue, 142, 145, 149, 151, 158, 170, 190 Consciousness, 140, 151, 153, 154, 163, 185 Constipation, 104, 151, 168, 179 Constitutional, 151, 186 Constriction, 59, 151, 168 Consultation, 9, 151 Contraindications, ii, 151 Contrast medium, 151, 171 Control group, 8, 151 Controlled clinical trial, 16, 151 Convulsions, 141, 151, 154, 162, 181 Coordination, 151, 173 Cornea, 151, 186, 193 Coronary, 151, 173 Coronary Thrombosis, 151, 173 Cortex, 151 Corticosteroid, 151, 181 Creatinine, 96, 152, 168, 193 Creatinine clearance, 96, 152 Critical Care, 5, 36, 57, 68, 152 Crossing-over, 152, 184 Curative, 152, 190 Cutaneous, 152, 169, 170 Cyanosis, 152, 156 Cyclic, 24, 152, 161, 175 Cyst, 7, 152, 177 Cysteine, 15, 16, 54, 146, 147, 152 Cysteine Endopeptidases, 146, 152 Cystic Duct, 149, 152, 163 Cystine, 152 Cytochrome, 15, 152 Cytokine, 11, 37, 70, 74, 152, 167 Cytoplasm, 141, 143, 147, 152, 161, 170, 172 Cytotoxic, 98, 152, 187

200

Acute pancreatitis

D Decarboxylation, 152, 163 Decontamination, 75, 152 Degenerative, 153, 163, 176 Deletion, 17, 141, 153 Dementia, 137, 153 Depolarization, 153, 187 Deuterium, 153, 164 Diabetes Mellitus, 22, 153, 160, 162, 176 Diabetic Ketoacidosis, 50, 153 Diagnostic procedure, 91, 109, 153 Dialyzer, 153, 162 Diarrhea, 153, 168, 171 Diastolic, 153, 165 Dicyclomine, 141, 153 Dietary Fats, 153, 169 Diffusion, 145, 153, 166, 175, 192 Digestion, 19, 55, 97, 139, 143, 144, 145, 148, 153, 154, 166, 167, 169, 170, 177, 178, 189, 193 Digestive system, 16, 153, 159 Digestive tract, 153, 188 Dilation, 59, 145, 153 Direct, iii, 18, 23, 26, 27, 92, 154, 177, 184 Discrete, 99, 154 Disease Progression, 9, 154 Disinfectant, 154, 157 Dissection, 6, 154 Dissociation, 138, 154 Distal, 42, 154, 159, 183 Double-blind, 63, 81, 154 Drug Interactions, 154 Duct, 10, 15, 24, 41, 62, 77, 97, 100, 110, 139, 149, 154, 155, 157, 183, 186, 189 Duodenum, 10, 100, 110, 143, 148, 154, 155, 174, 177, 178, 186, 189 Dyspepsia, 103, 154, 166 Dyspnea, 154, 156 E Eating Disorders, 104, 154 Eclampsia, 143, 154, 181 Edema, 22, 154, 173, 181, 193 Effector, 15, 137, 149, 154 Efficacy, 6, 16, 22, 27, 68, 86, 154 Elastic, 154, 160, 177, 188 Elastin, 149, 154, 177 Electrocoagulation, 148, 154 Electrolyte, 24, 94, 120, 151, 155, 158, 162, 169, 175, 188, 193 Electrons, 141, 143, 155, 168, 176, 184 Emaciation, 137, 155 Embolus, 155, 166

Embryo, 146, 147, 155, 166 Emodin, 84, 155 Encephalopathy, 71, 102, 155 Endogenous, 22, 74, 144, 155, 182, 192 Endoscope, 155 Endoscopic, 6, 7, 8, 9, 11, 13, 16, 38, 39, 41, 57, 65, 66, 69, 104, 109, 134, 155 Endoscopic retrograde cholangiopancreatography, 7, 8, 9, 38, 39, 66, 104, 155 Endothelial cell, 155 Endothelium, 155, 175 Endothelium-derived, 155, 175 Endotoxic, 155, 169 Endotoxin, 41, 51, 52, 67, 155, 192 End-stage renal, 148, 155 Enteral Nutrition, 8, 56, 84, 155 Enteropeptidase, 93, 156, 192 Environmental Exposure, 156, 176 Environmental Health, 114, 116, 156 Enzymatic, 15, 98, 99, 145, 149, 156, 163, 171 Enzyme, 14, 16, 22, 77, 99, 100, 139, 142, 146, 148, 154, 156, 160, 161, 168, 169, 173, 177, 178, 180, 182, 183, 184, 185, 186, 187, 189, 190, 194, 195 Epigastric, 94, 156, 177 Epithelial, 23, 24, 56, 137, 156, 163 Epithelial Cells, 23, 24, 156, 163 Epithelium, 155, 156, 177 Epitope, 19, 156 Erythema, 156, 193 Erythrocyte Volume, 144, 156 Erythrocytes, 140, 144, 145, 156, 162, 184, 187 Erythromycin, 148, 156, 186 Esophageal, 104, 156, 159, 192 Esophageal Atresia, 104, 156, 192 Esophageal Motility Disorders, 104, 156 Esophagitis, 94, 95, 156, 159 Esophagus, 153, 156, 159, 162, 170, 178, 179, 184, 189, 192 Estrogens, 82, 156 Ethanol, 17, 77, 157 Ethionine, 86, 157 Eukaryotic Cells, 157, 176 Evacuation, 151, 157, 169 Excrete, 141, 157, 168 Exhaustion, 140, 157 Exocrine, 11, 23, 24, 26, 76, 93, 147, 157, 177 Exocytosis, 15, 26, 157

201

Exogenous, 22, 155, 157, 182 Exon, 26, 157 Extensor, 157, 183 Extracellular, 17, 151, 157, 188, 190 Extravasation, 22, 157, 162 Exudate, 56, 85, 148, 157, 176 Eye Infections, 138, 157 F Failure to Thrive, 104, 157 Family Planning, 115, 157 Fat, 49, 77, 133, 134, 141, 144, 145, 151, 155, 157, 168, 169, 170, 173, 192 Fatty acids, 18, 138, 153, 157, 161, 182, 191 Feces, 151, 157, 189 Fibrin, 144, 157, 177, 179, 180, 190 Fibroblasts, 157, 167 Fibrosis, 21, 26, 102, 104, 139, 158, 186 Finasteride, 64, 158 Fine-needle aspiration, 158, 174 Fistula, 66, 158, 176 Fixation, 158, 187 Fluid Therapy, 158, 175 Fold, 17, 158, 171 Foramen, 158, 179 Forearm, 144, 158 Frameshift, 158, 192 Frameshift Mutation, 158, 192 Free Radicals, 10, 65, 78, 141, 154, 158, 173 Fulminant Hepatic Failure, 103, 158 G Gabexate, 45, 46, 64, 158 Gallbladder, 26, 64, 101, 102, 103, 110, 137, 144, 147, 152, 153, 155, 159 Gangrene, 60, 137, 159 Gas, 139, 153, 159, 164, 166, 168, 171, 175, 189 Gastric, 46, 47, 94, 142, 145, 156, 159, 162, 163, 178 Gastric Acid, 156, 159 Gastric Juices, 159, 178 Gastrin, 159, 164 Gastritis, 104, 159 Gastroenterologist, 102, 159 Gastroesophageal Reflux, 103, 104, 159 Gastroesophageal Reflux Disease, 103, 159 Gastrointestinal Hemorrhage, 98, 103, 159 Gastrointestinal Hormones, 25, 159 Gastrointestinal tract, 28, 102, 103, 104, 143, 157, 159, 169, 189 Gastrostomy, 155, 159 Gemfibrozil, 85, 159

Gene, 19, 20, 21, 23, 25, 26, 74, 75, 83, 138, 144, 159, 160, 164, 176, 187 Gene Expression, 20, 23, 25, 75, 83, 159, 160 Gene Therapy, 138, 159 Genetic Code, 160, 175 Genetic Engineering, 97, 144, 148, 160 Genetic testing, 6, 20, 160 Genital, 160, 186 Genotype, 160, 179 Germ cell tumors, 81, 160 Gingivitis, 94, 95, 160 Gland, 5, 93, 94, 96, 97, 99, 138, 151, 160, 170, 177, 178, 182, 186, 189, 191 Glomerular, 160, 168, 185 Glucocorticoid, 160, 164, 181 Glucose, 133, 142, 144, 153, 160, 161, 162, 166, 167, 188 Glucose Intolerance, 153, 160 Glucuronic Acid, 160, 162 Glutathione Peroxidase, 160, 187 Gluten, 103, 146, 160 Glyburide, 61, 161 Glycerol, 145, 161, 179 Glycerophospholipids, 161, 179 Glycine, 143, 161, 174, 187 Glycodeoxycholic Acid, 18, 161 Glycogen, 77, 161 Glycoprotein, 26, 74, 161, 190, 192 Glycoside, 161, 164 Governing Board, 161, 181 Grade, 4, 161 Grading, 12, 13, 103, 161 Gram-negative, 143, 155, 161 Gram-positive, 161, 169 Granule, 15, 26, 161 Granulocytes, 161, 169, 187, 194 Guanylate Cyclase, 161, 175 H Habitual, 147, 161 Haptens, 138, 162 Heartburn, 162, 166 Helix-loop-helix, 23, 162 Hematocrit, 69, 144, 162 Hematoma, 53, 162 Hemlock, 63, 162 Hemobilia, 102, 162 Hemochromatosis, 103, 162 Hemodialysis, 5, 153, 158, 162, 168, 169, 192 Hemofiltration, 35, 162, 192 Hemoglobin, 140, 144, 152, 156, 162, 177

202

Acute pancreatitis

Hemolysis, 50, 162 Hemorrhage, 53, 63, 94, 98, 102, 154, 162, 173, 190 Heparin, 51, 76, 162, 180 Hepatic, 98, 102, 103, 138, 149, 155, 162, 163, 170, 181 Hepatic Duct, Common, 155, 163 Hepatic Encephalopathy, 103, 163 Hepatitis, 29, 49, 65, 97, 102, 103, 104, 158, 163, 194 Hepatitis, Chronic, 102, 163 Hepatobiliary, 31, 35, 41, 42, 48, 49, 51, 61, 62, 64, 84, 102, 163 Hepatocellular, 102, 103, 163 Hepatocellular carcinoma, 102, 103, 163 Hepatocytes, 163 Hepatology, 10, 13, 29, 32, 33, 47, 48, 49, 52, 65, 77, 102, 103, 104, 163 Hepatorenal Syndrome, 98, 103, 163 Hepatotoxicity, 47, 163 Hereditary, 12, 19, 21, 49, 102, 120, 163 Heredity, 137, 159, 163 Hernia, 49, 138, 163 Heterodimer, 23, 163 Heterogeneity, 138, 163 Histamine, 9, 140, 163 Histidine, 163 Histology, 68, 163 Homeostasis, 24, 163 Homodimer, 23, 163 Homologous, 22, 152, 160, 163, 187, 190, 192 Hormonal, 120, 142, 151, 164 Hormone, 25, 151, 159, 164, 167, 176, 186, 187, 190, 191 Hybridomas, 164, 167 Hydration, 4, 99, 164 Hydrocortisone, 29, 164 Hydrogen, 92, 139, 143, 145, 146, 153, 160, 164, 169, 172, 174, 176, 183, 190 Hydrogen Peroxide, 146, 160, 164, 169, 190 Hydrolases, 15, 164, 179 Hydrolysis, 164, 178, 179, 181, 183, 192 Hyperaemia, 150, 164 Hyperbaric, 84, 85, 164 Hyperbaric oxygen, 84, 85, 164 Hyperbilirubinemia, 164, 168 Hyperlipidemia, 74, 164 Hyperlipoproteinemia, 164, 165 Hyperplasia, 25, 164 Hypersensitivity, 139, 164, 169, 186, 187

Hyperstimulation, 17, 24, 25, 164 Hypertension, 10, 22, 102, 164, 176, 181, 193 Hypertriglyceridemia, 38, 50, 51, 82, 85, 165 Hypertrophy, 143, 164, 165 Hypotension, 92, 151, 165, 174, 180 Hypothalamus, 165, 174 Hypoxanthine, 165, 195 Hypoxemia, 32, 165 Hypoxia, 10, 57, 165 I Iatrogenic, 98, 165 Idiopathic, 10, 12, 13, 21, 26, 33, 36, 37, 49, 51, 69, 77, 165 Ileum, 165, 174 Ileus, 42, 145, 165 Immune response, 141, 143, 151, 162, 165, 187, 189, 194 Immune system, 143, 165, 169, 173, 194 Immunity, 137, 165 Immunization, 165, 187 Immunodeficiency, 63, 137, 165 Immunogenic, 165, 169 Immunology, 138, 165 Impaction, 9, 165 Impairment, 5, 11, 157, 165 In situ, 64, 165 In vitro, 14, 15, 17, 19, 21, 82, 160, 165, 166 In vivo, 17, 82, 160, 162, 165, 166, 191 Incision, 26, 166, 167, 169 Incompetence, 159, 166 Incontinence, 104, 153, 166 Incubated, 14, 166 Indigestion, 103, 131, 132, 166 Induction, 18, 24, 32, 76, 97, 98, 166 Infarction, 95, 99, 166, 185 Infertility, 94, 95, 166 Infiltration, 22, 24, 37, 166, 182 Inflammatory bowel disease, 104, 166 Infusion, 14, 16, 166, 173 Ingestion, 77, 104, 166, 180, 190 Initiation, 17, 20, 22, 46, 166, 192 Inositol, 24, 166 Insight, 19, 166 Insulator, 167, 173 Insulin, 23, 25, 51, 110, 153, 167, 168 Insulin-dependent diabetes mellitus, 167 Insulin-like, 25, 167 Intensive Care, 4, 7, 9, 41, 57, 62, 77, 98, 167 Interleukin-2, 67, 167

203

Interleukin-6, 33, 53, 74, 167 Interleukin-8, 47, 167 Intermittent, 93, 96, 158, 167, 179 Internal Medicine, 16, 17, 18, 47, 54, 74, 75, 77, 78, 81, 84, 159, 167 Interstitial, 12, 75, 167, 185 Intestinal, 24, 45, 46, 53, 60, 67, 82, 96, 143, 146, 147, 156, 167, 169, 171 Intestinal Mucosa, 24, 143, 146, 147, 167 Intestine, 26, 110, 141, 143, 145, 149, 167, 169, 194 Intracellular, 10, 14, 17, 24, 25, 83, 146, 166, 167, 171, 175, 187 Intramuscular, 167, 178 Intraocular, 167, 191 Intraocular pressure, 167, 191 Intravascular, 7, 11, 78, 86, 98, 158, 167 Intravenous, 4, 8, 16, 54, 77, 120, 134, 166, 167, 178 Intrinsic, 93, 138, 167 Intussusception, 138, 167 Invasive, 26, 109, 165, 167, 170 Ions, 143, 154, 155, 164, 168, 188 Irritable Bowel Syndrome, 103, 168 Ischemia, 6, 10, 17, 24, 45, 60, 142, 168, 173, 185 Isoenzymes, 133, 168 Isotretinoin, 74, 168 J Jaundice, 103, 132, 163, 164, 168 Jejunostomy, 155, 168 K Kallidin, 145, 168 Kb, 114, 168 Keratinocytes, 167, 168 Ketone Bodies, 153, 168 Ketosis, 153, 168 Kidney Failure, 5, 155, 168, 169 Kidney Failure, Acute, 168 Kidney Failure, Chronic, 168, 169 L Labile, 149, 169 Lactobacillus, 56, 84, 169 Laparotomy, 12, 169 Large Intestine, 149, 153, 167, 169, 184, 188, 194 Larynx, 169, 191 Laxative, 138, 155, 169, 188 Leishmaniasis, 29, 169 Lesion, 94, 132, 169, 192 Lethal, 14, 58, 78, 143, 169 Leucocyte, 33, 37, 66, 169

Leukemia, 30, 82, 160, 169 Leukotrienes, 95, 142, 169 Ligation, 24, 169 Lipase, 4, 6, 9, 50, 93, 97, 133, 169 Lipid, 25, 28, 100, 120, 141, 142, 145, 147, 159, 161, 167, 169, 170, 173, 177, 192 Lipid A, 28, 169 Lipid Peroxidation, 169, 177 Lipofuscin, 147, 170 Lipopolysaccharide, 36, 161, 170 Liver Cirrhosis, 163, 170 Liver Neoplasms, 157, 170 Liver Transplantation, 103, 170 Localized, 10, 16, 22, 99, 137, 139, 158, 162, 166, 170, 180, 192, 193 Loop, 138, 163, 170 Lower Esophageal Sphincter, 156, 159, 170 Lupus, 170, 190 Lymph, 143, 155, 170 Lymph node, 143, 170 Lymphatic, 155, 166, 170, 189 Lymphatic system, 170, 189 Lymphocyte Count, 137, 170 Lymphocytes, 40, 137, 141, 164, 165, 167, 169, 170, 189, 194 Lymphoid, 140, 169, 170 Lymphoma, 30, 77, 82, 85, 170 Lysine, 93, 170, 192 M Macronutrients, 8, 170 Magnetic Resonance Imaging, 10, 36, 49, 170 Malabsorption, 24, 104, 146, 171 Malabsorption syndrome, 104, 171 Malignancy, 10, 171 Malignant, 58, 137, 160, 171, 174 Malnutrition, 24, 138, 142, 145, 171 Mediate, 15, 22, 171 Mediator, 25, 45, 57, 98, 147, 167, 171, 180 Medical Records, 171, 186 MEDLINE, 115, 171 Meglumine, 29, 171 Membrane Lipids, 171, 179 Menstruation, 49, 171 Mental, iv, 13, 114, 116, 150, 153, 154, 166, 171, 193 Meperidine, 11, 171 Mesenteric, 60, 99, 143, 171, 181 Mesentery, 171, 179 Metabolic acidosis, 153, 171 Metastasis, 171, 174 Microbiology, 137, 172

204

Acute pancreatitis

Microcirculation, 12, 64, 170, 172 Micronutrients, 8, 172 Microorganism, 149, 172, 194 Microscopy, 22, 172 Microspheres, 17, 172 Migration, 57, 172 Mitochondria, 172, 173, 176 Mitochondrial Swelling, 172, 174 Mitosis, 141, 172 Modification, 160, 172, 184 Monitor, 9, 50, 152, 172, 175 Monoclonal, 95, 164, 172, 184 Monoclonal antibodies, 95, 172 Monocytes, 37, 50, 167, 172, 180 Mononuclear, 47, 172, 173, 192 Morphine, 74, 94, 171, 173, 174, 176 Motility, 102, 173 Motion Sickness, 173, 174 Motor Activity, 151, 159, 173 Mucinous, 49, 173 Mucocutaneous, 169, 173 Mucosa, 24, 159, 170, 173 Mucus, 173, 192 Multiple Organ Failure, 33, 98, 173 Multiple sclerosis, 94, 173 Mydriatic, 153, 173 Myelin, 173 Myocardial infarction, 94, 95, 143, 151, 173 Myocardial Reperfusion, 173, 185 Myocardial Reperfusion Injury, 173, 185 Myocardium, 173 N N-acetyl, 54, 173 Narcotic, 171, 173 Nasogastric, 7, 9, 155, 174 Nausea, 4, 5, 96, 132, 166, 168, 174, 193 Needle biopsy, 68, 158, 174 Neoplasms, 59, 102, 137, 146, 162, 174 Nephrosis, 163, 174 Nervous System, 138, 147, 162, 171, 174, 189 Neural, 62, 138, 174, 188 Neurogenic, 22, 174 Neurogenic Inflammation, 22, 174 Neuronal, 17, 69, 174 Neurons, 174, 190 Neuropeptides, 174 Neuroretinitis, 174, 186 Neurotensin, 25, 174 Neurotransmitter, 137, 142, 145, 161, 163, 174, 187, 189 Neutralization, 100, 174

Neutrons, 139, 174, 184 Neutropenia, 175, 180 Neutrophil, 22, 56, 64, 175 Neutrophil Infiltration, 22, 175 Nifedipine, 78, 175 Nitric Oxide, 17, 52, 62, 85, 175 Nitrogen, 8, 139, 158, 168, 175 Nosocomial, 104, 175 Nuclear, 18, 23, 66, 150, 155, 157, 174, 175 Nuclei, 139, 150, 155, 160, 171, 172, 174, 175, 176, 183 Nucleic acid, 100, 160, 165, 175, 183 Nucleotidases, 164, 175 Nucleus, 141, 143, 148, 152, 153, 157, 170, 172, 173, 174, 175, 183, 189 Nutritional Support, 7, 8, 16, 44, 159, 175 O Observational study, 82, 175 Octreotide, 8, 11, 13, 49, 77, 82, 84, 108, 176 Oliguria, 168, 176 Oncogene, 56, 176 Operon, 176, 185 Opiate, 173, 176 Opium, 173, 176 Opportunistic Infections, 137, 176 Optic Nerve, 174, 176, 185, 186 Organelles, 16, 147, 152, 172, 176, 180 Orthostatic, 176 Osteoarthritis, 94, 176 Osteoporosis, 94, 176 Overdose, 158, 176 Oxidation, 141, 152, 153, 160, 169, 176, 177 Oxidative metabolism, 169, 177 Oxidative Stress, 64, 65, 177 Oxygenation, 108, 165, 177 P Palliative, 177, 190 Pancreatic cancer, 21, 23, 99, 102, 177 Pancreatic Ducts, 155, 177 Pancreatic Elastase, 38, 177 Pancreatic enzymes, 10, 99, 177 Pancreatic Fistula, 102, 103, 177 Pancreatic Juice, 24, 93, 97, 100, 110, 148, 159, 177 Pancreatic Pseudocyst, 12, 71, 177 Papilla, 155, 177 Papillary, 49, 177 Parasite, 177 Parasitic, 103, 177 Parasitic Diseases, 103, 177 Parathyroid, 35, 177, 178, 190 Parathyroid Glands, 177, 178

205

Parathyroid hormone, 35, 178 Parenteral, 8, 11, 24, 47, 51, 104, 178 Parenteral Nutrition, 8, 24, 47, 51, 104, 178 Particle, 178, 188, 192 Pathologic, 15, 17, 33, 94, 141, 144, 151, 164, 178, 183 Pathologic Processes, 141, 178 Pathophysiology, 4, 19, 20, 37, 43, 65, 75, 178 Patient Education, 120, 126, 128, 135, 178 Pelvis, 137, 178, 193 Penicillin, 140, 178 Pepsin, 178, 186 Peptic, 94, 95, 99, 104, 178 Peptic Ulcer, 94, 95, 99, 104, 178 Peptide, 25, 41, 68, 69, 147, 148, 156, 164, 178, 181, 182, 183 Peptide Chain Elongation, 148, 178 Peptide Hydrolases, 164, 178 Percutaneous, 7, 12, 26, 48, 178 Perforation, 54, 62, 96, 158, 178, 194 Perfusion, 17, 46, 165, 178 Pericardium, 178, 190 Periodontitis, 160, 178 Peripheral blood, 37, 67, 179 Peritoneal, 5, 7, 13, 56, 97, 105, 142, 179 Peritoneal Cavity, 105, 142, 179 Peritoneal Dialysis, 5, 179 Peritoneal Lavage, 5, 7, 13, 105, 179 Peritoneum, 171, 179, 186 Peritonitis, 103, 179, 194 Pharmacologic, 17, 140, 179, 191 Pharynx, 159, 179 Phenotype, 19, 179 Phenyl, 171, 179 Phospholipases, 179, 187 Phospholipids, 95, 157, 166, 171, 179 Phosphoric Monoester Hydrolases, 164, 179 Phosphorus, 145, 178, 179 Photocoagulation, 148, 179 Physiologic, 17, 25, 138, 144, 171, 172, 179, 184 Physiology, 18, 20, 21, 31, 84, 103, 110, 159, 179 Pigment, 147, 170, 179 Plants, 139, 142, 155, 160, 161, 162, 180, 191 Plaque, 94, 95, 180 Plasma, 22, 56, 62, 75, 77, 97, 99, 138, 140, 143, 144, 147, 160, 162, 164, 168, 180, 185 Plasma cells, 140, 180

Plasma Volume, 144, 180 Plasmin, 158, 180 Plastids, 176, 180 Platelet Activating Factor, 10, 180 Platelet Activation, 180, 187 Platelet Aggregation, 140, 175, 180, 191 Platelet Factor 4, 167, 180 Platelets, 143, 175, 180, 190 Pneumonia, 151, 180 Poisoning, 174, 180, 187 Polymerase, 15, 180, 185 Polypeptide, 139, 149, 180, 181, 182, 183, 195 Polyposis, 149, 181 Polysaccharide, 141, 181 Portal Hypertension, 102, 103, 181 Portal System, 18, 181 Portal Vein, 181 Posterior, 148, 177, 181, 186 Postmenopausal, 176, 181 Postoperative, 6, 171, 173, 181 Postsynaptic, 181, 187 Potentiation, 181, 187 Practice Guidelines, 12, 116, 121, 181 Preclinical, 22, 181 Precursor, 140, 142, 154, 156, 181 Prednisolone, 29, 181 Preeclampsia, 94, 95, 181 Pregnancy Maintenance, 157, 181 Preoperative, 8, 181 Primary Biliary Cirrhosis, 102, 103, 181 Primary Sclerosing Cholangitis, 103, 181 Procaine, 34, 76, 182 Proctocolectomy, 103, 182 Proenzymes, 93, 182 Prognostic factor, 66, 182 Progression, 10, 21, 69, 140, 182 Progressive, 110, 146, 148, 153, 169, 173, 174, 176, 180, 182, 185 Promoter, 19, 26, 182 Prone, 26, 182 Prophylaxis, 11, 31, 104, 107, 182 Prospective study, 45, 69, 182 Prostaglandins, 78, 95, 142, 182 Prostaglandins A, 95, 182 Prostaglandins D, 182 Prostate, 143, 182 Protease, 78, 86, 97, 149, 177, 182 Protease Inhibitors, 97, 182 Protein Binding, 23, 182 Protein C, 16, 24, 97, 138, 139, 141, 182, 193 Protein Conformation, 139, 182

206

Acute pancreatitis

Protein S, 16, 144, 148, 156, 160, 183 Proteinuria, 181, 183 Proteolytic, 15, 17, 19, 93, 149, 156, 180, 183 Protons, 139, 164, 183, 184 Protozoa, 150, 169, 172, 183, 193 Proximal, 154, 183 Pseudocysts, 10, 13, 102, 183 Psoriasis, 94, 95, 183 Public Policy, 115, 183 Publishing, 5, 7, 8, 10, 11, 27, 76, 101, 103, 104, 109, 183 Pulmonary, 18, 32, 144, 162, 168, 169, 183, 194 Pulmonary Artery, 144, 183, 194 Pulmonary Edema, 168, 183 Pulse, 172, 183 Pupil, 151, 153, 173, 183 Purines, 183, 187, 195 Putrefaction, 159, 184 Q Quality of Life, 5, 57, 62, 184, 190 R Race, 172, 184 Radiation, 98, 156, 158, 164, 184, 195 Radiation therapy, 164, 184 Radioactive, 152, 164, 172, 175, 184 Radiolabeled, 24, 184 Radiological, 47, 178, 184 Radiologist, 102, 184 Randomized, 8, 16, 27, 34, 51, 53, 56, 81, 84, 154, 184 Receptor, 9, 22, 24, 25, 28, 67, 75, 92, 137, 141, 184, 187 Recombinant, 19, 21, 184, 194 Recombination, 22, 150, 160, 184 Rectum, 141, 145, 149, 153, 159, 166, 169, 182, 184 Recurrence, 41, 120, 184 Red blood cells, 64, 156, 184, 188 Reductase, 158, 184 Refer, 1, 145, 149, 158, 175, 184 Reflux, 156, 159, 184 Refractory, 84, 155, 184 Regeneration, 24, 75, 84, 184 Regimen, 154, 184 Regurgitation, 156, 159, 162, 184 Remission, 184, 185 Renal failure, 11, 96, 163, 185 Renin, 57, 140, 185 Renin-Angiotensin System, 57, 185 Reperfusion, 10, 94, 95, 173, 185

Reperfusion Injury, 10, 94, 95, 185 Repressor, 23, 176, 185 Resection, 24, 185 Respiration, 172, 177, 185 Respiratory distress syndrome, 8, 18, 185 Restitution, 24, 185 Resuscitation, 12, 185 Retina, 148, 174, 176, 185, 186, 193 Retinitis, 94, 95, 185 Retrograde, 65, 186 Retroperitoneal, 6, 27, 94, 138, 186 Retrospective, 54, 109, 186 Retrospective study, 54, 109, 186 Reversion, 186, 192 Rheumatoid, 44, 94, 149, 186 Rheumatoid arthritis, 44, 94, 149, 186 Rhinitis, 94, 95, 186 Ribonuclease, 97, 186 Ribose, 15, 186 Risk factor, 5, 6, 45, 61, 64, 182, 186 Rod, 169, 186 Roxithromycin, 34, 186 S Saliva, 186 Salivary, 100, 153, 177, 186 Salivary glands, 153, 186 Salivation, 156, 186 Sclera, 148, 150, 186, 193 Sclerosis, 95, 142, 149, 173, 186 Screening, 96, 103, 108, 148, 186 Secretin, 18, 186 Secretion, 16, 17, 93, 99, 137, 145, 151, 153, 159, 163, 167, 173, 176, 186, 193 Secretory, 11, 15, 21, 186 Sedative, 162, 186 Segregation, 184, 187 Selenium, 54, 187 Semisynthetic, 146, 148, 186, 187 Senile, 12, 176, 187 Sensitization, 18, 187 Sepsis, 5, 8, 11, 44, 50, 93, 143, 171, 187 Septic, 46, 71, 187 Septicemia, 16, 187 Serine, 148, 158, 187, 192 Serous, 142, 155, 187 Sex Characteristics, 156, 187, 190 Shock, 15, 22, 47, 53, 71, 76, 94, 98, 164, 187, 192 Side effect, 138, 187, 190, 191 Signal Transduction, 24, 25, 166, 187 Sludge, 33, 188

207

Small intestine, 23, 100, 110, 148, 152, 154, 155, 164, 165, 167, 174, 188, 192 Smooth muscle, 139, 140, 145, 163, 173, 185, 188, 189 Social Environment, 184, 188 Sodium, 100, 161, 188, 193 Sodium Bicarbonate, 100, 188 Sodium Channels, 188, 193 Solvent, 157, 161, 188 Sorbitol, 171, 188 Sound wave, 184, 188 Spastic, 168, 188 Specialist, 122, 153, 188 Species, 169, 172, 177, 184, 188, 192, 195 Specificity, 6, 24, 93, 98, 99, 138, 177, 188 Spectrum, 146, 186, 188 Sperm, 160, 188 Sphincter, 6, 10, 37, 77, 100, 109, 169, 188 Spleen, 70, 140, 143, 170, 189 Stabilizer, 85, 189 Staging, 38, 189 Standard therapy, 104, 189 Stenosis, 59, 189 Stent, 109, 189 Sterile, 12, 58, 177, 189 Sterility, 166, 189 Sterilization, 7, 189 Stimulant, 163, 168, 189 Stimulus, 167, 174, 189, 190 Stool, 149, 165, 166, 168, 169, 189 Strand, 180, 189 Stress, 4, 15, 77, 168, 174, 177, 186, 189, 193 Stricture, 44, 189 Subacute, 166, 189 Subcapsular, 53, 189 Subclinical, 166, 189 Subcutaneous, 154, 178, 189 Substance P, 156, 186, 189 Substrate, 16, 98, 164, 189 Suction, 7, 189 Superoxide, 78, 189, 190 Superoxide Dismutase, 78, 190 Supplementation, 105, 190 Supportive care, 4, 9, 12, 190 Survival Rate, 98, 190 Symptomatic, 13, 95, 177, 190 Synaptic, 174, 187, 190 Systemic lupus erythematosus, 29, 54, 66, 149, 190 Systolic, 165, 190 T Tachycardia, 190, 191

Tamponade, 35, 190 Teratogenic, 168, 190 Testosterone, 158, 184, 190 Tetany, 178, 190 Therapeutics, 39, 92, 190 Threshold, 164, 190 Thrombin, 157, 158, 180, 182, 190 Thrombocytopenia, 180, 190 Thrombomodulin, 182, 190 Thrombosis, 143, 183, 191 Thromboxanes, 142, 191 Thyroid, 78, 177, 178, 191 Thyroid Gland, 177, 178, 191 Tomography, 3, 50, 191 Tonic, 156, 191 Tonicity, 162, 191 Tonometry, 46, 191 Tooth Preparation, 137, 191 Topical, 157, 164, 168, 188, 191 Torsades de Pointes, 60, 191 Torsion, 166, 191 Toxaemia, 181, 191 Toxic, iv, 93, 150, 156, 162, 165, 187, 191 Toxicity, 154, 155, 191 Toxicology, 116, 191 Toxins, 10, 141, 160, 166, 172, 187, 191 Trace element, 8, 191 Trachea, 22, 145, 169, 179, 191, 192 Tracheoesophageal Fistula, 156, 192 Transcription Factors, 20, 23, 192 Transduction, 24, 25, 187, 192 Transfection, 144, 160, 192 Translocating, 143, 192 Translocation, 18, 32, 99, 143, 148, 156, 192 Transmitter, 137, 171, 192 Transplantation, 102, 103, 104, 148, 165, 169, 192 Trauma, 10, 93, 98, 102, 120, 156, 162, 174, 177, 179, 192 Triglyceride, 82, 164, 165, 192 Trypsin, 9, 15, 16, 17, 19, 20, 21, 65, 76, 93, 97, 148, 156, 182, 192, 195 Tube-feeding, 16, 192 Tuberculosis, 170, 192 Tumor Necrosis Factor, 10, 18, 78, 192 Tunica, 173, 192 Typhimurium, 60, 192 U Ulcer, 95, 103, 192 Ulceration, 178, 192 Ulcerative colitis, 29, 103, 166, 181, 192 Ultrafiltration, 162, 192

208

Acute pancreatitis

Ultrasonography, 4, 9, 69, 70, 97, 193 Uraemia, 177, 193 Urea, 168, 193 Uremia, 93, 168, 185, 193 Urethra, 143, 182, 193 Uric, 139, 183, 193 Urinary, 6, 41, 69, 108, 153, 166, 176, 193, 195 Urine, 68, 93, 94, 134, 141, 143, 144, 152, 166, 168, 176, 183, 193 Urticaria, 94, 95, 193 Uterus, 171, 174, 190, 193 Uvea, 193 Uveitis, 94, 95, 193 V Vaccines, 193, 194 Vacuoles, 15, 176, 193 Vagina, 169, 171, 190, 193 Valproic Acid, 43, 193 Vascular, 6, 10, 21, 46, 70, 94, 95, 139, 148, 155, 162, 166, 170, 172, 174, 175, 191, 193 Vasculitis, 93, 177, 194 Vasoactive, 94, 194 Vasodilatation, 22, 168, 194 Vasodilator, 145, 163, 173, 175, 194 Vector, 177, 192, 194 Vein, 63, 142, 167, 175, 181, 194 Venous, 142, 143, 144, 183, 194

Ventricle, 165, 183, 190, 194 Ventricular, 60, 173, 191, 194 Ventricular Dysfunction, 60, 194 Ventricular fibrillation, 191, 194 Venules, 144, 145, 172, 194 Veterinary Medicine, 115, 194 Villous, 146, 194 Viral, 65, 102, 103, 163, 192, 194 Viral Hepatitis, 65, 102, 103, 163, 194 Virus, 63, 65, 137, 160, 180, 192, 194 Visceral, 29, 169, 179, 194 Vitamin A, 166, 194 Vitro, 15, 17, 162, 194 Vivo, 17, 194 Volvulus, 49, 138, 194 W White blood cell, 93, 141, 166, 170, 173, 175, 180, 194 Withdrawal, 171, 194 X Xanthine, 28, 139, 195 Xanthine Oxidase, 28, 139, 195 Xenograft, 140, 195 X-ray, 142, 150, 151, 155, 175, 184, 189, 195 Y Yeasts, 179, 195 Z Zymogen, 17, 26, 93, 99, 148, 182, 195