Henoch-Schonlein Purpura: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References

HENOCH-SCHONLEIN PURPURA A 3-IN-1 MEDICAL REFERENCE Medical Dictionary Bibliography & Annotated Research Guide TO I NTE...

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HENOCH-SCHONLEIN PURPURA

A 3-IN-1 MEDICAL REFERENCE Medical Dictionary Bibliography & Annotated Research Guide TO I NTERNET

R EFERENCES

HENOCH-SCHONLEIN PURPURA A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES

J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS

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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright 2004 by ICON Group International, Inc. Copyright 2004 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1

Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Henoch-Schonlein Purpura: 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: 0-497-00531-X 1. Henoch-Schonlein Purpura-Popular works. I. Title.

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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.

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.

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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on Henoch-Schonlein purpura. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.

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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications. Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.

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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes&Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health

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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON HENOCH-SCHONLEIN PURPURA ............................................................. 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Henoch-Schonlein Purpura........................................................... 4 E-Journals: PubMed Central ....................................................................................................... 11 The National Library of Medicine: PubMed ................................................................................ 11 CHAPTER 2. NUTRITION AND HENOCH-SCHONLEIN PURPURA.................................................... 55 Overview...................................................................................................................................... 55 Finding Nutrition Studies on Henoch-Schonlein Purpura ......................................................... 55 Federal Resources on Nutrition ................................................................................................... 56 Additional Web Resources ........................................................................................................... 56 CHAPTER 3. ALTERNATIVE MEDICINE AND HENOCH-SCHONLEIN PURPURA ............................. 59 Overview...................................................................................................................................... 59 National Center for Complementary and Alternative Medicine.................................................. 59 Additional Web Resources ........................................................................................................... 61 General References ....................................................................................................................... 62 CHAPTER 4. PATENTS ON HENOCH-SCHONLEIN PURPURA .......................................................... 63 Overview...................................................................................................................................... 63 Patents on Henoch-Schonlein Purpura........................................................................................ 63 Patent Applications on Henoch-Schonlein Purpura.................................................................... 64 Keeping Current .......................................................................................................................... 66 CHAPTER 5. BOOKS ON HENOCH-SCHONLEIN PURPURA .............................................................. 67 Overview...................................................................................................................................... 67 Chapters on Henoch-Schonlein Purpura ..................................................................................... 67 APPENDIX A. PHYSICIAN RESOURCES ............................................................................................ 71 Overview...................................................................................................................................... 71 NIH Guidelines............................................................................................................................ 71 NIH Databases............................................................................................................................. 73 Other Commercial Databases....................................................................................................... 75 APPENDIX B. PATIENT RESOURCES ................................................................................................. 77 Overview...................................................................................................................................... 77 Patient Guideline Sources............................................................................................................ 77 Finding Associations.................................................................................................................... 79 APPENDIX C. FINDING MEDICAL LIBRARIES .................................................................................. 81 Overview...................................................................................................................................... 81 Preparation................................................................................................................................... 81 Finding a Local Medical Library.................................................................................................. 81 Medical Libraries in the U.S. and Canada ................................................................................... 81 ONLINE GLOSSARIES.................................................................................................................. 87 Online Dictionary Directories ..................................................................................................... 92 HENOCH-SCHONLEIN PURPURA DICTIONARY................................................................ 93 INDEX .............................................................................................................................................. 125

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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with Henoch-Schonlein purpura 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 Henoch-Schonlein purpura, 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 Henoch-Schonlein purpura, 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 Henoch-Schonlein purpura. 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 HenochSchonlein purpura, 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 Henoch-Schonlein purpura. The Editors

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

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CHAPTER 1. STUDIES ON HENOCH-SCHONLEIN PURPURA Overview In this chapter, we will show you how to locate peer-reviewed references and studies on Henoch-Schonlein purpura.

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

Henoch-Schonlein Purpura Nephritis: Course of Disease and Efficacy of Cyclophosphamide Source: Pediatric Nephrology. 19(1): 51-56. January 2004. Summary: Nephritis (inflammation of the filtering units of the kidneys) in HenochSchonlein purpura (HSP) is the primary cause of morbidity and mortality. Although many therapeutic regimens have been reported to be effective, no therapy has been shown in a controlled trial to be beneficial. This article reports on a study of 56 patients with histopathologically severe HSP nephritis who were randomized to receive supportive therapy with or without cyclosphosphamide. Patients were classified according to status at final followup: fully recovered 48.2 percent, persistent abnormalities 39.3 percent, and end stage renal disease (ESRD) or death, 12.5 percent.

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There were no differences in onset date or outcome between the two trial groups or in outcome between trial and 23 nontrial patients followed concurrently. Only 5 of 28 patients with nephrotic levels of proteinuria (protein in the urine) and severe onset histopathology recovered fully. The authors conclude that nephrotic syndrome, decreased glomerular filtration rate (GFR, a measure of kidney function), and more severe histopathology at onset, as well as persistence of urinary abnormalities for several years, are ominous signs. 2 figures. 4 tables. 29 references. •

Chronic Glomerulonephritis in Childhood: Membranoproliferative Glomerulonephritis, Henoch-Schonlein Purpura Nephritis, and IgA Nephropathy Source: Pediatric Clinics of North America. 42(6): 1487-1503. December 1995. Contact: Available from W.B. Saunders Company, Periodicals Fulfillment, 6277 Sea Harbor Drive, Orlando, FL 32887. (800) 654-2452. Summary: This article reviews various presentations of common childhood glomerulonephritides and provides an approach to management and potential therapy. The chronic glomerulonephritides that lead to permanent loss of renal function may present with an acute nephritic syndrome, nephrotic syndrome, or asymptomatic hematuria and proteinuria. The author covers membranoproliferative glomerulonephritis, Henoch-Schonlein purpura nephritis, and IgA nephropathy. For each, the clinical, laboratory, and pathologic features are outlined and management and therapeutic strategies proposed. 5 figures. 60 references. (AA-M).

Federally Funded Research on Henoch-Schonlein Purpura The U.S. Government supports a variety of research studies relating to Henoch-Schonlein purpura. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to Henoch-Schonlein purpura. 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 Henoch-Schonlein purpura. The following is typical of the type of information found when searching the CRISP database for Henoch-Schonlein purpura: •

Project Title: ALTERNATE DAY PREDNISONE & FISH OIL SUPPLEMENTS IN IGA NEPHROPATHY Principal Investigator & Institution: Jackson, Elizabeth; University of Kentucky 109 Kinkead Hall Lexington, Ky 40506

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Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).

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Timing: Fiscal Year 2002 Summary: This study evaluates alternate day prednisone and fish oil supplementation in young adults on IgA nephropathy. Patients under age 30 will be given therapy based on renal biopsy and persistent proteinuria. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CORE--CLINICAL RESOURCES AND BIOSTATISTICS Principal Investigator & Institution: Julian, Bruce A.; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2007 Summary: The aim of this Program Project is to identify the genes and pathways responsible for development of familial IgA nephropathy (IgAN). The approaches in the 3 Projects will refine the genetic location of the recently identified disease locus on chromosome 6q22-23 (IGAM1), evaluate the biosynthesis of IgA1 and its glycosylation in B lymphocytes, and assess the pathogenic role of cir5cuylating immune complexes with undergalactosylated IgA1. These studies require many patients with well- defined clinical phenotypes and appropriate family members and controls. Patients with familial or sporadic IgAN, Henoch-Schonlein purpura (HSP), family members, and non-IgAN disease- and healthy control subjects in a 7-stage catchment area will be enrolled. To provide clinical resources and statistical support for the 3 Projects, Core A will collect blood and urine samples (and residual renal tissue if biopsy done within 30 days), compile clinical and laboratory data in aq centralized database, and correlate laboratory and clinical data. The Specific Aims of Core A are: 1. Enroll 1515 subjects for the 3 Projects: 20 pedigrees with 50 familial IgAN/HSP patients and about 150 of their family members, 150 Caucasian sporadic IgAN patients and 375 of their family members, 50 HSP patients and 125 of their family members, 50 African-American IgAN patients and 200 of their family members, 65 non-IgAN disease- controls, and 200 Caucasian and 100 African-American healthy controls. 2. Establish and manage the computerized database for the entire Program Project: (a) compile the demographic, clinical, laboratory, histopathologic, and genetic data; (b) coordinate and manage statistical analyses to ensure investigators have ready access to statistical consultation and support; (c) provide statistical expertise including sample-size estimation and power calculations, randomization procedures, and design of data collection forms; and (d) perform interim reviews and final analyses. 3. Coordinate collection and distribution of blood and urine samples from patients and controls, and establish immortalized cell lines from selected subjects. 4. Perform detailed histologic analyses of residual renal tissue of newly biopsied IgAN/HSP and non-IgAN glomerulonephritis patients from whom blood and urine samples will be obtained for contemporaneous in vitro studies. The findings from this Program Project will substantially increase the understanding of the pathogenesis of a common renal disease and may be the foundation for future development of a diseasespecific therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: DIETARY LIPIDS AND EXPERIMENTAL IGA NEPHROPATHY Principal Investigator & Institution: Pestka, James J.; Professor; Food Science & Human Nutrition; Michigan State University 301 Administration Bldg East Lansing, Mi 48824 Timing: Fiscal Year 2002; Project Start 01-FEB-2001; Project End 31-DEC-2004 Summary: The goal of this research will be to understand specific mechanisms by which dietary polyunsaturated fatty acids (n-3 PUFA) in marine and plant oils impair

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development and progression of immunoglobulin A nephropathy (IgAN). Although IgAN is the most common glomerulonephritis worldwide, effective treatments for it remain elusive. Fish oil consumption has recently shown promise in retarding disease progression and renal failure in IgAN patients. An experimental mouse model is now available in which immunopathological hallmarks of IgAN are induced by dietary exposure to the mycotoxin vomitoxin (VT). Interestingly, replacement of corn oil in a semi-purified diet with menhaden fish oil markedly impairs immunopathogenesis in this model. The sequential activation of mitogen-activated protein kinases (MAPKs), upregulation of interleukin-6 (IL-6) gene expression and polyclonal activation of IgAsecreting cells appear to be critical early events in VT-induced IgAN. The guiding hypothesis for this project is that ingestion of n-3 PUFA in fish oil attenuates VTinduced IgAN by interfering with upstream regulation of IL-6 gene expression. Five specific aims are proposed. In AIM 1, a sub-chronic VT feeding model will be used to determine the capacity of feeding fish oil or the n-3 PUFAs, eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA), to attenuate VT-induced IgAN markers. In AIM 2, an acute VT exposure model will be used to evaluate the in vivo and ex vivo effects of feeding fish oil on IL-6 and IgA expression. In AIM 3, the role of transcription in n-3 PUFA-attenuated IL-6 expression will be assessed in VT-treated macrophage cultures by measuring transcription factor binding and nuclear runoff of IL-6 mRNA. In AIM 4, the role of post-transcriptional mechanisms in n-3 PUFA-attenuated IL-6 expression will be evaluated by measuring IL-6 mRNA stability in macrophage cultures. In AIM 5, the effects of n-3 PUFAs on activation of the MAPKs SAPK/JNK 1/2, ERK1/2 and p38 will be assessed in macrophages cultured with VT. Long-term impacts of increased mechanistic understanding of n-PUFA effects in this model may include improved nutritional and pharmacological strategies for inhibiting the progression of IgAN and potentially other autoimmune diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: FAMILIAL IGA NEPHROPATHY: GENETIC AND METABOLIC STUDIES Principal Investigator & Institution: Mestecky, Jiri F.; Professor; Microbiology; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2002; Project Start 15-JUN-2002; Project End 31-MAR-2007 Summary: IgA nephropathy (IgAN) is the most common primary glomerulonephritis in the world. Because of its frequently unfavorable cou7rse and lack of specific therapy, IgAN represents a serious healthy care and economic problem. The overall objective of the proposed Program Project is to determine the genetic and molecular basis of this common disease through integrated studies of patients with IgAN or HenochSchonlein purpura (HSP), commonly considered the systemic form of the disease process causing IgAN. We will enroll 20 multiplex families with 50 member5s afflicted with IgAN or HSP and 150 other family members; 150 Caucasian patients with sporadic IgAN (no affected relatives) and 375 of their family members, 50 patients with HSP and 125 of their relatives, 50 African-American patients with IgAN and 200 family members, 50 patients with non-IgAN glomerulonephritis, and 200 Caucasians and 100 AfricanAmericans as health controls. This proposal is based on novel findings generated in the laboratories of the participating investigators, with respect to genetic, biosynthetic, and metabolic studies of IgA molecules, immune complexes, and relevant receptors involved in IgA catabolism. The Program Project consists of three component research project and two core facilities: Project 1: Genetic Studies of IgA Nephropathy Project 2: Biosynthesis and Glycosylation of IgA1 Molecules in IgA Nephropathy Project 3: Immune

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Complexes and Mesangial Cells in IgA Nephropathy Core A: Clinical Resources and Biostatistics Core B: Administrative The results generated through extensive collaboration among the participating investigators are likely to provide information concerning the genetic and molecular defects characteristic of IgAN, identify mechanisms of the pathogenesis of this disease, and ultimately provide a basis to develop rational therapeutic approaches. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: IGA NEPHROPATHY

GLYCANS

AND

IMMUNE

COMPLEXES

IN

IGA

Principal Investigator & Institution: Tomana, Milan; Medicine; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2002; Project Start 01-FEB-2001; Project End 31-JAN-2005 Summary: (Applicant's Description Verbatim): IgA nephropathy (IgAN), the most common glomerulonephritis in the world is characterized by elevated levels of IgA1 in its polymeric form in circulation, presence of circulating immune complexes (CIC) and deposition of IgA1, frequently with C3 component of complement and IgG and/or IgM in glomerular mesangium. Earlier studies have shown that IgA1 in IgAN patients displays aberrant structural features in the heavy chain hinge region glycans. Carbohydrate analysis and lectin-binding studies have shown that the hinge region glycans bound by O-glycosidic bonds to Ser or Thr residues are deficient in galactose (Gal), resulting in an increased exposure of N-acetylgalactosamine (GalNAc). Furthermore, our earlier studies have shown that Gal deficient IgA1 molecules are present mainly in high molecular mass CIC that also contain IgG molecules. Our preliminary studies indicate that the interaction of Gal-deficient IgA1 with IgG, and probably other major isotypes, is based on antigen (IgA1) and antibody (IgG) recognition. Experimental approaches proposed in this application are designed to test the following hypothesis: An altered glycosylation of IgA1 hinge region results, due to the Gal deficiency, in exposure of GalNAc-Ser/Thr associated antigenic determinant(s) which are recognized by ubiquitous, naturally occurring antibodies, predominantly of the IgG isotype, which are involved in the formation of CIC and mesangial depositions. The following specific aims are proposed to test this hypothesis: 1) Determine the localization of antigenic determinants in IgA1 with aberrantly glycosylated hinge region glycans, involved in the formation of CIC; 2) Examine whether the Gal-deficient molecules are of systemic or mucosal origin; 3) Characterize the specificities and molecular properties of IgG, IgA, and IgM antibodies that bind to epitopes in the aberrantly glycosylated IgA1 hinge region; 4) Investigate the biological consequences of the formation of CIC containing Gal-deficient IgA1 and IgG. With GalNAc-Ser/Thr specificity; 5) Determine whether immune complexes composed of Gal-deficient IgA1IgG with GalNAc-Ser/Thr binding activity are present in mesangial deposits of patients with IgAN; and 6) Correlate levels of Gal-deficient serum or secretory IgA1 and levels of IgG, IgA1, or IgM antibodies with GalNAc-Ser/Thr specificity with disease activity. Results of these studies may lead to the elucidation of molecular defects of IgA1 in IgAN and provide experimental basis for rational approach to the treatment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: IGA NEPHROPATHY--PILOT STUDY WITH VITAMIN E Principal Investigator & Institution: Chan, James C.; Professor of Pediatrics; Virginia Commonwealth University Richmond, Va 232980568

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Timing: Fiscal Year 2003 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: IMMUNE COMPLEXES AND MESANGIAL CELLS IN IGA NEPHROPATHY Principal Investigator & Institution: Novak, Jan; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2007 Summary: IgA nephropathy (IgAN) is characterized by IgA1-containing immune complexes (IC) in the glomerular mesangium. Proliferation of mesangial cells (MC) and extracellular matrix (ECM) expansion occur from early stages, progressing to glomerular and interstitial sclerosis and development of end-stage renal disease in 3040% patients within 20 years. IgA1 containing deposits patients produce galactosedeficient O- linked glycans in the hinge region of IgA1. This aberrantly glycosylated IgA1 is bound to antibodies (IgG, IgA1) with anti-glycan specificity in CIC. We postulated that these CIC deposit in the mesangium. Highly undergalactosylated IgA1 was detected in IgAN mesangial deposits which support this hypothesis Our Preliminary Studies show that CIC with aberrantly glycosylated IgA1 from IgAN patients (IgAN-CIC) bound to MC in vitro and activated them. In four Specific Aims, we propose to test the hypothesis that CIC containing undergalactosylated IgA1 are involved in the pathogenesis of IgAN. In Specific Aim 1, we will examine presence and composition of these CIC in patients with familial and non-familial IgAN, and in nonIgAN glomerulonephritides controls and healthy individuals, and we will study binding as well as receptors involved in the binding of these IgAN-CIC (proliferation, apoptosis, cytokine synthesis, formation of reactive oxygen species). With selected samples of CIC (based on properties and activities of the CIC), we will identify MC genes induced or repressed by CIC. In Specific Aim 3, we will examine whether contemporaneously collected renal biopsies parallel the in vitro observed effects of CIC on MC and whether the same IgG and IgA receptors are expressed. Furthermore, results of Specific Aim 2 will identify other potential targets (IgAN- specific genes, ECM, upregulated genes, etc.) In Specific Aim 4, we will study mechanisms of activation of MC by CIC and we will examine whether MC activation can be prevented by inhibition of CIC binding or by inhibition of signaling by the bound CIC. Understanding how the IgAN-specific IC are generated and how they bind to MC and discovering the key signals triggering the chain of events in MC that lead to IgAN may offer potential new therapeutic targets. Considering that current IgAN therapies are not especially effective, new pharmacological intervention would be beneficial. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: PILOT TRIAL IN YOUNG PATIENTS WITH IGA NEPHROPATHY Principal Investigator & Institution: Hogg, Ronald J.; Medical City Dallas Hospital 7777 Forest Ln Dallas, Tx 75230 Timing: Fiscal Year 2002; Project Start 30-SEP-1994; Project End 31-AUG-2003 Summary: The objective of this application is to describe a pilot study to evaluate the efficacy of alternate-day prednisone in the treatment of IgA nephropathy (IgAN) in children, adolescents, and young adults. Details of the study design, administration, and statistical analysis are provided. Although IgAN is a disorder of the kidneys that was first described in France in 1967, none of the current treatment options are of proven

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benefit. Over the past few years, a number of small studies have suggested that prednisone is beneficial, but none of these have been definitive. The lack of proven therapy for IgAN is of concern because it is now apparent that untreated IgAN progresses to end-stage renal disease in up to 50% of patients and is a significant contributor to the total ESRD population in the United States. The proposed pilot study is a multicenter, double-blind, placebo- controlled, randomized clinical trial of the efficacy and safety of 2 years of therapy with alternate-day prednisone in approximately 90-100 children, adolescents, and young adults with moderately severe IgAN. Since we have defined rather strict criteria for patient entry into this trial, the number of eligible patients in individual nephrology centers will be small. Hence, a large number of centers (34) will be participating in order to recruit sufficient patients for valid statistical analysis. In order to successfully complete this study, it is essential that the activities of the 34 centers are carefully coordinated. This will be achieved through the Administration Center of the Southwest Pediatric Nephrology Study Group (SPNSG), a collaborative group that has been studying various aspects of IgAN for 14 years. To handle the complexities of this multicenter, clinical trial, we will establish rigorous procedures for monitoring medication administration and patient compliance, data management and analysis, clinical and laboratory measurements, and will maintain close communication with the 34 participating centers. Results from this 3-year pilot study will be analyzed by members of an experienced Data and Statistics Core in Birmingham, Alabama. From these pilot data, we will determine if a full- scale clinical trial is justified and feasible. if this is the case, a competitive renewal application will be submitted to the NIH. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: T CELLS CONTROL IGA GLYCOSYLATION, EVOKE IGA NEPHROPATHY Principal Investigator & Institution: Emancipator, Steven N.; Professor; Pathology; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2002; Project Start 01-MAY-2002; Project End 30-APR-2006 Summary: (Provided by applicant): As the most common form of glomerulonephritis throughout the world, IgA nephropathy (IgAN) continues to be a major financial and social burden. We believe that the pathogenesis of IgAN is usually related to dysregulation of the mucosal immune response, particularly to viral pathogens. We have therefore established an experimental model of IgAN in mice by immunization and challenge with a common rodent respiratory pathogen (Sendai virus), for which the immune response is genetically restricted. Based upon prior clinical and experimental observations and our new data, we hypothesize that the genetically determined T cell repertoire of a host determines susceptibility to IgAN, in association with other factors. We will emphasize complementary studies in two strains of mice (BALB/c and C57B1/6) that differ in severity of virally-induced IgAN. The Specific Aims of this proposal are to: 1) determine if the polarity of helper T cells towards type 2 (Th2) versus type 1 (Thi) is a critical determinant of the severity of IgAN; 2) offer direct assessment of the contribution of the B cell response to Th2 cytokines to the genesis of IgAN; 3) assess the role of non-lymphoid cells' response to T cell cytokines in the genesis of IgAN; 4) evaluate the applicability of our hypothesis to the immune response in humans. To achieve this last goal, we will reconstitute a functional human immune system in congenitally immunodeficient mice. In all experiments, we will compare the frequency and severity of IgAN provoked by immunization and challenge with virus among the various groups of mice, and correlate these parameters to the polarity of the antigen-

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specific T cell cytokine responses and IgA glycosylation. As our experiments unfold, we anticipate gaining insights not only to the pathogenesis of this currently incurable and poorly treated form of glomerulonephritis, but also to gain information about the factors that govern the character of immune responses to microbes and other antigens that gain access to mammals via mucosal routes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: VIRAL IGA NEPHROPATHY Principal Investigator & Institution: Lamm, Michael E.; Professor; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2002 Summary: As the most common form of glomerulonephritis throughout the world, IgA nephropathy (IgAN) continues to be a major financial and social burden. We believe the pathogenesis of IgAN is related to dysregulation of the mucosal immune response, particularly to viral pathogens. We have therefore established an experimental model of IgAN in mice by immunization and challenge with common rodent respiratory pathogen (Sendai virus), for which the immune response is genetically restricted. Based upon prior clinical and experimental observations and our new data, we hypothesize. Based upon prior clinical and experimental observations and our new data, we hypothesize that the genetically determined T cell repertoire of a host determines susceptibility to IgAN, in association with other factors. We will emphasize complementary studies in two strains of mice (BALB/c and C57BL/6) that differ in severity of virally-induced IgAN. The Specific Aims of this proposal are to:1) demonstrate that differences in IgA glycosylation are critical determinants of nephritis, and assess a possible contribution of non-Ig humoral factors; 2) investigate viral replication in and antigen presentation to virus-specific T cells by mesangial cells in culture; 3) determine the influence of the interaction of mesangial cells with monocytes/macrophages on selected functions of each cell lineage, measure modulation of such effects by immune complexes, and quantify any differences in such altered cell functions between the strains; and 4) define the elements of the immune response that lead to severe versus load nephritis, by reconstitution of immuno-deficient mice with genetically engineered lymphocytes, and repolarization of cytokine responses. These studies offer the potential for significant insights into the pathogenesis of IgAN and new therapeutic approaches. These studies also will aid understanding of regulation of the mucosal immune response, which is pertinent to mucosal vaccine development. The influence of the cytokine response to infectious mucosal pathogens is a major theme shared by the other Projects; we will also utilize the resources of Hybridoma Core B. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: VITAMIN E IN TREATMENT OF IGA NEPHROPATHY IN CHILDREN Principal Investigator & Institution: Flynn, Joseph T.; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2002 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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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 “Henoch-Schonlein purpura” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for HenochSchonlein purpura in the PubMed Central database: •

Selective deposition of immunoglobulin A1 in immunoglobulin A nephropathy, anaphylactoid purpura nephritis, and systemic lupus erythematosus. by Conley ME, Cooper MD, Michael AF.; 1980 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=371631

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

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A case of Kawasaki disease accompanied by Henoch-Schonlein purpura. Author(s): Miura M, Mochizuki T, Fukushima H, Ishihara J. Source: Clin Exp Rheumatol. 2004 May-June; 22(3): 377-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15144140

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. 6 PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.

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A case of pediatric Henoch-Schonlein purpura and thrombosis of spermatic veins. Author(s): Diana A, Gaze H, Laubscher B, De Meuron G, Tschantz P. Source: Journal of Pediatric Surgery. 2000 December; 35(12): 1843. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11101753

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A case of refractory Henoch-Schonlein purpura treated with thalidomide. Author(s): Choi SJ, Park SK, Uhm WS, Hong DS, Park HS, Park YL, Kwon KW. Source: Korean J Intern Med. 2002 December; 17(4): 270-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12647645

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A fatal case of bowel and cardiac involvement in Henoch-Schonlein purpura. Author(s): Carmichael P, Brun E, Jayawardene S, Abdulkadir A, O'Donnell PJ. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 2002 March; 17(3): 497-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11865100

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A patient with juvenile chronic arthritis and Henoch-Schonlein purpura. Author(s): Ballantyne FC, Capell HA. Source: Annals of Clinical Biochemistry. 2000 March; 37 ( Pt 2): 224-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10735370

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A patient with Wegener's granulomatosis with initial clinical presentations of Henoch-Schonlein purpura. Author(s): Miyata M, Kanno K, Nishimaki T, Sakuma F, Iwatsuki K, Kasukawa R. Source: Intern Med. 2001 October; 40(10): 1050-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11688833

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Abnormal IgA glycosylation in Henoch-Schonlein purpura restricted to patients with clinical nephritis. Author(s): Allen AC, Willis FR, Beattie TJ, Feehally J. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1998 April; 13(4): 930-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9568852

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Acenocoumarol-induced Henoch-Schonlein purpura. Author(s): Borras-Blasco J, Girona E, Navarro-Ruiz A, Matarredona J, Gimenez ME, Gutierrez A, Enriquez R, Martinez A. Source: The Annals of Pharmacotherapy. 2004 February; 38(2): 261-4. Epub 2003 December 23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14742763

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Acute abdomen in Henoch-Schonlein purpura. Author(s): Lawes D, Wood J. Source: Journal of the Royal Society of Medicine. 2002 October; 95(10): 505-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12356974

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Acute infantile hemorrhagic edema and Henoch-Schonlein purpura overlap in a child. Author(s): Shah D, Goraya JS, Poddar B, Parmar VR. Source: Pediatric Dermatology. 2002 January-February; 19(1): 92-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11860586

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Acute infantile hemorrhagic edema and Henoch-Schonlein purpura: is IgA the missing link? Author(s): Goraya JS, Kaur S. Source: Journal of the American Academy of Dermatology. 2002 November; 47(5): 801; Author Reply 801-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12399785

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Acute poststreptococcal glomerulonephritis mimicking Henoch-Schonlein purpura. Author(s): Matsukura H, Ohtsuki A, Fuchizawa T, Miyawaki T. Source: Clinical Nephrology. 2003 January; 59(1): 64-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12572934

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Acute renal failure in Henoch-Schonlein purpura due to interstitial haemorrhage of the kidney. Author(s): Costa de Beauregard MA, Ades L, Mougenot B, Akposso K, Lahlou A, Haymann JP, Rondeau E, Sraer JD. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1998 September; 13(9): 2355-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9761523

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Acute reversible renal failure with macroscopic hematuria in Henoch-Schonlein purpura. Author(s): Kobayashi Y, Omori S, Kamimaki I, Ikeda M, Akaoka K, Honda M, Ogata K, Morikawa Y. Source: Pediatric Nephrology (Berlin, Germany). 2001 September; 16(9): 742-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11511991

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Acute rheumatic carditis in Henoch-Schonlein purpura. Author(s): Ocal B, Karademir S, Oguz D, Erdogan, Oner A, Senocak F. Source: International Journal of Cardiology. 2000 June 12; 74(1): 97-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10912443

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Acute rheumatic fever associated with Henoch-Schonlein purpura: report of three cases and review of the literature. Author(s): Eisenstein EM, Navon-Elkan P. Source: Acta Paediatrica (Oslo, Norway : 1992). 2002; 91(11): 1265-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12463331

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Acute scrotal swelling in Henoch-Schonlein purpura: a case report. Author(s): Sakai N, Kawamoto K, Fukuoka H, Nakajima S, Kurozumi H. Source: Hinyokika Kiyo. 2000 October; 46(10): 739-41. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11215203

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Acute scrotum in Henoch-Schonlein purpura. Author(s): Choong CS, Liew KL, Liu PN, Kuo TU, Su CM. Source: Zhonghua Yi Xue Za Zhi (Taipei). 2000 July; 63(7): 577-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10934812

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Additional cases of ureteral obstruction associated with Henoch-Schonlein purpura. Author(s): Garcia-Nieto V, Claverie-Martin F. Source: Pediatric Nephrology (Berlin, Germany). 1998 February; 12(2): 168-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9543383

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Adrenal haematoma in Henoch-Schonlein purpura. Author(s): Landron C, Paccalin M, Chameau AM, Bonnefoy M, Roblot P, Becq-Giraudon B. Source: Rheumatology (Oxford, England). 2001 June; 40(6): 717. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11426042

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Adrenomedullin and total nitrite levels in children with Henoch-Schonlein purpura. Author(s): Islek I, Balat A, Cekmen M, Yurekli M, Muslu A, Sahinoz S, Sivasli E. Source: Pediatric Nephrology (Berlin, Germany). 2003 November; 18(11): 1132-7. Epub 2003 August 12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12920627

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Adult Henoch-Schonlein purpura associated with malignancy. Author(s): Pertuiset E, Liote F, Launay-Russ E, Kemiche F, Cerf-Payrastre I, Chesneau AM. Source: Seminars in Arthritis and Rheumatism. 2000 June; 29(6): 360-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10924021

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Adult Henoch-Schonlein purpura with fatal complications. Author(s): McCarthy R, Rosen T, Chen SH, Raimer SS. Source: Archives of Dermatology. 2001 January; 137(1): 19-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11176655

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Adult Henoch-Schonlein purpura with glomerulonephritis and paroxysmal nocturnal haemoglobinuria: an uncommon association. Author(s): Cozzi F, Botsios C, Ostuni P, Sfriso P, Piva E, Marson P, Punzi L, Todesco S. Source: Clinical Rheumatology. 2002 September; 21(5): 408-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12223993

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Alterations in the O-linked glycosylation of IgA1 in children with Henoch-Schonlein purpura. Author(s): Saulsbury FT. Source: The Journal of Rheumatology. 1997 November; 24(11): 2246-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9375892

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An audit of the management of the acute scrotum in children with Henoch-Schonlein Purpura. Author(s): Ioannides AS, Turnock R. Source: Journal of the Royal College of Surgeons of Edinburgh. 2001 April; 46(2): 98-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11329751

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Anaphylactoid purpura and familial IgA nephropathy. Author(s): Miyagawa S, Dohi K, Hanatani M, Yamanaka F, Okuchi T, Sakamoto K, Ishikawa H. Source: The American Journal of Medicine. 1989 March; 86(3): 340-2. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2645774

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Are Henoch-Schonlein purpura and hypersensitivity vasculitis in adults truly distinct entities? A dermatologist's perspective. Author(s): Callen JP. Source: Clin Exp Rheumatol. 2000 November-December; 18(6): 659-60. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11138325

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Association of Henoch-Schonlein purpura with varicella zoster. Author(s): Kalyoncu M, Odemis E, Yaris N, Okten A. Source: Indian Pediatrics. 2003 March; 40(3): 274-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12657772

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Ataxia and peripheral neuropathy: rare manifestations in Henoch-Schonlein purpura. Author(s): Bulun A, Topaloglu R, Duzova A, Saatci I, Besbas N, Bakkaloglu A. Source: Pediatric Nephrology (Berlin, Germany). 2001 December; 16(12): 1139-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11793117

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Bilateral subperiosteal orbital hematomas and Henoch-Schonlein purpura. Author(s): Ma'luf RN, Zein WM, El Dairi MA, Bashshur ZF. Source: Archives of Ophthalmology. 2002 October; 120(10): 1398-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12365928

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Binding sites for carrier-immobilized carbohydrates in the kidney: implication for the pathogenesis of Henoch-Schonlein purpura and/or IgA nephropathy. Author(s): Sediva A, Smetana K Jr, Stejskal J, Bartunkova J, Liu FT, Bovin NV, Gabius HJ. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1999 December; 14(12): 2885-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10570092

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Carbamazepine-induced thrombocytopenia and leucopenia complicated by HenochSchonlein purpura symptoms. Author(s): Kaneko K, Igarashi J, Suzuki Y, Niijima S, Ishimoto K, Yabuta K. Source: European Journal of Pediatrics. 1993 September; 152(9): 769-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8223813

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Cardiac vasculitis in Henoch-Schonlein purpura. Author(s): Osman A, McCreery CJ. Source: Circulation. 2000 February 8; 101(5): E69-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10662762

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Cardiopulmonary manifestations of Henoch-Schonlein purpura. Author(s): Agraharkar M, Gokhale S, Le L, Rajaraman S, Campbell GA. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2000 February; 35(2): 319-22. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10676734

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Cerebral vasculitis in Henoch-Schonlein purpura. Author(s): Bakkaloglu SA, Ekim M, Tumer N, Deda G, Erden I, Erdem T. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 2000 February; 15(2): 246-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10648674

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Cerebral vasculitis in Henoch-Schonlein purpura: a case report with sequential magnetic resonance imaging changes and treated with plasmapheresis alone. Author(s): Chen CL, Chiou YH, Wu CY, Lai PH, Chung HM. Source: Pediatric Nephrology (Berlin, Germany). 2000 December; 15(3-4): 276-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11149126

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Cerebral vasculitis in Henoch-Schonlein purpura: a case report with sequential magnetic resonance imaging. Author(s): Ha TS, Cha SH. Source: Pediatric Nephrology (Berlin, Germany). 1996 October; 10(5): 634-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8897572

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Cerebral vasculitis in Henoch-Schonlein purpura: MRI and MRA findings, treated with plasmapheresis alone. Author(s): Eun SH, Kim SJ, Cho DS, Chung GH, Lee DY, Hwang PH. Source: Pediatrics International : Official Journal of the Japan Pediatric Society. 2003 August; 45(4): 484-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12911492

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Chronic glomerulonephritis in childhood. Membranoproliferative glomerulonephritis, Henoch-Schonlein purpura nephritis, and IgA nephropathy. Author(s): Andreoli SP. Source: Pediatric Clinics of North America. 1995 December; 42(6): 1487-503. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8614597

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Ciprofloxacin-induced Henoch-Schonlein purpura. Author(s): Gamboa F, Rivera JM, Gomez Mateos JM, Gomez-Gras E. Source: The Annals of Pharmacotherapy. 1995 January; 29(1): 84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7711355

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Circulating adhesion molecules ICAM-1, E-selectin, and von Willebrand factor in Henoch-Schonlein purpura. Author(s): Soylemezoglu O, Sultan N, Gursel T, Buyan N, Hasanoglu E. Source: Archives of Disease in Childhood. 1996 December; 75(6): 507-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9014604

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Clinical and laboratory correlation of acute Henoch-Schonlein purpura in children. Author(s): Lin SJ, Huang JL, Hsieh KH. Source: Zhonghua Min Guo Xiao Er Ke Yi Xue Hui Za Zhi. 1998 March-April; 39(2): 948. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9599897

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Clinical features of Henoch-Schonlein purpura. Italian Group of Renal Immunopathology. Author(s): Coppo R, Amore A, Gianoglio B. Source: Annales De Medecine Interne. 1999 February; 150(2): 143-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10392263

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Clostridium difficile-related necrotizing pseudomembranous enteritis in association with Henoch-Schonlein purpura. Author(s): Boey CC, Ramanujam TM, Looi LM. Source: Journal of Pediatric Gastroenterology and Nutrition. 1997 April; 24(4): 426-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9144126

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Colchicine for the treatment of recurrent Henoch-Schonlein purpura in an adult. Author(s): Pyne D, Mootoo R, Bhanji A. Source: Rheumatology (Oxford, England). 2001 December; 40(12): 1430-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11752528

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Colo-colic intussusception in Henoch-Schonlein purpura. Author(s): Choong CK, Kimble RM, Pease P, Beasley SW. Source: Pediatric Surgery International. 1998 December; 14(3): 173-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9880740

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Colonic biopsy in Henoch-Schonlein purpura. Author(s): Novak J, Ottlakan A, Toth K. Source: Gastrointestinal Endoscopy. 1995 May; 41(5): 519. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7615237

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Colonoscopic findings in an adult patient with Henoch-Schonlein purpura. Author(s): Nakasone H, Hokama A, Fukuchi J, Makishi T, Yamashiro T, Sakugawa H, Kinjo F, Saito A. Source: Gastrointestinal Endoscopy. 2000 September; 52(3): 392. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10968856

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Combined diagnostic imaging of intestinal involvement in Henoch-Schonlein purpura. Author(s): Maggi F, Minordi LM, Macis G, Vecchioli A. Source: Rays. 2003 April-June; 28(2): 157-66. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14509190

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Comparative clinical and epidemiological study of hypersensitivity vasculitis versus Henoch-Schonlein purpura in adults. Author(s): Garcia-Porrua C, Gonzalez-Gay MA. Source: Seminars in Arthritis and Rheumatism. 1999 June; 28(6): 404-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10406408

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Complement activation in Henoch-Schonlein purpura. Author(s): Smith GC, Davidson JE, Hughes DA, Holme E, Beattie TJ. Source: Pediatric Nephrology (Berlin, Germany). 1997 August; 11(4): 477-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9260249

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Complement activation through the lectin pathway in patients with HenochSchonlein purpura nephritis. Author(s): Endo M, Ohi H, Ohsawa I, Fujita T, Matsushita M. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2000 March; 35(3): 401-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10692265

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Concurrent Henoch-Schonlein purpura and papular-purpuric gloves-and-socks syndrome. Author(s): Hakim A. Source: Scandinavian Journal of Rheumatology. 2000; 29(2): 131-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10777129

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Concurrent occurrence of chylothorax and chylous ascites in a patient with HenochSchonlein purpura. Author(s): Lee TH, Lee EY, Cho YS, Yoo B, Moon HB, Lee CK. Source: Scandinavian Journal of Rheumatology. 2003; 32(6): 378-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15080272

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Corticosteroid therapy does not prevent nephritis in Henoch-Schonlein purpura. Author(s): Mollica F, Li Volti S, Garozzo R, Russo G. Source: Pediatric Nephrology (Berlin, Germany). 1994 February; 8(1): 131. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8142215

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Corticosteroid therapy in Henoch-Schonlein purpura. Author(s): Lane W, Robson M, Leung AK. Source: Pediatric Nephrology (Berlin, Germany). 1993 August; 7(4): 507-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8280218

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Crohn's disease presenting with Henoch-Schonlein purpura. Author(s): Saulsbury FT, Hart MH. Source: Journal of Pediatric Gastroenterology and Nutrition. 2000 August; 31(2): 173-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10941970

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Cryofibrinogenemia due to Henoch-Schonlein purpura in a patient on peritoneal dialysis. Author(s): Alexopoulos E, Kirmizis D, Visvardis G, Flaris N, Fylaktou A, Kokolina E, Memmos D. Source: Perit Dial Int. 2003 January-February; 23(1): 85-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12691514

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Cutaneous manifestations of Henoch-Schonlein purpura in young children. Author(s): Nussinovitch M, Prais D, Finkelstein Y, Varsano I. Source: Pediatric Dermatology. 1998 November-December; 15(6): 426-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9875962

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Cyclosporin A therapy for steroid-dependent Henoch-Schonlein purpura. Author(s): Huang DC, Yang YH, Lin YT, Chiang BL. Source: J Microbiol Immunol Infect. 2003 March; 36(1): 61-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12741736

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Cyclosporine A for heavy proteinuria in a child with Henoch-Schonlein purpura nephritis. Author(s): Someya T, Kaneko K, Fujinaga S, Ohtaki R, Hira M, Yamashiro Y. Source: Pediatrics International : Official Journal of the Japan Pediatric Society. 2004 February; 46(1): 111-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15043680

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Danazol for Henoch-Schonlein purpura. Author(s): Lee YJ, Horstman LL, Ahn YS. Source: Annals of Internal Medicine. 1993 May 15; 118(10): 827. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8470863

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Dapsone in Henoch-Schonlein purpura. Author(s): Sarma PS. Source: Postgraduate Medical Journal. 1994 June; 70(824): 464-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8029176

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Dapsone in Henoch-Schonlein purpura--worth a trial. Author(s): Hoffbrand BI. Source: Postgraduate Medical Journal. 1991 November; 67(793): 961-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1775419

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Deletion polymorphism of the angiotensin converting enzyme gene predicts persistent proteinuria in Henoch-Schonlein purpura nephritis. Author(s): Yoshioka T, Xu YX, Yoshida H, Shiraga H, Muraki T, Ito K. Source: Archives of Disease in Childhood. 1998 November; 79(5): 394-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10193250

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Dendrocytoclasis in Henoch-Schonlein purpura. Author(s): Estrada JA, Goffin F, Cornil F, Pierard-Franchimont C, Pierard GE. Source: Acta Dermato-Venereologica. 1991; 71(4): 358-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1681660

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Development of immunoglobulin A nephropathy in a kidney transplant in a patient with previous history of Henoch-Schonlein purpura glomerulonephritis. Author(s): Mousa DH, al-Harbi W, Dhar JM, al-Sulaiman MH, al-Khader AA. Source: Nephron. 1993; 63(2): 247-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8450927

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Diagnosis of Henoch-Schonlein purpura: renal or skin biopsy? Author(s): Davin JC, Weening JJ. Source: Pediatric Nephrology (Berlin, Germany). 2003 December; 18(12): 1201-3. Epub 2003 September 16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=13680332

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Differences in tumor necrosis factor-alpha soluble receptor serum concentrations between patients with Henoch-Schonlein purpura and pediatric systemic lupus erythematosus: pathogenetic implications. Author(s): Gattorno M, Picco P, Barbano G, Stalla F, Sormani MP, Buoncompagni A, Gusmano R, Borrone C, Pistoia V. Source: The Journal of Rheumatology. 1998 February; 25(2): 361-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9489835

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Diffuse gastrointestinal involvement in Henoch-Schonlein purpura. Author(s): Patel RP, Parikh SS, Phadke VA, Vora IM, Kalro RH. Source: Indian J Gastroenterol. 1996 January; 15(1): 32. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8840629

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Diffuse intrapulmonary hemorrhage and renal failure in adult Henoch-Schonlein purpura. Author(s): Shichiri M, Tsutsumi K, Yamamoto I, Ida T, Iwamoto H. Source: American Journal of Nephrology. 1987; 7(2): 140-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3605235

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Disturbances of lipoprotein and PGI2 metabolism in IgA nephropathy and HenochSchonlein purpura. Author(s): Turi S, Nagy J, Haszon I, Havass Z, Nemeth M, Bereczki C. Source: Contrib Nephrol. 1988; 67: 37-43. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3061744

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Does steroid treatment of abdominal pain prevent renal involvement in HenochSchonlein purpura? Author(s): Reinehr T, Burk G, Andler W. Source: Journal of Pediatric Gastroenterology and Nutrition. 2000 September; 31(3): 3234. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10997386

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Drug-related Henoch-Schonlein Purpura. Author(s): Escudero A, Lucas E, Vidal JB, Sanchez-Guerrero I, Martinez A, Illan F, Ramos J. Source: Allergologia Et Immunopathologia. 1996 January-February; 24(1): 22-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8882757

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Dual positivity for cytoplasmic and perinuclear anti-neutrophil antibodies in a patient with Henoch-Schonlein purpura. Author(s): Ferraz-Amaro I, Herrero MJ, Jurado A, Diaz-Gonzalez F. Source: Clin Exp Rheumatol. 2004 March-April; 22(2): 233-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15083894

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Duodenal obstruction due to Henoch-Schonlein purpura. Author(s): Kawasaki M, Suekane H, Imagawa E, Iida M, Hizawa K, Aoyagi K, Fujishima M. Source: Ajr. American Journal of Roentgenology. 1997 April; 168(4): 969-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9124152

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Duodenojejunitis: is it idiopathic or is it Henoch-Schonlein purpura without the purpura? Author(s): Gunasekaran TS, Berman J, Gonzalez M. Source: Journal of Pediatric Gastroenterology and Nutrition. 2000 January; 30(1): 22-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10630435

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Early tubular proteinuria and the development of nephritis in Henoch-Schonlein purpura. Author(s): Muller D, Greve D, Eggert P. Source: Pediatric Nephrology (Berlin, Germany). 2000 November; 15(1-2): 85-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11095020

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Effect of vitamin E treatment on the oxidative damage occurring in Henoch-Schonlein purpura. Author(s): Erdogan O, Oner A, Aydin A, Isimer A, Demircin G, Bulbul M. Source: Acta Paediatrica (Oslo, Norway : 1992). 2003 May; 92(5): 546-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12839282

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Effective therapy for severe Henoch-Schonlein purpura nephritis with prednisone and azathioprine: a clinical and histopathologic study. Author(s): Foster BJ, Bernard C, Drummond KN, Sharma AK. Source: The Journal of Pediatrics. 2000 March; 136(3): 370-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10700695

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Electron-dense subepithelial glomerular deposits in Henoch-Schonlein purpura syndrome. Author(s): Kim CK, Aikawa M, Makker SP. Source: Archives of Pathology & Laboratory Medicine. 1979 October; 103(11): 595-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=384959

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Elevated levels of anti-Helicobacter pylori antibodies in Henoch-Schonlein purpura. Author(s): Novak J, Szekanecz Z, Sebesi J, Takats A, Demeter P, Bene L, Sipka S, Csiki Z. Source: Autoimmunity. 2003 August; 36(5): 307-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14567560

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Encephalopathy complicating Henoch-Schonlein purpura: reversible MRI changes. Author(s): Woolfenden AR, Hukin J, Poskitt KJ, Connolly MB. Source: Pediatric Neurology. 1998 July; 19(1): 74-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9682892

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Endomyocardial biopsy in Henoch-Schonlein purpura. Author(s): Kereiakes DJ, Ports TA, Finkbeiner W. Source: American Heart Journal. 1984 February; 107(2): 382-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6364755

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Endoscopic findings in Henoch-Schonlein purpura. Author(s): Banerjee B, Rashid S, Singh E, Moore J. Source: Gastrointestinal Endoscopy. 1991 September-October; 37(5): 569-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1936842

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Endoscopic findings in pediatric patients with Henoch-Schonlein purpura and gastrointestinal symptoms. Author(s): Tomomasa T, Hsu JY, Itoh K, Kuroume T. Source: Journal of Pediatric Gastroenterology and Nutrition. 1987 September-October; 6(5): 725-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3694367

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Endoscopic hemostasis of bleeding duodenal ulcer in a child with Henoch-Schonlein purpura. Author(s): Ebina K, Kato S, Abukawa D, Nakagawa H. Source: The Journal of Pediatrics. 1997 December; 131(6): 934-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9427906

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Endoscopically and histologically documented gastrointestinal lesions in an adult patient with Henoch-Schonlein purpura. Author(s): Sasaki K, Nukuda Y, Masuda T, Sato E. Source: Endoscopy. 1994 September; 26(7): 629-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8001494

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Endothelin levels in Henoch-Schonlein purpura. Author(s): Muslu A, Islek I, Gok F, Aliyazicioglu Y, Dagdemir A, Dundaroz R, Kucukoduk S, Sakarcan A. Source: Pediatric Nephrology (Berlin, Germany). 2002 November; 17(11): 920-5. Epub 2002 September 25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12432435

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Eosinophil cationic protein in Henoch-Schonlein purpura and in IgA nephropathy. Author(s): Namgoong MK, Lim BK, Kim JS. Source: Pediatric Nephrology (Berlin, Germany). 1997 December; 11(6): 703-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9438647

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Epidemiology of a cluster of Henoch-Schonlein purpura. Author(s): Farley TA, Gillespie S, Rasoulpour M, Tolentino N, Hadler JL, Hurwitz E. Source: Am J Dis Child. 1989 July; 143(7): 798-803. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2741850

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Epidemiology of Henoch-Schonlein purpura. Author(s): Saulsbury FT. Source: Cleve Clin J Med. 2002; 69 Suppl 2: Sii87-9. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12086273

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Epididymal involvement in Henoch-Schonlein purpura mimicking testicular torsion. Author(s): Ross WB, Davis-Reynolds LM. Source: Journal of the Royal College of Surgeons of Edinburgh. 1987 August; 32(4): 247. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3681804

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Epididymoorchitis mimicking testicular torsion in Henoch-Schonlein purpura. Author(s): Dayanir YO, Akdilli A, Karaman CZ, Sonmez F, Karaman G. Source: European Radiology. 2001; 11(11): 2267-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11702171

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Esophageal stricture as a complication in Henoch-Schonlein purpura. Author(s): van Wieringen PM, van der Zee CL, Hoevenaars F, Joosten HJ, Rieu PN. Source: European Journal of Pediatric Surgery : Official Journal of Austrian Association of Pediatric Surgery. [et Al] = Zeitschrift Fur Kinderchirurgie. 1992 August; 2(4): 236-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1390554

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Evidence of enhanced immunoglobulin synthesis and defective immune regulation in Henoch-Schonlein purpura. Author(s): Beale MG, Nash GS, Bertovich MJ, MacDermott RP. Source: Contrib Nephrol. 1983; 35: 46-60. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6600994

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Evolution of immunoglobulin A nephropathy into Henoch-Schonlein purpura in an adult patient. Author(s): Araque A, Sanchez R, Alamo C, Torres N, Praga M. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1995 February; 25(2): 340-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7847363

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Excretion of epidermal growth factor-like material in acute Henoch-Schonlein purpura nephritis. Author(s): Goodyer PR, Fata J, Goodyer CG. Source: Pediatric Nephrology (Berlin, Germany). 1990 March; 4(2): 101-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2397173

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Expression of interferon-inducible Mx-proteins in patients with IgA nephropathy or Henoch-Schonlein purpura. Author(s): Floege J, Burg M, Al Masri AN, Grone HJ, von Wussow P. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1999 March; 33(3): 434-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10070906

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Fatal adult Henoch-Schonlein purpura due to small intestinal infarction. Author(s): Chan JC, Li PK, Lai FM, Lai KN. Source: Journal of Internal Medicine. 1992 August; 232(2): 181-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1506816

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Fatal pulmonary hemorrhage in Henoch-Schonlein purpura. Author(s): Weiss VF, Naidu S. Source: Cutis; Cutaneous Medicine for the Practitioner. 1979 May; 23(5): 687-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=456038

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Fate of renal grafts with recurrent Henoch-Schonlein purpura nephritis in children. Author(s): Hasegawa A, Kawamura T, Ito H, Hasegawa O, Ogawa O, Honda M, Ohara T, Hajikano H. Source: Transplantation Proceedings. 1989 February; 21(1 Pt 2): 2130-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2652687

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Functional intestinal obstruction in Henoch-Schonlein purpura. Author(s): Sharief N, Ward HC, Wood CB. Source: Journal of Pediatric Gastroenterology and Nutrition. 1991 February; 12(2): 272-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2051279

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Gastrointestinal and renal involvement in vasculitis: management strategies in Henoch-Schonlein purpura. Author(s): Szer IS. Source: Cleve Clin J Med. 1999 May; 66(5): 312-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10330784

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Gastrointestinal endoscopy in Henoch-Schonlein purpura. Author(s): Kato S, Shibuya H, Naganuma H, Nakagawa H. Source: European Journal of Pediatrics. 1992 July; 151(7): 482-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1396906

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Gastrointestinal involvement as the initial manifestation in children with HenochSchonlein purpura--clinical analysis of 27 cases. Author(s): Lin SJ, Chao HC, Huang JL. Source: Zhonghua Min Guo Xiao Er Ke Yi Xue Hui Za Zhi. 1998 May-June; 39(3): 186-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9684524

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Gastrointestinal lesions in an adult patient with Henoch-Schonlein purpura. Author(s): Yoshikawa N, Yamamura F, Akita Y, Sato T, Mitamura K. Source: Hepatogastroenterology. 1999 September-October; 46(29): 2823-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10576353

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Gastrointestinal manifestations and complications of Henoch-Schonlein purpura. Author(s): Chen SY, Kong MS. Source: Chang Gung Med J. 2004 March; 27(3): 175-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15148994

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Gastrointestinal manifestations of Henoch-Schonlein purpura. Author(s): Park SH, Kim CJ, Chi JG, Seo JK, Park KW. Source: Journal of Korean Medical Science. 1990 June; 5(2): 101-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2278663

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GI involvement in Henoch-Schonlein purpura. Author(s): Esaki M, Matsumoto T, Nakamura S, Kawasaki M, Iwai K, Hirakawa K, Tarumi K, Yao T, Iida M. Source: Gastrointestinal Endoscopy. 2002 December; 56(6): 920-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12447314

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GI lesions in Henoch-Schonlein purpura. Author(s): Pore G. Source: Gastrointestinal Endoscopy. 2002 February; 55(2): 283-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11818944

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Glomerulonephritis without IgA deposits in a case of Henoch-Schonlein purpura. Author(s): Tanaka H, Onodera N, Waga S, Monma N. Source: Pediatric Nephrology (Berlin, Germany). 1999 September; 13(7): 597-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10460509

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Grading of acute and chronic renal lesions in Henoch-Schonlein purpura. Author(s): Szeto CC, Choi PC, To KF, Li PK, Hui J, Chow KM, Leung CB, Lui SF, MacMoune Lai F. Source: Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc. 2001 July; 14(7): 635-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11454994

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Granulocyte colony-stimulating factor associated leukocytoclastic vasculitis mimicking Henoch-Schonlein purpura. Author(s): Yang YM, Mankad VN, Manci E. Source: Pediatric Hematology and Oncology. 1993 April-June; 10(2): 193-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7686389

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Group A beta-haemolytic streptococcal infection and Henoch-Schonlein purpura with cardiac, renal and neurological complications. Author(s): Mattoo TK, al-Mutair A, al-Khatib Y, Ali A, al-Sohaibani MO. Source: Annals of Tropical Paediatrics. 1997 December; 17(4): 381-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9578800

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Guillain-Barre syndrome in a child with Henoch-Schonlein Purpura. Author(s): Goraya JS, Jayashree M, Ghosh D, Singh S, Singhi SC, Kumar L. Source: Scandinavian Journal of Rheumatology. 1998; 27(4): 310-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9751475

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Henoch-Schonlein purpura (treatment and outcome). Author(s): Dillon MJ. Source: Cleve Clin J Med. 2002; 69 Suppl 2: Sii121-3. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12086251

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Henoch-Schonlein purpura and cutaneous leukocytoclastic angiitis exhibit different HLA-DRB1 associations. Author(s): Amoli MM, Thomson W, Hajeer AH, Calvino MC, Garcia-Porrua C, Ollier WE, Gonzalez-Gay MA. Source: The Journal of Rheumatology. 2002 May; 29(5): 945-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12022354

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Henoch-Schonlein purpura and priapism. Author(s): Lind J, Mackay A, Withers SJ. Source: Journal of Paediatrics and Child Health. 2002 October; 38(5): 526-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12354274

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Henoch-Schonlein purpura and pulmonary tuberculosis. Author(s): Islek I, Muslu A, Totan M, Gok F, Sanic A. Source: Pediatrics International : Official Journal of the Japan Pediatric Society. 2002 October; 44(5): 545-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12225561

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Henoch-Schonlein Purpura as a cause of renal failure in an elderly African-American female. Author(s): Klein MN, Schlessinger S. Source: J Miss State Med Assoc. 2002 April; 43(4): 110-1. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11989193

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Henoch-Schonlein purpura associated with clarithromycin. Case report and review of literature. Author(s): Borras-Blasco J, Enriquez R, Amoros F, Cabezuelo JB, Navarro-Ruiz A, Perez M, Fernandez J. Source: Int J Clin Pharmacol Ther. 2003 May; 41(5): 213-6. Erratum In: Int J Clin Pharmacol Ther. 2003 September; 41(9): 420. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12776812

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Henoch-Schonlein purpura associated with hepatitis A infection. Author(s): Islek I, Kalayci AG, Gok F, Muslu A. Source: Pediatrics International : Official Journal of the Japan Pediatric Society. 2003 February; 45(1): 114-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12654084

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Henoch-Schonlein purpura following a meningococcal vaccine. Author(s): Lambert EM, Liebling A, Glusac E, Antaya RJ. Source: Pediatrics. 2003 December; 112(6 Pt 1): E491. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14654652

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Henoch-Schonlein purpura following hepatitis B vaccination. Author(s): Chave T, Neal C, Camp R. Source: The Journal of Dermatological Treatment. 2003 September; 14(3): 179-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14522629

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Henoch-Schonlein purpura in adulthood and childhood: comment on the article by Blanco et al. Author(s): Uthman I, Kassak K, Nasr FW. Source: Arthritis and Rheumatism. 1998 August; 41(8): 1518-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9704658

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Henoch-Schonlein purpura in an adult. Author(s): Ly MN, Breza TS Jr. Source: Skinmed. 2003 July-August; 2(4): 262-4. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14673285

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Henoch-Schonlein purpura in children and adults: clinical differences in a defined population. Author(s): Garcia-Porrua C, Calvino MC, Llorca J, Couselo JM, Gonzalez-Gay MA. Source: Seminars in Arthritis and Rheumatism. 2002 December; 32(3): 149-56. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12528079

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Henoch-Schonlein purpura in Chinese children and adults. Author(s): Lin SJ, Huang JL. Source: Asian Pac J Allergy Immunol. 1998 March; 16(1): 21-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9681125

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Henoch-Schonlein purpura in pregnancy. Author(s): Cummins DL, Mimouni D, Rencic A, Kouba DJ, Nousari CH. Source: The British Journal of Dermatology. 2003 December; 149(6): 1282-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14674910

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Henoch-Schonlein purpura in two brothers imprisoned in the same jail: presentation two months apart. Author(s): Cakir N, Pamuk ON, Donmez S. Source: Clin Exp Rheumatol. 2004 March-April; 22(2): 235-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15083895

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Henoch-Schonlein purpura involving the glans penis. Author(s): David S, Schiff JD, Poppas DP. Source: Urology. 2003 May; 61(5): 1035. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12736035

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Henoch-Schonlein purpura mimicking acute appendicitis and Crohn's disease. Author(s): Yentis I. Source: The British Journal of Radiology. 1973 July; 46(547): 555-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4718298

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Henoch-Schonlein purpura nephritis associated with methicillin-resistant Staphylococcus aureus infection. Author(s): Hirayama K, Kobayashi M, Kondoh M, Muro K, Iwabuchi S, Yoh K, Ishizu T, Kikuchi S, Yamaguchi N, Nagase S, Koyama A. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1998 October; 13(10): 2703-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9794595

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Henoch-Schonlein purpura nephritis. Author(s): Fervenza FC. Source: International Journal of Dermatology. 2003 March; 42(3): 170-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12653909

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Henoch-Schonlein purpura occurring in three members of a family. Author(s): Lofters WS, Pineo GF, Luke KH, Yaworsky RG. Source: Can Med Assoc J. 1973 July 7; 109(1): 46-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4541508

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Henoch-Schonlein purpura secondary to subacute bacterial endocarditis. Author(s): Galaria NA, Lopressti NP, Magro CM. Source: Cutis; Cutaneous Medicine for the Practitioner. 2002 April; 69(4): 269-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12080945

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Henoch-Schonlein purpura with particular reference to the prognosis of the renal lesion. Author(s): Ansell BM. Source: The British Journal of Dermatology. 1970 March; 82(3): 211-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5441756

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Henoch-Schonlein purpura. Author(s): Joseph PR. Source: Archives of Pediatrics & Adolescent Medicine. 1998 July; 152(7): 715. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9667551

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Henoch-Schonlein purpura. Author(s): Mrusek S, Kruger M, Greiner P, Kleinschmidt M, Brandis M, Ehl S. Source: Lancet. 2004 April 3; 363(9415): 1116. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15064030

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Henoch-Schonlein purpura. Author(s): Ballinger S. Source: Current Opinion in Rheumatology. 2003 September; 15(5): 591-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12960486

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Henoch-Schonlein purpura: a review. Author(s): Kraft DM, Mckee D, Scott C. Source: American Family Physician. 1998 August; 58(2): 405-8, 411. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9713395

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Henoch-Schonlein purpura: clinical manifestations and long-term outcomes in Thai children. Author(s): Pabunruang W, Treepongkaruna S, Tangnararatchakit K, Chunharas A, Phuapradit P. Source: J Med Assoc Thai. 2002 November; 85 Suppl 4: S1213-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12549797

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Henoch-Schonlein purpura: the Chandigarh experience. Author(s): Kumar L, Singh S, Goraya JS, Uppal B, Kakkar S, Walker R, Sehgal S. Source: Indian Pediatrics. 1998 January; 35(1): 19-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9707900

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HLA-B35 association with nephritis in Henoch-Schonlein purpura. Author(s): Amoli MM, Thomson W, Hajeer AH, Calvino MC, Garcia-Porrua C, Ollier WE, Gonzalez-Gay MA. Source: The Journal of Rheumatology. 2002 May; 29(5): 948-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12022355

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Hypoalbuminemia in Henoch-Schonlein purpura following streptococcal infection. Description of a case in a child. Author(s): Taylor WF, Amin LA, Mruthyunjaya GT. Source: Clinical Pediatrics. 1971 December; 10(12): 737-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5139951

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IgA myeloma presenting as Henoch-Schonlein purpura with nephritis. Author(s): Zickerman AM, Allen AC, Talwar V, Olczak SA, Brownlee A, Holland M, Furness PN, Brunskill NJ, Feehally J. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2000 September; 36(3): E19. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10977812

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IgA1 is the major IgA subclass in cutaneous blood vessels in Henoch-Schonlein purpura. Author(s): Egan CA, Taylor TB, Meyer LJ, Petersen MJ, Zone JJ. Source: The British Journal of Dermatology. 1999 November; 141(5): 859-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10583167

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Ileal vasculitis in Henoch-Schonlein purpura. Author(s): Kim HS, Lee DK, Baik SK, Kwon SO. Source: Gastrointestinal Endoscopy. 2001 October; 54(4): 493-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11577315

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Ileitis caused by Henoch-Schonlein purpura. An endoscopic view of the terminal ileum. Author(s): Kawasaki M, Hizawa K, Aoyagi K, Kuroki F, Nakahara T, Sakamoto K, Iida M, Fujishima M. Source: Journal of Clinical Gastroenterology. 1997 July; 25(1): 396-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9412933

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Ileitis terminalis in a patient with Henoch-Schonlein purpura. Author(s): Ortego-Centeno N, Callejas-Rubio JL, Lopez-Manas JG, Troncoso-Garcia E, de la Higuera Torres-Puchol J. Source: Digestive Diseases and Sciences. 1999 August; 44(8): 1590-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10492137

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Images in clinical medicine. Henoch-Schonlein purpura. Author(s): Marinella MA. Source: The New England Journal of Medicine. 2004 July 15; 351(3): 278. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15254286

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Imbalances in serum proinflammatory cytokines and their soluble receptors: a putative role in the progression of idiopathic IgA nephropathy (IgAN) and HenochSchonlein purpura nephritis, and a potential target of immunoglobulin therapy? Author(s): Rostoker G, Rymer JC, Bagnard G, Petit-Phar M, Griuncelli M, Pilatte Y. Source: Clinical and Experimental Immunology. 1998 December; 114(3): 468-76. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9844059

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Immunoconglutinin and complement studies in congenital nephrotic syndrome and nephritis of Henoch-Schonlein purpura in children. Author(s): Shulman ST, Barratt TM, Soothill JF. Source: Archives of Disease in Childhood. 1971 December; 46(250): 838-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5001946

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Immunoglobulin A multiple myeloma presenting with Henoch-Schonlein purpura associated with reduced sialylation of IgA1. Author(s): Van Der Helm-Van Mil AH, Smith AC, Pouria S, Tarelli E, Brunskill NJ, Eikenboom HC. Source: British Journal of Haematology. 2003 September; 122(6): 915-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12956761

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Impaired activation of the fibrinolytic system in children with Henoch-Schonlein purpura: beneficial effect of hydrocortisone plus Sigma-aminocaproic acid therapy on disappearance rate of cutaneous vasculitis and fibrinolysis. Author(s): Prandota J, Pankow-Prandota L, Kotecki L. Source: American Journal of Therapeutics. 2001 January-February; 8(1): 11-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11304653

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Incidence of Henoch-Schonlein purpura, Kawasaki disease, and rare vasculitides in children of different ethnic origins. Author(s): Gardner-Medwin JM, Dolezalova P, Cummins C, Southwood TR. Source: Lancet. 2002 October 19; 360(9341): 1197-202. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12401245

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Increased serum IgD concentrations in children with Henoch-Schonlein purpura. Author(s): Saulsbury FT. Source: British Journal of Rheumatology. 1998 May; 37(5): 570-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9651087

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Increased transforming growth factor-beta (TGF-beta)-secreting T cells and IgA anticardiolipin antibody levels during acute stage of childhood Henoch-Schonlein purpura. Author(s): Yang YH, Huang MT, Lin SC, Lin YT, Tsai MJ, Chiang BL. Source: Clinical and Experimental Immunology. 2000 November; 122(2): 285-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11091287

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Infantile Henoch-Schonlein purpura. Author(s): Shetty AK, Desselle BC, Ey JL, Correa H, Galen WK, Gedalia A. Source: Archives of Family Medicine. 2000 June; 9(6): 553-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10862218

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Interleukin 1 receptor antagonist gene polymorphism is associated with severe renal involvement and renal sequelae in Henoch-Schonlein purpura. Author(s): Amoli MM, Thomson W, Hajeer AH, Calvino MC, Garcia-Porrua C, Ollier WE, Gonzalez-Gay MA. Source: The Journal of Rheumatology. 2002 July; 29(7): 1404-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12136897

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Interleukin 1beta gene polymorphism association with severe renal manifestations and renal sequelae in Henoch-Schonlein purpura. Author(s): Amoli MM, Calvino MC, Garcia-Porrua C, Llorca J, Ollier WE, Gonzalez-Gay MA. Source: The Journal of Rheumatology. 2004 February; 31(2): 295-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14760799

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Intra-abdominal manifestations of Henoch-Schonlein purpura. Author(s): Choong CK, Beasley SW. Source: Journal of Paediatrics and Child Health. 1998 October; 34(5): 405-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9767498

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Intravenous immunoglobulin in Henoch-Schonlein purpura. Author(s): Hamidou MA, Pottier MA, Dupas B. Source: Annals of Internal Medicine. 1996 December 15; 125(12): 1013-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8967701

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Intravenous immunoglobulin therapy for severe digestive manifestations of HenochSchonlein purpura. Author(s): Lamireau T, Rebouissoux L, Hehunstre JP. Source: Acta Paediatrica (Oslo, Norway : 1992). 2001 September; 90(9): 1081-2. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11683201

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Intussusception in Henoch-Schonlein purpura. A report of two cases requiring operation. Author(s): Noussias M, Blandy AC, Ward-Mcquaid N. Source: The British Journal of Surgery. 1969 July; 56(7): 503-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5306177

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Is there IgA from gut mucosal origin in the serum of children with Henoch-Schonlein purpura? Author(s): Moja P, Quesnel A, Resseguier V, Lambert C, Freycon F, Berthoux F, Genin C. Source: Clinical Immunology and Immunopathology. 1998 March; 86(3): 290-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9557162

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Jejunal IgA and C3 deposition in adult Henoch-Schonlein purpura with severe intestinal manifestations. Author(s): Morichau-Beauchant M, Touchard G, Maire P, Briaud M, Babin P, Alcalay D, Matuchansky C. Source: Gastroenterology. 1982 June; 82(6): 1438-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7067961

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Laboratory signs of activated coagulation are common in Henoch-Schonlein purpura. Author(s): Brendel-Muller K, Hahn A, Schneppenheim R, Santer R. Source: Pediatric Nephrology (Berlin, Germany). 2001 December; 16(12): 1084-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11793106

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Lack of association between endothelial nitric oxide synthase polymorphisms and Henoch-Schonlein purpura. Author(s): Amoli MM, Garcia-Porrua C, Calvino MC, Ollier WE, Gonzalez-Gay MA. Source: The Journal of Rheumatology. 2004 February; 31(2): 299-301. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14760800

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Lack of evidence for herpesvirus, retrovirus, or parvovirus infection in HenochSchonlein purpura. Author(s): Eisenstein EM. Source: Clin Exp Rheumatol. 2002 September-October; 20(5): 734. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12412214

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Lack of IgA antineutrophil cytoplasmic antibodies in Henoch-Schonlein purpura and IgA nephropathy. Author(s): Sinico RA, Tadros M, Radice A, Pozzi C, Quarenghi M, Comotti C, Gregorini G, Castiglione A, Arrigo G, D'Amico G. Source: Clinical Immunology and Immunopathology. 1994 October; 73(1): 19-26. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7923914

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Legionella longbeachae pneumonia and Henoch-Schonlein purpura. Author(s): Gowardman JR, Havill J. Source: Aust N Z J Med. 1996 April; 26(2): 236-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8744628

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Letter: Dermal IgA deposits in Henoch-Schonlein purpura and Berger's nephritis. Author(s): Tsai CC, Giangiacomo J, Zuckner J. Source: Lancet. 1975 February 8; 1(7902): 342-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=46492

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Letter: Henoch-Schonlein purpura in a family. Author(s): De Veber LL. Source: Can Med Assoc J. 1974 July 6; 111(1): 16. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4841937

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Letter: Mycoplasmal pneumonia preceding Henoch-Schonlein purpura. Author(s): Liew SW, Kessel I. Source: Archives of Disease in Childhood. 1974 November; 49(11): 912-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4441126

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Letter: Renal involvement in Henoch-Schonlein purpura. Author(s): Haahr J, Thomsen K, Sparrevohn S. Source: British Medical Journal. 1974 November 16; 4(5941): 405. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4425897

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Letter: Unusual gastrointestinal manifestations of Henoch-Schonlein purpura. Author(s): Klein GL, Stafford S 3rd. Source: Am J Dis Child. 1975 October; 129(10): 1238-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1190152

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Leukocytoclastic vasculitis, not associated with Henoch-Schonlein purpura, causing recurrent massive painless gastrointestinal hemorrhage. Author(s): Powers BJ, Brown G, Williams RW, Speers W. Source: The American Journal of Gastroenterology. 1992 September; 87(9): 1191-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1519579

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Life-threatening gastrointestinal bleeding due to a jejunal lesion of HenochSchonlein purpura. Author(s): Lippl F, Huber W, Werner M, Nekarda H, Berger H, Weigert N. Source: Endoscopy. 2001 September; 33(9): 811-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11558038

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Long term renal prognosis of Henoch-Schonlein purpura in an unselected childhood population. Author(s): Stewart M, Savage JM, Bell B, McCord B. Source: European Journal of Pediatrics. 1988 February; 147(2): 113-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3366130

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Long-term prognosis of Henoch-Schonlein nephritis in adults and children. Italian Group of Renal Immunopathology Collaborative Study on Henoch-Schonlein purpura. Author(s): Coppo R, Mazzucco G, Cagnoli L, Lupo A, Schena FP. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1997 November; 12(11): 2277-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9394311

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Low serum C3, leukopenia, and thrombocytopenia: unusual features of henochschonlein purpura. Author(s): Krause I, Garty BZ, Davidovits M, Cleper R, Tamary H, Rosenmann E, Eisenstein B. Source: European Journal of Pediatrics. 1999 November; 158(11): 906-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10541946

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Lymph node pathology in Henoch-Schonlein purpura. Author(s): Akosa AB, Ali MH. Source: Histopathology. 1989 September; 15(3): 297-301. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2807187

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Lymph nodes in Henoch-Schonlein purpura. Author(s): Howat AJ. Source: Histopathology. 1990 May; 16(5): 514-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2361665

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Magnetic resonance imaging of central nervous system vasculitis. A case report of Henoch-Schonlein purpura. Author(s): Elinson P, Foster KW Jr, Kaufman DB. Source: Acta Paediatr Scand. 1990 June-July; 79(6-7): 710-3. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2386069

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Major histocompatibility complex antigens in Turkish children with HenochSchonlein purpura. Author(s): Mir S, Kutukculer N, Coker M, Keskinoglu A. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1994; 9(5): 586-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8090348

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Management of Henoch-Schonlein purpura and polyarteritis nodosa. Author(s): Ford EG, Jennings LM, Andrassy RJ. Source: Tex Med. 1987 August; 83(8): 54-8. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2889276

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Management of intra-abdominal Henoch-Schonlein purpura. The role of surgery. Author(s): Toledo-Pereyra LH, Von Reuden T, Cich JA, Yonehiro EG. Source: Minn Med. 1976 June; 59(6): 376-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1083937

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Massive gastric hemorrhage: an unusual complication of Henoch-Schonlein purpura. Author(s): Weber TR, Grosfeld JL, Bergstein J, Fitzgerald J. Source: Journal of Pediatric Surgery. 1983 October; 18(5): 576-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6644497

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Membrane attack complex of complement in Henoch-Schonlein purpura skin and nephritis. Author(s): Kawana S, Shen GH, Kobayashi Y, Nishiyama S. Source: Archives of Dermatological Research. 1990; 282(3): 183-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2369144

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Mesangial cell autoantigens in immunoglobulin A nephropathy and HenochSchonlein purpura. Author(s): O'Donoghue DJ, Darvill A, Ballardie FW. Source: The Journal of Clinical Investigation. 1991 November; 88(5): 1522-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1939642

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Methotrexate used as a steroid-sparing agent in non-renal chronic Henoch-Schonlein purpura. Author(s): Rettig P, Cron RQ. Source: Clin Exp Rheumatol. 2003 November-December; 21(6): 767-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14740458

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Microscopic polyangiitis mimicking Henoch-Schonlein purpura followed by severe renal involvement: a diagnostic role for antineutrophil cytoplasmic autoantibody. Author(s): Akimoto S, Ishikawa O, Tsukada Y, Yano S, Miyachi Y. Source: The British Journal of Dermatology. 1997 February; 136(2): 298-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9068765

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Mononeuritis multiplex complicating Henoch-Schonlein purpura. Author(s): Campbell SB, Hawley CM, Staples C. Source: Aust N Z J Med. 1994 October; 24(5): 580. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7848168

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More on ureteral obstruction associated with Henoch-Schonlein purpura. Author(s): Lane W, Robson M, Leung AK. Source: Pediatric Nephrology (Berlin, Germany). 1998 February; 12(2): 169. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9543384

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Multiple entero-entero fistulae: an unusual complication of Henoch-Schonlein purpura. Author(s): Gow KW, Murphy JJ 3rd, Blair GK, Magee JF, Hailey J. Source: Journal of Pediatric Surgery. 1996 June; 31(6): 809-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8783109

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Mycoplasma pneumoniae infection associated with Henoch-Schonlein purpura. Author(s): Steare SE, Wiselka MJ, Kurinczuk JJ, Nicholson KG. Source: The Journal of Infection. 1988 May; 16(3): 305-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3397582

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Mycoplasma pneumoniae-associated Henoch-Schonlein purpura nephritis. Author(s): Kaneko K, Fujinaga S, Ohtomo Y, Nagaoka R, Obinata K, Yamashiro Y. Source: Pediatric Nephrology (Berlin, Germany). 1999 November; 13(9): 1000-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10671029

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Myocardial infarction - a rare complication in Henoch-Schonlein purpura. Author(s): Abdel-Hadi O, Greenstone MA, Hartley RB, Kidner PH. Source: Postgraduate Medical Journal. 1981 June; 57(668): 390-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7301688

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Nailfold capillaroscopy in Henoch-Schonlein purpura: a follow-up study of 31 cases. Author(s): Martino F, Agolini D, Tsalikova E, Bederti O, Principessa L, Martino E, Carnevali E, Giardini O. Source: The Journal of Pediatrics. 2002 July; 141(1): 145. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12091868

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Nailfold capillary abnormalities in Henoch-Schonlein purpura. Author(s): Greenberg LW. Source: The Journal of Pediatrics. 1983 October; 103(4): 665-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6620036

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Nitric oxide in Henoch-Schonlein purpura. Author(s): Soylemezoglu O, Ozkaya O, Erbas D, Akkok N, Buyan N, Hasanoglu E. Source: Scandinavian Journal of Rheumatology. 2002; 31(5): 271-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12455816

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No pathogenic role of enhanced plasma IgA binding capacity to fibronectin and IgAfibronectin aggregates in Henoch-Schonlein purpura. Author(s): Davin JC, Li Vecchi M, Mahieu P. Source: Nephron. 1996; 74(2): 435-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8893175

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Occurrence of Henoch-Schonlein purpura in a child with Wilms' tumor. Author(s): Sivak LE, Virshup DM. Source: Medical and Pediatric Oncology. 1995 March; 24(3): 213-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7838045

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Outcome after childhood Henoch-Schonlein purpura. Author(s): Thervet E, Pillebout E, Guillevin L; CESAR study group. Source: Lancet. 2003 January 4; 361(9351): 81; Author Reply 82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12517499

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Paediatric patients with Henoch-Schonlein purpura followed up at Cumhuriyet University, Sivas, Turkey during 1993-1996: role of parasitosis in the aetiology of Henoch-Schonlein purpura. Author(s): Ergur AT, Cetinkaya O, Onarlioglu B. Source: Journal of Tropical Pediatrics. 1999 June; 45(3): 177-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10401201

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Pancreatitis associated with Henoch-Schonlein purpura. Author(s): Cheung KM, Mok F, Lam P, Chan KH. Source: Journal of Paediatrics and Child Health. 2001 June; 37(3): 311-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11468053

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Parvovirus B19 and parvovirus V9 are not associated with Henoch-Schonlein purpura in children. Author(s): Heegaard ED, Taaning EB. Source: The Pediatric Infectious Disease Journal. 2002 January; 21(1): 31-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11791095

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Penile involvement in Henoch-Schonlein purpura. Author(s): Sandell J, Ramanan R, Shah D. Source: Indian J Pediatr. 2002 June; 69(6): 529-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12139142

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Pericarditis as a presenting feature of Henoch-Schonlein purpura. Author(s): Cimaz R, Boccazzi A, Milone V, Careddu P. Source: Clin Exp Rheumatol. 2000 November-December; 18(6): 785. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11138351

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Plasma E-selectin and ICAM-1 in acute Henoch-Schonlein purpura. Author(s): Willis FR, Smith GC, Beattie TJ. Source: Archives of Disease in Childhood. 1997 July; 77(1): 94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9279172

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Plasmapheresis as the sole therapy for rapidly progressive Henoch-Schonlein purpura nephritis in children. Author(s): Hattori M, Ito K, Konomoto T, Kawaguchi H, Yoshioka T, Khono M. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1999 March; 33(3): 427-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10070905

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Polyangitis overlap syndrome: a fatal case combined with adult Henoch-Schonlein purpura and polyarteritis nodosa. Author(s): Watanabe K, Abe H, Mishima T, Ogura G, Suzuki T. Source: Pathology International. 2003 August; 53(8): 569-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12895238

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Polymorphism at codon 469 of the intercellular adhesion molecule-1 locus is associated with protection against severe gastrointestinal complications in HenochSchonlein purpura. Author(s): Amoli MM, Mattey DL, Calvino MC, Garcia-Porrua C, Thomson W, Hajeer AH, Ollier WE, Gonzalez-Gay MA. Source: The Journal of Rheumatology. 2001 May; 28(5): 1014-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11361181

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Polymorphism of the ACE gene in Henoch-Schonlein purpura nephritis. Author(s): Dudley J, Afifi E, Gardner A, Tizard EJ, McGraw ME. Source: Pediatric Nephrology (Berlin, Germany). 2000 March; 14(3): 218-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10752761

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Positive NBT test associated with Henoch-Schonlein purpura (HSP). Author(s): Matula G, Chang C. Source: The Journal of Pediatrics. 1974 April; 84(4): 558-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4834248

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Predictive factors for renal sequelae in adults with Henoch-Schonlein purpura. Author(s): Garcia-Porrua C, Gonzalez-Louzao C, Llorca J, Gonzalez-Gay MA. Source: The Journal of Rheumatology. 2001 May; 28(5): 1019-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11361182

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Prevalence and significance of mutations in the familial Mediterranean fever gene in Henoch-Schonlein purpura. Author(s): Gershoni-Baruch R, Broza Y, Brik R. Source: The Journal of Pediatrics. 2003 November; 143(5): 658-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14615741

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Primary antiphospholipid syndrome presenting as complicated Henoch-Schonlein purpura. Author(s): Monastiri K, Selmi H, Tabarki B, Yacoub M, Mahjoub T, Essoussi AS. Source: Archives of Disease in Childhood. 2002 February; 86(2): 132-3. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11827910

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Primary manifestation of Henoch-Schonlein purpura during immunosuppressive treatment. Author(s): Schwab M, Behrens R, Ruder H, Korn K. Source: Archives of Disease in Childhood. 1997 August; 77(2): 184-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9301369

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Proceedings: Henoch-Schonlein purpura in Southampton. Author(s): Atkinson S, Barker DJ. Source: Br J Prev Soc Med. 1974 February; 28(1): 66-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4819790

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Properties of circulating IgA molecules in Henoch-Schonlein purpura nephritis with focus on neutrophil cytoplasmic antigen IgA binding (IgA-ANCA): new insight into a debated issue. Italian Group of Renal Immunopathology Collaborative Study on Henoch-Schonlein purpura in adults and in children. Author(s): Coppo R, Cirina P, Amore A, Sinico RA, Radice A, Rollino C. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1997 November; 12(11): 2269-76. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9394310

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Pulmonary function abnormalities in children with Henoch-Schonlein purpura. Author(s): Cazzato S, Bernardi F, Cinti C, Tassinari D, Canzi A, Bergamaschi R, Corsini I, Capecchi V, Cacciari E. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 1999 March; 13(3): 597-601. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10232432

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Pulmonary haemorrhage in a 6-year-old boy with Henoch-Schonlein purpura. Author(s): Besbas N, Duzova A, Topaloglu R, Gok F, Ozaltin F, Ozen S, Bakkaloglu A. Source: Clinical Rheumatology. 2001; 20(4): 293-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11529643

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Pulmonary hemorrhage associated with Henoch-Schonlein purpura. Author(s): Eichenfield LF, Wright WK. Source: Pediatric Dermatology. 1998 March-April; 15(2): 143. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9572702

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Rapidly progressive glomerulonephritis in association with Henoch-Schonlein purpura in a patient with advanced liver cirrhosis. Author(s): Ogawa M, Makino Y, Ueda S, Ohto M, Akikusa B. Source: Nephron. 1995; 71(3): 365-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8569993

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Recurrence of Henoch-Schonlein purpura glomerulonephritis in transplanted kidneys. Author(s): Baliah T, Kim KH, Anthone S, Anthone R, Montes M, Andres GA. Source: Transplantation. 1974 October; 18(4): 343-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4609069

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Recurrence of Henoch-Schonlein purpura in association with colitis. Author(s): Gimenez-Esparza Vich JA, Arguelles BF, Martin IH, Gutierrez Fernandez MJ, Porras Vivas JJ. Source: Journal of Clinical Gastroenterology. 2002 April; 34(4): 492-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11907375

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Recurrent episodes of testicular swelling preceding Henoch-Schonlein purpura by 11 months. Author(s): Hardoff D, Jaffe M, Front H. Source: European Journal of Pediatrics. 1987 November; 146(6): 613-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3428298

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Recurrent gastrointestinal Henoch-Schonlein purpura. Author(s): Nathan K, Gunasekaran TS, Berman JH. Source: Journal of Clinical Gastroenterology. 1999 July; 29(1): 86-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10405241

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Recurrent Henoch-Schonlein purpura controlled with ciclosporin. Author(s): Harries MJ, McWhinney P, Melsom R. Source: Journal of the Royal Society of Medicine. 2004 April; 97(4): 184-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15056743

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Recurrent Henoch-Schonlein purpura presenting as gingival petechiae and mandibular pain. Author(s): Enzenauer RJ, Sutley SH, Enzenauer RW. Source: Journal of Oral and Maxillofacial Surgery : Official Journal of the American Association of Oral and Maxillofacial Surgeons. 1990 June; 48(6): 634-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2341945

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Recurrent systemic Henoch-Schonlein purpura in an adult following renal transplantation. Author(s): Crown AL, Woolfson RG, Griffiths MH, Mansell MA, Neild GH. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1994; 9(4): 423-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8084458

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Recurrent ureteric obstruction in association with Henoch-Schonlein purpura. Author(s): Powell JM, Ware H, Williams G. Source: Postgraduate Medical Journal. 1987 August; 63(742): 699-701. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3422877

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Relapsing Henoch-Schonlein purpura associated with a tubo-ovarian abscess due to Morganella morganii. Author(s): Pomeranz A, Korzets Z, Eliakim A, Pomeranz M, Uziel Y, Wolach B. Source: American Journal of Nephrology. 1997; 17(5): 471-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9382169

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Relapsing Henoch-Schonlein purpura associated with Pseudomonas aeruginosa pyelonephritis. Author(s): Egan CA, O'Reilly MA, Meadows KP, Zone JJ. Source: Journal of the American Academy of Dermatology. 2000 February; 42(2 Pt 2): 381-3. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10640939

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Renal changes in Henoch-Schonlein purpura. Author(s): Glasgow EF. Source: Archives of Disease in Childhood. 1970 February; 45(239): 151. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5440202

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Renal colic due to Henoch-Schonlein purpura. Author(s): Robson WL, Leung AK, Mathers MS. Source: J S C Med Assoc. 1994 December; 90(12): 592-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7869696

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Renal involvement in Henoch-Schonlein purpura: a multivariate analysis of prognostic factors. Author(s): Kaku Y, Nohara K, Honda S. Source: Kidney International. 1998 June; 53(6): 1755-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9607209

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Renal vasculitis in a nonfatal case of Henoch-Schonlein purpura. Author(s): Falls WF Jr, Ford KL, Ashworth CT, Carter NW. Source: Annals of Internal Medicine. 1966 June; 64(6): 1276-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5933427

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Rheumatoid arthritis associated with Henoch-Schonlein purpura. Author(s): Nishiya K, Oosaki F, Nakamura T, Hashimoto K, Kariya K, Seike M, Kodama H. Source: Clin Exp Rheumatol. 2000 September-October; 18(5): 653-4. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11072618

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Rifampin therapy in Henoch-Schonlein purpura nephritis accompanied by nephrotic syndrome. Author(s): Kim PK, Kim KS, Lee JK, Lee JS, Jeong HJ, Choi IJ. Source: Child Nephrol Urol. 1988-89; 9(1-2): 50-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3251621

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Risk factors of renal involvement and significant proteinuria in Henoch-Schonlein purpura. Author(s): Sano H, Izumida M, Shimizu H, Ogawa Y. Source: European Journal of Pediatrics. 2002 April; 161(4): 196-201. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12014385

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Role of Bartonella henselae in the etiology of Henoch-Schonlein purpura. Author(s): Ayoub EM, McBride J, Schmiederer M, Anderson B. Source: The Pediatric Infectious Disease Journal. 2002 January; 21(1): 28-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11791094

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Role of free oxygen radicals and prostanoids in the pathogenesis of HenochSchonlein Purpura. Author(s): Buyan N, Erbas D, Akkok N, Oz E, Biberoglu G, Hasanoglu E. Source: Prostaglandins, Leukotrienes, and Essential Fatty Acids. 1998 September; 59(3): 181-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9844990

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Scrotal involvement in Henoch-Schonlein purpura in children. Author(s): Mintzer CO, Nussinovitch M, Danziger Y, Mimouni M, Varsano I. Source: Scandinavian Journal of Urology and Nephrology. 1998 April; 32(2): 138-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9606788

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Scrotal involvement in Henoch-Schonlein purpura: a case report and review of the literature. Author(s): Chamberlain RS, Greenberg LW. Source: Pediatric Emergency Care. 1992 August; 8(4): 213-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1513732

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Scrotal ultrasonography in Henoch-Schonlein purpura. Author(s): Laor T, Atala A, Teele RL. Source: Pediatric Radiology. 1992; 22(7): 505-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1491907

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Seizures complicating adult Henoch-Schonlein purpura. Author(s): Fielding RE, Hawkins CP, Hand MF, Heath PD, Davies SJ. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1998 March; 13(3): 761-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9550663

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Septicemia as a complication of Henoch-Schonlein purpura. Author(s): Robberecht E, Vlaminck H, Gamiz-Jimenez J, Renders F, Van Winckel M, Carton D. Source: Journal of Pediatric Gastroenterology and Nutrition. 1997 August; 25(2): 222-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9252913

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Sequential occurrence of IgA nephropathy and Henoch-Schonlein purpura: support for common pathogenesis. Author(s): Silverstein DM, Greifer I, Folkert V, Bennett B, Corey HE, Spitzer A. Source: Pediatric Nephrology (Berlin, Germany). 1994 December; 8(6): 752-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7696119

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Serum hepatocyte growth factor levels in Henoch-Schonlein purpura. Author(s): Nishida M, Kawakatsu H, Ishiwari K, Tamai M, Sawada T, Nishimura M, Yoshimura M. Source: Pediatrics International : Official Journal of the Japan Pediatric Society. 1999 October; 41(5): 474-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10530056

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Serum IgA-fibronectin aggregates in patients with IgA nephropathy and HenochSchonlein purpura: diagnostic value and pathogenic implications. The Glomerular Disease Collaborative Network. Author(s): Jennette JC, Wieslander J, Tuttle R, Falk RJ. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1991 October; 18(4): 466-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1928066

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Serum SC5b-9 (terminal complement complex) level, a sensitive indicator of disease activity in patients with Henoch-Schonlein purpura. Author(s): Kawana S, Nishiyama S. Source: Dermatology (Basel, Switzerland). 1992; 184(3): 171-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1392107

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Severe hypertension without urinary abnormalities in a patient with HenochSchonlein purpura. Author(s): Whyte DA, Van Why SK, Siegel NJ. Source: Pediatric Nephrology (Berlin, Germany). 1997 December; 11(6): 750-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9438659

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Severe scrotal pain in boys with Henoch-Schonlein purpura: incidence and sonography. Author(s): Ben-Sira L, Laor T. Source: Pediatric Radiology. 2000 February; 30(2): 125-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10663526

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Small bowel stricture due to vascular compromise: a late complication of HenochSchonlein purpura. Author(s): Lipsett J, Byard RW. Source: Pediatric Pathology & Laboratory Medicine : Journal of the Society for Pediatric Pathology, Affiliated with the International Paediatric Pathology Association. 1995 March-April; 15(2): 333-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8597821

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Soluble thrombomodulin and antibodies to bovine glomerular endothelial cells in patients with Henoch-Schonlein purpura. Author(s): Fujieda M, Oishi N, Naruse K, Hashizume M, Nishiya K, Kurashige T, Ito K. Source: Archives of Disease in Childhood. 1998 March; 78(3): 240-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9613354

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Sonographic evaluation of the abdomen in Henoch-Schonlein purpura. Author(s): Connolly B, O'Halpin D. Source: Clinical Radiology. 1994 May; 49(5): 320-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8013195

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Specific T-cell receptor usage with cytokinemia in Henoch-Schonlein purpura nephritis associated with Staphylococcus aureus infection. Author(s): Hirayama K, Kobayashi M, Muro K, Yoh K, Yamagata K, Koyama A. Source: Journal of Internal Medicine. 2001 April; 249(4): 289-95. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11298848

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Subcutaneous nodules in Henoch-Schonlein purpura. Author(s): Robson WL, Leung AK. Source: Pediatric Nephrology (Berlin, Germany). 2000 June; 14(6): 493-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10872192

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Successful treatment of adult-onset Henoch-Schonlein purpura nephritis with highdose immunoglobulins. Author(s): Kusuda A, Migita K, Tsuboi M, Degawa M, Matsuoka N, Tominaga M, Kawakami A, Kawabe Y, Taguchi T, Eguchi K. Source: Intern Med. 1999 April; 38(4): 376-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10361914

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Successful treatment of chronic Henoch-Schonlein purpura with colchicine and aspirin. Author(s): Padeh S, Passwell JH. Source: Isr Med Assoc J. 2000 June; 2(6): 482-3. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10897246

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Successful treatment of mesenteric vasculitis caused by Henoch-Schonlein purpura with methylprednisolone pulse therapy. Author(s): Wang L, Huang FC, Ko SF, Cheng MT. Source: Clinical Rheumatology. 2003 May; 22(2): 140-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12740680

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Successful treatment with leukocytapheresis in refractory Henoch-Schonlein purpura: case report. Author(s): Nakahata T, Tanaka H, Suzuki K, Ito E. Source: Clinical Rheumatology. 2003 September; 22(3): 248-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14505222

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The absence of anti-neutrophil cytoplasmic antibodies in patients with HenochSchonlein purpura. Author(s): Robson WL, Leung AK, Woodman RC. Source: Pediatric Nephrology (Berlin, Germany). 1994 June; 8(3): 295-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7917854

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The adult kidney 24 years after childhood Henoch-Schonlein purpura: a retrospective cohort study. Author(s): Ronkainen J, Nuutinen M, Koskimies O. Source: Lancet. 2002 August 31; 360(9334): 666-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12241872

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The American College of Rheumatology 1990 criteria for the classification of HenochSchonlein purpura. Author(s): Mills JA, Michel BA, Bloch DA, Calabrese LH, Hunder GG, Arend WP, Edworthy SM, Fauci AS, Leavitt RY, Lie JT, et al. Source: Arthritis and Rheumatism. 1990 August; 33(8): 1114-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2202310

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The clinical spectrum of Henoch-Schonlein purpura in infants and young children. Author(s): Al-Sheyyab M, El-Shanti H, Ajlouni S, Sawalha D, Daoud A. Source: European Journal of Pediatrics. 1995 December; 154(12): 969-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8801104

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The complement system in IgA nephropathy and Henoch-Schonlein purpura: functional and genetic aspects. Author(s): Wyatt RJ. Source: Contrib Nephrol. 1993; 104: 82-91. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8325036

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The level of IgA antibodies to human umbilical vein endothelial cells can be enhanced by TNF-alpha treatment in children with Henoch-Schonlein purpura. Author(s): Yang YH, Wang SJ, Chuang YH, Lin YT, Chiang BL. Source: Clinical and Experimental Immunology. 2002 November; 130(2): 352-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12390327

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The nephritis of Henoch-Schonlein purpura. Author(s): Striker GE, Quadracci LJ, Larter W, Hickman RO, Kelly MR, Schaller J. Source: Perspect Nephrol Hypertens. 1973; 1 Pt 2(0): 1105-21. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4803306

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The rheumatic poison: a survey of some published investigations of the immunopathogenesis of Henoch-Schonlein purpura. Author(s): Knight JF. Source: Pediatric Nephrology (Berlin, Germany). 1990 September; 4(5): 533-41. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2242325

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The role of apoptosis in childhood Henoch-Schonlein purpura. Author(s): Ozaltin F, Besbas N, Uckan D, Tuncer M, Topaloglu R, Ozen S, Saatci U, Bakkaloglu A. Source: Clinical Rheumatology. 2003 October; 22(4-5): 265-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14576987

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The role of IgA1 rheumatoid factor in the formation of IgA-containing immune complexes in Henoch-Schonlein purpura. Author(s): Saulsbury FT. Source: J Clin Lab Immunol. 1987 July; 23(3): 123-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3669060

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The role of plasma arachidonic acid metabolites in the pathogenesis and the prognosis of Henoch-Schonlein purpura. Author(s): Buyan N, Hasanoglu E, Oguz A, Ercan S. Source: Prostaglandins, Leukotrienes, and Essential Fatty Acids. 1994 June; 50(6): 353-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7938089

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The role of streptococcal infection in Henoch-Schonlein purpura. Author(s): Ercan G, Kasapcopur O, Akdenizli E, Arisoy N. Source: Journal of Tropical Pediatrics. 2004 June; 50(3): 187-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15233200

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The value of colour Doppler ultrasonography for small bowel involvement of adult Henoch-Schonlein purpura. Author(s): Shirahama M, Umeno Y, Tomimasu R, Dohmen K, Miyamoto Y, Shimoda Y, Irie K, Ishibashi H. Source: The British Journal of Radiology. 1998 July; 71(847): 788-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9771392

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Therapeutics. XV. The management of Henoch-Schonlein purpura. Author(s): Ashton H, Frenk E, Stevenson CJ. Source: The British Journal of Dermatology. 1971 August; 85(2): 199-203. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4936860

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Three cases of Henoch-Schonlein purpura preceded by IgA nephropathy. Author(s): Watanabe T, Takada T, Kihara I, Oda Y. Source: Pediatric Nephrology (Berlin, Germany). 1995 October; 9(5): 674. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8580041

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Thrombomodulin, tissue plasminogen activator and plasminogen activator inhibitor1 in Henoch-Schonlein purpura. Author(s): Besbas N, Erbay A, Saatci U, Ozdemir S, Bakkaloglu A, Ozen S, Topaloglu R. Source: Clin Exp Rheumatol. 1998 January-February; 16(1): 95-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9543574

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Total bilateral ureteral replacement for stenosing ureteritis in Henoch-Schonlein purpura. Author(s): Pfister C, Liard-Zmuda A, Dacher J, Dubois D, Grise P, Mitrofanoff P. Source: European Urology. 2000 July; 38(1): 96-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10859449

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Treatment of Henoch-Schonlein Purpura glomerulonephritis in children with highdose corticosteroids plus oral cyclophosphamide. Author(s): Flynn JT, Smoyer WE, Bunchman TE, Kershaw DB, Sedman AB. Source: American Journal of Nephrology. 2001 March-April; 21(2): 128-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11359020

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Tumor necrosis factor induced adhesion molecule serum concentrations in HenochSchonlein purpura and pediatric systemic lupus erythematosus. Author(s): Gattorno M, Vignola S, Barbano G, Sormani MP, Sabatini F, Buoncompagni A, Picco P, Pistoia V. Source: The Journal of Rheumatology. 2000 September; 27(9): 2251-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10990243

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Two cases of Henoch-Schonlein purpura with transient myocardial ischaemia. Author(s): Hayakawa K, Shiohara T. Source: Acta Dermato-Venereologica. 2003; 83(5): 393-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14609119

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Ultrasonographic and color Doppler imaging of hemorrhagic epididymitis in Henoch-Schonlein purpura. Author(s): Sudakoff GS, Burke M, Rifkin MD. Source: Journal of Ultrasound in Medicine : Official Journal of the American Institute of Ultrasound in Medicine. 1992 November; 11(11): 619-21. Erratum In: J Ultrasound Med 1993 February; 12(2): 78. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1433470

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Ultrasonographic gallbladder wall thickening in children with Henoch-Schonlein purpura. Author(s): Amemoto K, Nagita A, Aoki S, Azumagawa K, Hirano K, Mino M. Source: Journal of Pediatric Gastroenterology and Nutrition. 1994 July; 19(1): 126-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7965465

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Ultrasonography to diagnose and exclude intussusception in Henoch-Schonlein purpura. Author(s): Hu SC, Feeney MS, McNicholas M, O'Halpin D, Fitzgerald RJ. Source: Archives of Disease in Childhood. 1991 September; 66(9): 1065-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1929515

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Ultrasound diagnosis of acute scrotal hemorrhage in Henoch-Schonlein purpura. Author(s): Cooper SG, Sherman SB, Gross RI, Richman AH. Source: Journal of Clinical Ultrasound : Jcu. 1988 June; 16(5): 353-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3152394

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Uncommon multisystemic involvement in a case of Henoch-Schonlein purpura. Author(s): Kano K, Ozawa T, Kuwashima S, Ito S. Source: Acta Paediatr Jpn. 1998 April; 40(2): 159-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9581309

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Unusual manifestations of Henoch-Schonlein purpura. Author(s): Samuel SP, John E, Assadi F, Rao S. Source: Indian J Pediatr. 1984 November-December; 51(413): 751-4. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6537410

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Unusual problems in surgery. Henoch-Schonlein purpura. Author(s): Leichtling JJ. Source: J Mt Sinai Hosp N Y. 1969 January-February; 36(1): 65-70. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5249497

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Urinary tract tuberculosis in a child with Henoch-Schonlein purpura: a case report. Author(s): Saatci U, Ozen S, Bakkaloglu M, Tinaztepe K. Source: Turk J Pediatr. 1989 April-June; 31(2): 155-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2617718

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Urologic manifestations of Henoch-Schonlein purpura. Author(s): Stresing HA, Turner WR. Source: Urology. 1977 May; 9(5): 535-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=860343

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Use of intravenous hydrocortisone in Henoch-Schonlein purpura. Author(s): Leung SP. Source: Journal of Paediatrics and Child Health. 2001 June; 37(3): 309-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11468052

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Value of the assay for IgA-containing circulating immune complexes in HenochSchonlein purpura. Author(s): Kawana S, Ohta M, Nishiyama S. Source: Dermatologica. 1986; 172(5): 245-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3743843

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Vascular endothelial growth factor in Henoch-Schonlein purpura. Author(s): Topaloglu R, Sungur A, Baskin E, Besbas N, Saatci U, Bakkaloglu A. Source: The Journal of Rheumatology. 2001 October; 28(10): 2269-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11669168

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von Willebrand factor and factor XIII in children with Henoch-Schonlein purpura. Author(s): De Mattia D, Penza R, Giordano P, Del Vecchio GC, Aceto G, Altomare M, Schettini F. Source: Pediatric Nephrology (Berlin, Germany). 1995 October; 9(5): 603-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8580019

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CHAPTER 2. NUTRITION AND HENOCH-SCHONLEIN PURPURA Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and Henoch-Schonlein purpura.

Finding Nutrition Studies on Henoch-Schonlein Purpura 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 “Henoch-Schonlein purpura” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.

7 Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.

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

A cutaneous sign of IgA-associated small dermal vessel leukocytoclastic vasculitis in adults (Henoch-Schonlein purpura). Author(s): Department of Dermatology, University of Iowa Hospitals and Clinics, Iowa City 52242. Source: Piette, W W Stone, M S Arch-Dermatol. 1989 January; 125(1): 53-6 0003-987X

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Hepatobiliary involvement of Henoch-Schonlein purpura in children. Author(s): Department of Pediatrics, Chang Gung Children Hospital, Taoyuan, Taiwan. [email protected] Source: Chao, H C Kong, M S Lin, S J Acta-Paediatr-Taiwan. 2000 Mar-April; 41(2): 63-8

Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: •

healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0

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

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

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

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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/

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

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

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

Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: •

AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats

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

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

Nutrition

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

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

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

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

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

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The following is a specific Web list relating to Henoch-Schonlein purpura; 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 Lamb and Mutton Source: Healthnotes, Inc.; www.healthnotes.com Rabbit Source: Healthnotes, Inc.; www.healthnotes.com Turkey Source: Healthnotes, Inc.; www.healthnotes.com

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CHAPTER 3. ALTERNATIVE MEDICINE AND HENOCHSCHONLEIN PURPURA Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to Henoch-Schonlein purpura. 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 Henoch-Schonlein purpura 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 “Henoch-Schonlein purpura” (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 Henoch-Schonlein purpura: •

A test for antigen--antibody complexes in human sera using IgM of rabbit antisera to human immunoglobulins. Author(s): Levinsky RJ, Soothill JF. Source: Clinical and Experimental Immunology. 1977 September; 29(3): 428-35. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=589862

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Effect of Tripterygium wilfordii on nephritis of anaphylactoid purpura. Author(s): Pan YR, Zhu CY, Li P, Wei M, Xu DH. Source: Proc Chin Acad Med Sci Peking Union Med Coll. 1987; 2(1): 45-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3432251

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Factor XIII: inherited and acquired deficiency. Author(s): Board PG, Losowsky MS, Miloszewski KJ. Source: Blood Reviews. 1993 December; 7(4): 229-42. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8130686

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Fuzi xiexin tang for treatment of intractable pediatric diseases. Author(s): Xu R, Liu L, Xie C. Source: J Tradit Chin Med. 1999 September; 19(3): 185-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10921147

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Haemophilus influenzae type b purpura fulminans treated with hyperbaric oxygen. Author(s): Dollberg S, Nachum Z, Klar A, Engelhard D, Ginat-Israeli T, Hurvitz H, Melamed Y, Branski D. Source: The Journal of Infection. 1992 September; 25(2): 197-200. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1431173

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Hazards of misdiagnosis due to Vietnamese folk medicine. Author(s): Golden SM, Duster MC. Source: Clinical Pediatrics. 1977 October; 16(10): 949-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=891073

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Henoch-Schonlein IgA glomerulonephritis complicating myeloma kidneys: case report. Author(s): Arrizabalaga P, Saurina A, Sole M, Blade J. Source: Annals of Hematology. 2003 August; 82(8): 526-8. Epub 2003 July 03. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12844235

•

Henoch-Schonlein purpura associated with segmental and focal proliferative glomerulonephritis in a patient with Hodgkin's disease. Author(s): Blanco P, Denisi R, Rispal P, Deminiere C, Pellegrin JL, Leng B, Aparicio M. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1999 January; 14(1): 179-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10052501

•

Increased intestinal permeability to (51 Cr) EDTA is correlated with IgA immune complex-plasma levels in children with IgA-associated nephropathies. Author(s): Davin JC, Forget P, Mahieu PR. Source: Acta Paediatr Scand. 1988 January; 77(1): 118-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3130743

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•

Outcome of end-stage renal disease in patients with rare causes of renal failure. III. Systemic/vascular disorders. Author(s): Nissenson AR, Port FK. Source: The Quarterly Journal of Medicine. 1990 January; 74(273): 63-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1970184

•

Purpura haemorrhagica in 53 horses. Author(s): Pusterla N, Watson JL, Affolter VK, Magdesian KG, Wilson WD, Carlson GP. Source: The Veterinary Record. 2003 July 26; 153(4): 118-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12918829

•

Sequential measurements of intestinal permeability to [51Cr]EDTA in children with Henoch-Schonlein purpura nephritis. Author(s): Davin JC, Mahieu PR. Source: Nephron. 1992; 60(4): 498-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1584334

•

Systemically induced vasculitis in children. Author(s): Peterson-Sweeney KL. Source: Aacn Clinical Issues. 1995 November; 6(4): 657-69. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7493267

•

The cutaneous manifestations and common mimickers of physical child abuse. Author(s): Mudd SS, Findlay JS. Source: Journal of Pediatric Health Care : Official Publication of National Association of Pediatric Nurse Associates & Practitioners. 2004 May-June; 18(3): 123-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15129212

•

Traditional Chinese medicine in the treatment of autoimmune and immune disorders. Author(s): Shi JS. Source: Chinese Medical Journal. 1994 April; 107(4): 295-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8088199

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/

•


•

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

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•

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

•

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/

General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.

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CHAPTER 4. PATENTS ON HENOCH-SCHONLEIN PURPURA 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 “HenochSchonlein purpura” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on Henoch-Schonlein purpura, we have not necessarily excluded non-medical patents in this bibliography.

Patents on Henoch-Schonlein Purpura By performing a patent search focusing on Henoch-Schonlein purpura, 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.

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The following is an example of the type of information that you can expect to obtain from a patent search on Henoch-Schonlein purpura: •

Method and a kit for the diagnosis of IgA nephropathy Inventor(s): Bygren; Per (Lund, SE), Cederholm; Bo (Lund, SE), Heinegard; Dick (Lund, SE), Wieslander; Jorgen (Lund, SE) Assignee(s): BioCarb AB (Lund, SE) Patent Number: 5,139,932 Date filed: November 3, 1989 Abstract: A method for the diagnosis of IgA nephropathy using a specific binding reaction comprising the steps:a) preparing a substrate capable of binding fibronectin or IgAb) contacting the substrate resulting from step a) with a sample of body fluid drawn from a patient subject to diagnosis to bind any fibronectin-IgA-complex present in said sample to the substrate, andc) determining the presence of complex bound to the substrate using the reaction between the exposed part of such bound complex and a corresponding antibody thereto; anda diagnostic kit for use in such diagnosis. Excerpt(s): The present invention relates to a method for the diagnosis of IgA nephropathy using an antigen-antibody interaction, and the invention also includes a diagnostic kit for use in such a diagnosis. Patients with primary IgA nephropathy, also known as Berger's disease, have been shown to have circulating IgA antibodies, binding to collagen IV prepared from glomerular basement membrane (GBM) (1). It was also shown that the IgA antibodies bound equally well to collagen I, II and IV and that denatured collagens bound antibodies most efficiently (1). In view of the wide distribution of the various collagens, it is of interest to note the coexistence with IgA nephropathy of symptoms from extrarenal organs (2). Thus symptoms from skin, eye and joints are of particular interest since these structures contains collagen as a major component. Indeed one study reports presence of vascular IgA deposits in skin from patients with IgA nephropathy (3). The association of exacerbations of clinical disease with upper respiratory tract or gastrointestinal infections and the finding of IgA deposits in the glomerular mesangium is well known. The finding of increased levels of IgA-bearing peripheral lymphocytes (4) as well as decreased IgA-specific suppressor T cell activity (5) and increased IgA-specific helper T-alfa cells (6) suggests an immunological mechanism. Web site: http://www.delphion.com/details?pn=US05139932__

Patent Applications on Henoch-Schonlein Purpura 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 Henoch-Schonlein purpura:

9

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

Patents 65

•

IgA nephropathy-related DNA Inventor(s): Furuya, Akiko; (Tokyo, JP), Ishiwata, Tetsuyoshi; (Tokyo, JP), Kawabata, Ayako; (Tokyo, JP), Kuga, Tetsuro; (Yamaguchi, JP), Nakagawa, Satoshi; (Tokyo, JP), Nishi, Tatsunari; (Tokyo, JP), Sakurada, Mikiko; (Tokyo, JP), Sawada, Shigemasa; (Tokyo, JP), Shibata, Kenji; (Tokyo, JP), Takei, Masami; (Saitama, JP) Correspondence: Fitzpatrick Cella Harper & Scinto; 30 Rockefeller Plaza; New York; NY; 10112; US Patent Application Number: 20030207828 Date filed: December 7, 2000 Abstract: A novel DNA whose expression level fluctuates in leukocytes of IgA nephropathy patients in comparison with leukocytes of healthy persons, a process for isolating the DNA, a novel protein encoded by the DNA, an antibody recognizing the protein, methods for detecting the protein and the DNA, and methods of diagnosis and treatment of IgA nephropathy. Excerpt(s): This is a continuation-in-part application of U.S. patent application Ser. No. 09/090,672 filed on Jun. 4, 1998, which is a continuation-in-part application of PCT/JP97/04468 filed on Dec. 5, 1997. The present invention relates to a novel DNA whose expression level fluctuates in leukocytes of IgA nephropathy patients in comparison with leukocytes of healthy persons, a process for isolating the DNA, a novel protein encoded by the DNA, an antibody recognizing the protein, a method for detecting the protein or the DNA, and methods of diagnosis and treatment of IgA nephropathy. IgA nephropathy is a chronic glomerulonephritis which is characterized in that an IgA immune complex considered to be derived from blood deposits in glomerulus of the kidney. In Japan, the IgA nephropathy occupies 30% or more of primary renal diseases, having the highest frequency as a single renal disease, and 15 to 30% of the disease becomes renal failure due to poor prognosis. However, since the cause of the disease of IgA nephropathy is still unclear, a fundamental therapeutic method has not been found. Additionally, definite diagnosis of IgA nephropathy imposes heavy burden on patients, because the method is carried out by taking out a portion of the kidney by biopsy and recognizing deposition of the IgA immune complex in mesangium by means of immunological staining. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

•

Test method for IgA nephropathy Inventor(s): Arai, Kenji; (Shizuoka, JP), Rokubo, Tohru; (Kanagawa, JP), Toma, Kazunori; (Osaka, JP) Correspondence: Young & Thompson; 745 South 23rd Street 2nd Floor; Arlington; VA; 22202 Patent Application Number: 20030017619 Date filed: April 9, 2002 Abstract: A test method for IgA nephropathy involves determining antibody, which recognizes the core peptide of the hinge region in IgA1, in specimens. The method is a rapid and sample test method for IgA nephropathy having less emotional distress for the patients, low risk for peripheral hemorrhage of the kidney and reduced financial burden for the patients.

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Excerpt(s): This invention relates to a novel test method for IgA nephropathy. More particularly, the present invention pertains to a rapid and simple test method for IgA nephropathy and a determination method of antibody, which has low risks in emotional distress, peripheral hemorrhage in the kidney and financial burden to the patient, by determining antibody recognizing IgA1 hinge region core peptide in the specimen. IgA (immunoglobulin A) nephropathy is a disease concept provided by Berger et al. (J. Urol., 74, pp. 694-695, 1968), and is a primary glomerular nephritis having features with clinically poor symptoms except for continuous proteinuria and hematuria, and histological features with precipitants consisting of mainly IgA in the mesangium. The incidence of IgA nephropathy in Japan is high and accounts for 30% of the chronic nephritis. The long term prognosis is not so favorable, and 10-15% of patients with 10 years progress and about 3 0% of patients with 20 years progress suffer from terminal renal failure. Consequently, IgA nephropathy is especially noticed as a causal disease for terminal renal failure. At present, the only known test method for IgA nephropathy is the renal biopsy. This test method, however, causes emotional distress for the patients, and her may cause peripheral hemorrhage in the kidney after the biopsy. In addition, the patients must have absolute rest for more than 24 hours after the renal biopsy, and this requires the patients to stay in hospital for several days, and this causes a heavy financial burden for them. Furthermore, the test method has disadvantages including requiring many kinds of test facilities together with long term testing time. 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 HenochSchonlein purpura, 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 “Henoch-Schonlein purpura” (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 Henoch-Schonlein purpura. You can also use this procedure to view pending patent applications concerning HenochSchonlein purpura. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.

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CHAPTER 5. BOOKS ON HENOCH-SCHONLEIN PURPURA Overview This chapter provides bibliographic book references relating to Henoch-Schonlein purpura. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on Henoch-Schonlein purpura include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.

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

Glomerular Diseases Source: in Kher, K.K.; Makker, S.P., eds. Clinical Pediatric Nephrology. New York, NY: McGraw-Hill. 1992. p. 175-276. Contact: Available from McGraw-Hill, Inc. P.O. Box 545, Blacklick, OH 43004. (800) 2624729. PRICE: $85.00 plus $3.00 shipping and handling. ISBN: 0070345430. Summary: According to the author, glomerular diseases are the most common cause of end-stage renal failure in humans and are responsible for significant rates of morbidity in both children and adults. This chapter, from a book on clinical pediatric nephrology, discusses glomerular diseases. Topics include glomerular structure, morphologic terms used, classification, Alport syndrome, congenital nephrotic syndrome of the Finnish type, membranoproliferative glomerulonephritis, membranous glomerulonephropathy, IgA nephropathy, poststreptococcal glomerulonephritis, hepatitis-associated

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glomerulonephritis, glomerulonephritis associated with endocarditis, shunt nephritis, Henoch-Schonlein purpura nephritis, systemic lupus erythematosus nephritis, hemolytic uremic syndrome, and rapidly progressive glomerulonephritis. Twelve illustrative case histories are included. 19 figures. 22 tables. 402 references. •

Clinical Evaluation of the Kidney in Systemic and Collagen Diseases Source: in Barakat, A.Y. Renal Disease in Children: Clinical Evaluation and Diagnosis. Secaucus, NJ: Springer-Verlag. 1990. p. 357-369. Contact: No longer available from publisher. Summary: The specialized nature of the renal vasculature and the relatively large renal blood flow make kidney damage particularly likely whenever systemic illness threatens the patient's vascular integrity. Involvement may be minor, or kidney failure and homeostatic crisis may result. This chapter, from an extensive desk reference book about the clinical evaluation and diagnosis of renal disease in children, discusses the clinical evaluation of the kidney in systemic and collagen diseases. Eight sections cover: Henoch-Schonlein purpura; necrotizing vasculitis with nephritis; systemic lupus erythematosus and other collagen vascular diseases; renal injury from remote infection; rapidly progressive glomerulonephritis; hemolytic uremic syndrome; diabetic nephropathy; and lymphoid malignancy. The authors note that the prognosis in these situations will depend in part on the clinician's recognition of and response to the renal sequelae of the illness. One table summarizes the systemic diseases commonly associated with renal involvement in children. 20 references.

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APPENDICES

71

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.

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•

National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm

•

National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/

•

National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm

•

National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm

•

National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/

•

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

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

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•

Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html

•

Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html

The 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 “Henoch-Schonlein purpura” (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 2304 12 66 2 8 2392

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 “Henoch-Schonlein purpura” (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

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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.

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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on Henoch-Schonlein purpura 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 Henoch-Schonlein purpura. 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 Henoch-Schonlein purpura. 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 “Henoch-Schonlein purpura”:

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African-American Health http://www.nlm.nih.gov/medlineplus/africanamericanhealth.html Asthma http://www.nlm.nih.gov/medlineplus/asthma.html Autoimmune Diseases http://www.nlm.nih.gov/medlineplus/autoimmunediseases.html Bruises http://www.nlm.nih.gov/medlineplus/bruises.html Connective Tissue Disorders http://www.nlm.nih.gov/medlineplus/connectivetissuedisorders.html Diabetic Kidney Problems http://www.nlm.nih.gov/medlineplus/diabetickidneyproblems.html Immune System and Disorders http://www.nlm.nih.gov/medlineplus/immunesystemanddisorders.html Kidney Diseases http://www.nlm.nih.gov/medlineplus/kidneydiseases.html Kidney Failure http://www.nlm.nih.gov/medlineplus/kidneyfailure.html Kidney Transplantation http://www.nlm.nih.gov/medlineplus/kidneytransplantation.html Lupus http://www.nlm.nih.gov/medlineplus/lupus.html Multiple Sclerosis http://www.nlm.nih.gov/medlineplus/multiplesclerosis.html Multiple Sclerosis http://www.nlm.nih.gov/medlineplus/tutorials/multiplesclerosisloader.html Myositis http://www.nlm.nih.gov/medlineplus/myositis.html Skin Diseases http://www.nlm.nih.gov/medlineplus/skindiseases.html Vasculitis http://www.nlm.nih.gov/medlineplus/vasculitis.html Wegener's Granulomatosis http://www.nlm.nih.gov/medlineplus/wegenersgranulomatosis.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.

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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 Henoch-Schonlein purpura. 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: •


•

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

Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to Henoch-Schonlein purpura. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with Henoch-Schonlein purpura. 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 Henoch-Schonlein purpura. 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

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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 “Henoch-Schonlein purpura” (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 “Henoch-Schonlein purpura”. 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 “Henoch-Schonlein purpura” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months. The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “HenochSchonlein purpura” (or a synonym) into the search box, and click “Submit Query.”

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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.

Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.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.

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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)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

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•

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

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

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

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Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/

•

Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm

•

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/

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•

Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html

•

Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp

•

Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp

•

Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/

•

Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html

•

Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm

•

Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp

•

Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/

•

Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html

•

Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/

•

Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm

•

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

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•

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

•

New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/

•

New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm

•

New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm

•

New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/

•

New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html

•

New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/

•

New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html

•

New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/

•

Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm

•

Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp

•

Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/

•

Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/

•

Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml

•

Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html

•

Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html

•

Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml

•

Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp

•

Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm

•

Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/

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•

South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp

•

Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/

•

Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/

•

Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72

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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 Henoch-Schonlein purpura: •

Basic Guidelines for Henoch-Schonlein Purpura Allergic vasculitis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000874.htm Henoch-Schonlein purpura Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000425.htm IgA nephropathy (Berger's disease) Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000466.htm

•

Signs & Symptoms for Henoch-Schonlein Purpura Abdominal pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003120.htm Bleeding into the skin Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003235.htm

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Blindness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003040.htm Blisters Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003939.htm Blood in the urine Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003138.htm Bloody urine Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003138.htm Chorea Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003196.htm Convulsions Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003200.htm Decreased urine output Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003147.htm Diarrhea Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003126.htm Ecchymoses Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003235.htm Edema Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003103.htm Erythema Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003220.htm Fever Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003090.htm Headache Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003024.htm Hematomas Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003235.htm Hematuria Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003138.htm High blood pressure Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003082.htm Hyperactivity Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003256.htm

Online Glossaries 89

Irritability Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003214.htm Joint pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003261.htm Joint pains Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003261.htm Menstruation, painful Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003150.htm Nausea Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003117.htm Paralysis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003190.htm Petechiae Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003235.htm Purpura Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003232.htm Scrotal swelling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003161.htm Skin lesion Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003220.htm Skin lesions Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003220.htm Stools, bloody Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003130.htm Stress Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003211.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 Henoch-Schonlein Purpura Biopsy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003416.htm Blood pressure Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003398.htm

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BUN Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003474.htm C3 Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003539.htm Casts in the urine Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003586.htm Creatinine Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003475.htm Diffusing capacity Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003854.htm ESR Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003638.htm IgA Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003544.htm Immunoelectrophoresis - urine Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003592.htm Kidney biopsy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003907.htm Platelet aggregation test Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003669.htm Protein in the urine Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003580.htm Sed rate Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003638.htm Sedimentation rate Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003638.htm Skin biopsy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003840.htm Ulcers Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003228.htm Urinalysis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003579.htm X-ray Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003337.htm

Online Glossaries 91

•

Nutrition for Henoch-Schonlein Purpura Fats Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002468.htm Protein Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002467.htm

•

Background Topics for Henoch-Schonlein Purpura Acute Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002215.htm Allergic reaction Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000005.htm Antibodies Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002223.htm Antibody Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002223.htm Antigen Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002224.htm Incidence Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002387.htm Inflammatory response Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000821.htm Kidney disease - support group Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002172.htm Necrotic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002266.htm Physical examination Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002274.htm Renal Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002289.htm Respiratory Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002290.htm Support group Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002150.htm

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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

•

Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/

•

Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine

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HENOCH-SCHONLEIN PURPURA 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] Aberrant: Wandering or deviating from the usual or normal course. [EU] Abortion: 1. The premature expulsion from the uterus of the products of conception - of the embryo, or of a nonviable fetus. The four classic symptoms, usually present in each type of abortion, are uterine contractions, uterine haemorrhage, softening and dilatation of the cervix, and presentation or expulsion of all or part of the products of conception. 2. Premature stoppage of a natural or a pathological process. [EU] Abscess: A localized, circumscribed collection of pus. [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] Acetylgalactosamine: The N-acetyl derivative of galactosamine. [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] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [NIH] Aetiology: Study of the causes of disease. [EU] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alkaloid: A member of a large group of chemicals that are made by plants and have nitrogen in them. Some alkaloids have been shown to work against cancer. [NIH] Allografts: A graft of tissue obtained from the body of another animal of the same species but with genotype differing from that of the recipient; tissue graft from a donor of one genotype to a host of another genotype with host and donor being members of the same species. [NIH] Alopecia: Absence of hair from areas where it is normally present. [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]

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Amino acid: Any organic compound containing an amino (-NH2 and a carboxyl (- COOH) group. The 20 a-amino acids listed in the accompanying table are the amino acids from which proteins are synthesized by formation of peptide bonds during ribosomal translation of messenger RNA; all except glycine, which is not optically active, have the L configuration. Other amino acids occurring in proteins, such as hydroxyproline in collagen, are formed by posttranslational enzymatic modification of amino acids residues in polypeptide chains. There are also several important amino acids, such as the neurotransmitter y-aminobutyric acid, that have no relation to proteins. Abbreviated AA. [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] Ampulla: A sac-like enlargement of a canal or duct. [NIH] Anal: Having to do with the anus, which is the posterior opening of the large bowel. [NIH] 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] 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] Angiitis: Inflammation of a vessel, chiefly of a blood or a lymph vessel; called also vasculitis. [EU] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]

Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibodies, Anticardiolipin: Antiphospholipid antibodies found in association with systemic lupus erythematosus (lupus erythematosus, systemic), antiphospholipid syndrome, and in a variety of other diseases as well as in healthy individuals. The antibodies are detected by solid-phase immunoassay employing the purified phospholipid antigen cardiolipin. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue

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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] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antiphospholipid Syndrome: The presence of antibodies directed against phospholipids (antibodies, antiphospholipid). The condition is associated with a variety of diseases, notably systemic lupus erythematosus and other connective tissue diseases, thrombopenia, and arterial or venous thromboses. In pregnancy it can cause abortion. Of the phospholipids, the cardiolipins show markedly elevated levels of anticardiolipin antibodies (antibodies, anticardiolipin). Present also are high levels of lupus anticoagulant (lupus coagulation inhibitor). [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] Applicability: A list of the commodities to which the candidate method can be applied as presented or with minor modifications. [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Ascites: Accumulation or retention of free fluid within the peritoneal cavity. [NIH] Aspirin: A drug that reduces pain, fever, inflammation, and blood clotting. Aspirin belongs to the family of drugs called nonsteroidal anti-inflammatory agents. It is also being studied in cancer prevention. [NIH]

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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] Atrium: A chamber; used in anatomical nomenclature to designate a chamber affording entrance to another structure or organ. Usually used alone to designate an atrium of the heart. [EU] Attenuated: Strain with weakened or reduced virulence. [NIH] Autoantibodies: Antibodies that react with self-antigens (autoantigens) of the organism that produced them. [NIH] Autoantigens: Endogenous tissue constituents that have the ability to interact with autoantibodies and cause an immune response. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [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] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Barbiturate: A drug with sedative and hypnotic effects. Barbiturates have been used as sedatives and anesthetics, and they have been used to treat the convulsions associated with epilepsy. [NIH] Basement Membrane: Ubiquitous supportive tissue adjacent to epithelium and around smooth and striated muscle cells. This tissue contains intrinsic macromolecular components such as collagen, laminin, and sulfated proteoglycans. As seen by light microscopy one of its subdivisions is the basal (basement) lamina. [NIH] Basophils: Granular leukocytes characterized by a relatively pale-staining, lobate nucleus and cytoplasm containing coarse dark-staining granules of variable size and stainable by basic dyes. [NIH] 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] 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]

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Bladder: The organ that stores urine. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] 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] 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] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [EU] 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] Capsules: Hard or soft soluble containers used for the oral administration of medicine. [NIH] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, polyand heterosaccharides. [EU] Carcinogenic: Producing carcinoma. [EU] Cardiac: Having to do with the heart. [NIH] Cardiolipins: Acidic phospholipids composed of two molecules of phosphatidic acid covalently linked to a molecule of glycerol. They occur primarily in mitochondrial inner membranes and in bacterial plasma membranes. They are the main antigenic components of

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the Wassermann-type antigen that is used in nontreponemal syphilis serodiagnosis. [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] Catabolism: Any destructive metabolic process by which organisms convert substances into excreted compounds. [EU] Causal: Pertaining to a cause; directed against a cause. [EU] 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 Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [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 motility: The ability of a cell to move. [NIH] Cellulose: A polysaccharide with glucose units linked as in cellobiose. It is the chief constituent of plant fibers, cotton being the purest natural form of the substance. As a raw material, it forms the basis for many derivatives used in chromatography, ion exchange materials, explosives manufacturing, and pharmaceutical preparations. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Cerebrospinal: Pertaining to the brain and spinal cord. [EU] Cerebrospinal fluid: CSF. The fluid flowing around the brain and spinal cord. Cerebrospinal fluid is produced in the ventricles in the brain. [NIH] 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] 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] 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] Cholesterol Esters: Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] Chronic 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] Chylomicrons: A class of lipoproteins that carry dietary cholesterol and triglycerides from

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the small intestines to the tissues. [NIH] Clarithromycin: A semisynthetic macrolide antibiotic derived from erythromycin that is active against a variety of microorganisms. It can inhibit protein synthesis in bacteria by reversibly binding to the 50S ribosomal subunits. This inhibits the translocation of aminoacyl transfer-RNA and prevents peptide chain elongation. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient. [NIH]

Clinical 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] Codon: A set of three nucleotides in a protein coding sequence that specifies individual amino acids or a termination signal (codon, terminator). Most codons are universal, but some organisms do not produce the transfer RNAs (RNA, transfer) complementary to all codons. These codons are referred to as unassigned codons (codons, nonsense). [NIH] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Colchicine: A major alkaloid from Colchicum autumnale L. and found also in other Colchicum species. Its primary therapeutic use is in the treatment of gout, but it has been used also in the therapy of familial Mediterranean fever (periodic disease). [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] 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

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'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, 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] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue Diseases: A heterogeneous group of disorders, some hereditary, others acquired, characterized by abnormal structure or function of one or more of the elements of connective tissue, i.e., collagen, elastin, or the mucopolysaccharides. [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] Corn Oil: Oil from corn or corn plant. [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] Corpus: The body of the uterus. [NIH] Cortisone: A natural steroid hormone produced in the adrenal gland. It can also be made in

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the laboratory. Cortisone reduces swelling and can suppress immune responses. [NIH] Cutaneous: Having to do with the skin. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cyclophosphamide: Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the liver to form the active aldophosphamide. It is used in the treatment of lymphomas, leukemias, etc. Its side effect, alopecia, has been made use of in defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer. [NIH] 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] Data Collection: Systematic gathering of data for a particular purpose from various sources, including questionnaires, interviews, observation, existing records, and electronic devices. The process is usually preliminary to statistical analysis of the data. [NIH] 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] Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Dermal: Pertaining to or coming from the skin. [NIH] Dermatologist: A doctor who specializes in the diagnosis and treatment of skin problems. [NIH]

Diagnostic Imaging: Any visual display of structural or functional patterns of organs or tissues for diagnostic evaluation. It includes measuring physiologic and metabolic responses to physical and chemical stimuli, as well as ultramicroscopy. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Diastolic: Of or pertaining to the diastole. [EU] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] 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] 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] Duodenal Ulcer: An ulcer in the lining of the first part of the small intestine (duodenum). [NIH]

Duodenum: The first part of the small intestine. [NIH] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH]

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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] Elastin: The protein that gives flexibility to tissues. [NIH] Elective: Subject to the choice or decision of the patient or physician; applied to procedures that are advantageous to the patient but not urgent. [EU] Electrolytes: Substances that break up into ions (electrically charged particles) when they are dissolved in body fluids or water. Some examples are sodium, potassium, chloride, and calcium. Electrolytes are primarily responsible for the movement of nutrients into cells, and the movement of wastes out of cells. [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] Endemic: Present or usually prevalent in a population or geographical area at all times; said of a disease or agent. Called also endemial. [EU] Endocarditis: Exudative and proliferative inflammatory alterations of the endocardium, characterized by the presence of vegetations on the surface of the endocardium or in the endocardium itself, and most commonly involving a heart valve, but sometimes affecting the inner lining of the cardiac chambers or the endocardium elsewhere. It may occur as a primary disorder or as a complication of or in association with another disease. [EU] Endocardium: The innermost layer of the heart, comprised of endothelial cells. [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] Endoscopy: Endoscopic examination, therapy or surgery performed on interior parts of the body. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxins: Toxins closely associated with the living cytoplasm or cell wall of certain microorganisms, which do not readily diffuse into the culture medium, but are released upon lysis of the cells. [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] Enteritis: Inflammation of the intestine, applied chiefly to inflammation of the small intestine; see also enterocolitis. [EU] Enterocolitis: Inflammation of the intestinal mucosa of the small and large bowel. [NIH]

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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] Eosinophils: Granular leukocytes with a nucleus that usually has two lobes connected by a slender thread of chromatin, and cytoplasm containing coarse, round granules that are uniform in size and stainable by eosin. [NIH] Epidemic: Occurring suddenly in numbers clearly in excess of normal expectancy; said especially of infectious diseases but applied also to any disease, injury, or other healthrelated event occurring in such outbreaks. [EU] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermal: Pertaining to or resembling epidermis. Called also epidermic or epidermoid. [EU] Epidermal Growth Factor: A 6 kD polypeptide growth factor initially discovered in mouse submaxillary glands. Human epidermal growth factor was originally isolated from urine based on its ability to inhibit gastric secretion and called urogastrone. epidermal growth factor exerts a wide variety of biological effects including the promotion of proliferation and differentiation of mesenchymal and epithelial cells. [NIH] Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] 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] Epitopes: Sites on an antigen that interact with specific antibodies. [NIH] Erectile: The inability to get or maintain an erection for satisfactory sexual intercourse. Also called impotence. [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] Excrete: To get rid of waste from the body. [NIH] Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extrarenal: Outside of the kidney. [EU] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH]

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Fat: Total lipids including phospholipids. [NIH] Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three nonidentical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products. [NIH] Fibrinolysis: The natural enzymatic dissolution of fibrin. [NIH] Fibrinolytic: Pertaining to, characterized by, or causing the dissolution of fibrin by enzymatic action [EU] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibronectin: An adhesive glycoprotein. One form circulates in plasma, acting as an opsonin; another is a cell-surface protein which mediates cellular adhesive interactions. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Forearm: The part between the elbow and the wrist. [NIH] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gamma-interferon: Interferon produced by T-lymphocytes in response to various mitogens and antigens. Gamma interferon appears to have potent antineoplastic, immunoregulatory and antiviral activity. [NIH] Ganglion: 1. A knot, or knotlike mass. 2. A general term for a group of nerve cell bodies located outside the central nervous system; occasionally applied to certain nuclear groups within the brain or spinal cord, e.g. basal ganglia. 3. A benign cystic tumour occurring on a aponeurosis or tendon, as in the wrist or dorsum of the foot; it consists of a thin fibrous capsule enclosing a clear mucinous fluid. [EU] 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] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal Hemorrhage: Bleeding in the gastrointestinal tract. [NIH] Gastrointestinal tract: The stomach and intestines. [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] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]

Glomerular Filtration Rate: The volume of water filtered out of plasma through glomerular capillary walls into Bowman's capsules per unit of time. It is considered to be equivalent to inulin clearance. [NIH] Glomerular Mesangium: The thin membrane which helps to support the capillary loops in

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a renal glomerulus. It is connective tissue composed of mesangial cells - myofibroblasts phenotypically related to vascular smooth muscle cells (muscle, smooth, vascular), phagocytes, and the mesangial extracellular matrix. [NIH] Glomeruli: Plural of glomerulus. [NIH] Glomerulonephritis: Glomerular disease characterized by an inflammatory reaction, with leukocyte infiltration and cellular proliferation of the glomeruli, or that appears to be the result of immune glomerular injury. [NIH] Glomerulonephritis, Membranous: A disease of the glomerulus manifested clinically by proteinuria, and sometimes by other features of the nephrotic syndrome. It is histologically characterized by deposits in the glomerular capillary wall between the epithelial cell and the basement membrane and a thickening of the membrane. Also characteristic are outward projections of the membrane between the epithelial deposits in the form of "spikes". There is some agreement that the deposits are antigen-antibody complexes. [NIH] Glomerulus: A tiny set of looping blood vessels in the nephron where blood is filtered in the kidney. [NIH] Glucocorticoid: A compound that belongs to the family of compounds called corticosteroids (steroids). Glucocorticoids affect metabolism and have anti-inflammatory and immunosuppressive effects. They may be naturally produced (hormones) or synthetic (drugs). [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Glycosidic: Formed by elimination of water between the anomeric hydroxyl of one sugar and a hydroxyl of another sugar molecule. [NIH] Glycosylation: The chemical or biochemical addition of carbohydrate or glycosyl groups to other chemicals, especially peptides or proteins. Glycosyl transferases are used in this biochemical reaction. [NIH] Gonadal: Pertaining to a gonad. [EU] Gout: Hereditary metabolic disorder characterized by recurrent acute arthritis, hyperuricemia and deposition of sodium urate in and around the joints, sometimes with formation of uric acid calculi. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] 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] Haematoma: A localized collection of blood, usually clotted, in an organ, space, or tissue, due to a break in the wall of a blood vessel. [EU] Haemorrhage: The escape of blood from the vessels; bleeding. Small haemorrhages are classified according to size as petechiae (very small), purpura (up to 1 cm), and ecchymoses (larger). The massive accumulation of blood within a tissue is called a haematoma. [EU] Hematuria: Presence of blood in the urine. [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] Hemolytic: A disease that affects the blood and blood vessels. It destroys red blood cells,

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cells that cause the blood to clot, and the lining of blood vessels. HUS is often caused by the Escherichia coli bacterium in contaminated food. People with HUS may develop acute renal failure. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hemostasis: The process which spontaneously arrests the flow of blood from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements, and the process of blood or plasma coagulation. [NIH]

Hepatic: Refers to the liver. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatocyte: A liver cell. [NIH] Hepatocyte Growth Factor: Multifunctional growth factor which regulates both cell growth and cell motility. It exerts a strong mitogenic effect on hepatocytes and primary epithelial cells. Its receptor is proto-oncogene protein C-met. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Histocompatibility: The degree of antigenic similarity between the tissues of different individuals, which determines the acceptance or rejection of allografts. [NIH] Hormones: Chemical substances having a specific regulatory effect on the activity of a certain organ or organs. The term was originally applied to substances secreted by various endocrine glands and transported in the bloodstream to the target organs. It is sometimes extended to include those substances that are not produced by the endocrine glands but that have similar effects. [NIH] Humoral: Of, relating to, proceeding from, or involving a bodily humour - now often used of endocrine factors as opposed to neural or somatic. [EU] Humour: 1. A normal functioning fluid or semifluid of the body (as the blood, lymph or bile) especially of vertebrates. 2. A secretion that is itself an excitant of activity (as certain hormones). [EU] 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] 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] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxylysine: A hydroxylated derivative of the amino acid lysine that is present in certain collagens. [NIH]

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Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] 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] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hypnotic: A drug that acts to induce sleep. [EU] Idiopathic: Describes a disease of unknown cause. [NIH] Ileum: The lower end of the small intestine. [NIH] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]

Immune Sera: Serum that contains antibodies. It is obtained from an animal that has been immunized either by antigen injection or infection with microorganisms containing the antigen. [NIH] Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] 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] Immunoglobulin: A protein that acts as an antibody. [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunosuppressive: Describes the ability to lower immune system responses. [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 vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Infancy: The period of complete dependency prior to the acquisition of competence in walking, talking, and self-feeding. [NIH] Infantile: Pertaining to an infant or to infancy. [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,

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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]

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] Ingestion: Taking into the body by mouth [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] Intercellular Adhesion Molecule-1: A cell-surface ligand with a role in leukocyte adhesion and inflammation. Its production is induced by gamma-interferon and it is required for neutrophil migration into inflamed tissue. [NIH] Interferon: A biological response modifier (a substance that can improve the body's natural response to disease). Interferons interfere with the division of cancer cells and can slow tumor growth. There are several types of interferons, including interferon-alpha, -beta, and gamma. These substances are normally produced by the body. They are also made in the laboratory for use in treating cancer and other diseases. [NIH] Interferon-alpha: One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells when exposed to live or inactivated virus, double-stranded RNA, or bacterial products. It is the major interferon produced by virus-induced leukocyte cultures and, in addition to its pronounced antiviral activity, it causes activation of NK cells. [NIH] 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] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intestinal: Having to do with the intestines. [NIH] Intestinal Obstruction: Any impairment, arrest, or reversal of the normal flow of intestinal contents toward the anus. [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] 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]

Inulin: A starch found in the tubers and roots of many plants. Since it is hydrolyzable to fructose, it is classified as a fructosan. It has been used in physiologic investigation for determination of the rate of glomerular function. [NIH] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques.

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[EU]

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] 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] 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] Laminin: Large, noncollagenous glycoprotein with antigenic properties. It is localized in the basement membrane lamina lucida and functions to bind epithelial cells to the basement membrane. Evidence suggests that the protein plays a role in tumor invasion. [NIH] Lectin: A complex molecule that has both protein and sugars. Lectins are able to bind to the outside of a cell and cause biochemical changes in it. Lectins are made by both animals and plants. [NIH] Lesion: An area of abnormal tissue change. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Leukopenia: A condition in which the number of leukocytes (white blood cells) in the blood is reduced. [NIH] Lipid: Fat. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU] 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] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH]

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Low-density lipoprotein: Lipoprotein that contains most of the cholesterol in the blood. LDL carries cholesterol to the tissues of the body, including the arteries. A high level of LDL increases the risk of heart disease. LDL typically contains 60 to 70 percent of the total serum cholesterol and both are directly correlated with CHD risk. [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] 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] Lymphocyte: A white blood cell. Lymphocytes have a number of roles in the immune system, including the production of antibodies and other substances that fight infection and diseases. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells. [NIH] Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques. [NIH] Malignancy: A cancerous tumor that can invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant tumor: A tumor capable of metastasizing. [NIH] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Membranoproliferative: A disease that occurs primarily in children and young adults. Over time, inflammation leads to scarring in the glomeruli, causing proteinuria, hematuria, and sometimes chronic renal failure or end-stage renal disease. [NIH] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Mesenchymal: Refers to cells that develop into connective tissue, blood vessels, and lymphatic tissue. [NIH] Mesenteric: Pertaining to the mesentery : a membranous fold attaching various organs to the body wall. [EU] Mesentery: A layer of the peritoneum which attaches the abdominal viscera to the abdominal wall and conveys their blood vessels and nerves. [NIH] Methylprednisolone: (6 alpha,11 beta)-11,17,21-Trihydroxy-6-methylpregna-1,4-diene-3,2dione. A prednisolone derivative which has pharmacological actions similar to prednisolone. [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH]

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Mice Minute Virus: The type species of parvovirus prevalent in mouse colonies and found as a contaminant of many transplanted tumors or leukemias. [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] 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] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [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] Mitogen-Activated Protein Kinase Kinases: A serine-threonine protein kinase family whose members are components in protein kinase cascades activated by diverse stimuli. These MAPK kinases phosphorylate mitogen-activated protein kinases and are themselves phosphorylated by MAP kinase kinase kinases. JNK kinases (also known as SAPK kinases) are a subfamily. EC 2.7.10.- [NIH] Mitogen-Activated Protein Kinases: A superfamily of protein-serine-threonine kinases that are activated by diverse stimuli via protein kinase cascades. They are the final components of the cascades, activated by phosphorylation by mitogen-activated protein kinase kinases which in turn are activated by mitogen-activated protein kinase kinase kinases (MAP kinase kinase kinases). Families of these mitogen-activated protein kinases (MAPKs) include extracellular signal-regulated kinases (ERKs), stress-activated protein kinases (SAPKs) (also known as c-jun terminal kinases (JNKs)), and p38-mitogen-activated protein kinases. EC 2,7,1.- [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] Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecular mass: The sum of the atomic masses of all atoms in a molecule, based on a scale in which the atomic masses of hydrogen, carbon, nitrogen, and oxygen are 1, 12, 14, and 16, respectively. For example, the molecular mass of water, which has two atoms of hydrogen and one atom of oxygen, is 18 (i.e., 2 + 16). [NIH] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] 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] Mononuclear: A cell with one nucleus. [NIH] Mucosa: A mucous membrane, or tunica mucosa. [EU] Multiple Myeloma: A malignant tumor of plasma cells usually arising in the bone marrow;

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characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria, and anemia. [NIH] Multivariate Analysis: A set of techniques used when variation in several variables has to be studied simultaneously. In statistics, multivariate analysis is interpreted as any analytic method that allows simultaneous study of two or more dependent variables. [NIH] Muscle, Smooth, Vascular: The nonstriated, involuntary muscle tissue of blood vessels. [NIH]

Myeloma: Cancer that arises in plasma cells, a type of white blood cell. [NIH] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myositis: Inflammation of a voluntary muscle. [EU] 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] Neoplastic: Pertaining to or like a neoplasm (= any new and abnormal growth); pertaining to neoplasia (= the formation of a neoplasm). [EU] Nephritis: Inflammation of the kidney; a focal or diffuse proliferative or destructive process which may involve the glomerulus, tubule, or interstitial renal tissue. [EU] Nephrology: A subspecialty of internal medicine concerned with the anatomy, physiology, and pathology of the kidney. [NIH] Nephropathy: Disease of the kidneys. [EU] Nephrosis: Descriptive histopathologic term for renal disease without an inflammatory component. [NIH] Nephrotic: Pertaining to, resembling, or caused by nephrosis. [EU] Nephrotic Syndrome: Clinical association of heavy proteinuria, hypoalbuminemia, and generalized edema. [NIH] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH] 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] Neuropathy: A problem in any part of the nervous system except the brain and spinal cord. Neuropathies can be caused by infection, toxic substances, or disease. [NIH] Neutrophil: A type of white blood cell. [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]

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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] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [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] Orbit: One of the two cavities in the skull which contains an eyeball. Each eye is located in a bony socket or orbit. [NIH] Orbital: Pertaining to the orbit (= the bony cavity that contains the eyeball). [EU] 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] 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] Paroxysmal: Recurring in paroxysms (= spasms or seizures). [EU] Parvovirus: A genus of the family Parvoviridae, subfamily Parvovirinae, infecting a variety of vertebrates including humans. Parvoviruses are responsible for a number of important diseases but also can be non-pathogenic in certain hosts. The type species is mice minute virus. [NIH] Pathogen: Any disease-producing microorganism. [EU] Pathogenesis: The cellular events and reactions that occur in the development of disease. [NIH]

Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH] Patient Compliance: Voluntary cooperation of the patient in following a prescribed regimen. [NIH] Pelvis: The lower part of the abdomen, located between the hip bones. [NIH] Penis: The external reproductive organ of males. It is composed of a mass of erectile tissue enclosed in three cylindrical fibrous compartments. Two of the three compartments, the corpus cavernosa, are placed side-by-side along the upper part of the organ. The third compartment below, the corpus spongiosum, houses the urethra. [NIH] 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]

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Peripheral Neuropathy: Nerve damage, usually affecting the feet and legs; causing pain, numbness, or a tingling feeling. Also called "somatic neuropathy" or "distal sensory polyneuropathy." [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] 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] Petechiae: Pinpoint, unraised, round red spots under the skin caused by bleeding. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Phenotypes: An organism as observed, i. e. as judged by its visually perceptible characters resulting from the interaction of its genotype with the environment. [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] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] 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] Pilot study: The initial study examining a new method or treatment. [NIH] Plant Oils: Oils derived from plants or plant products. [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] 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] Plasmapheresis: Procedure whereby plasma is separated and extracted from anticoagulated whole blood and the red cells retransfused to the donor. Plasmapheresis is also employed for therapeutic use. [NIH] 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

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fibrin and quickly inactivated by antiplasmins. EC 3.4.21.7. [NIH] Plasminogen: Precursor of fibrinolysin (plasmin). It is a single-chain beta-globulin of molecular weight 80-90,000 found mostly in association with fibrinogen in plasma; plasminogen activators change it to fibrinolysin. It is used in wound debriding and has been investigated as a thrombolytic agent. [NIH] Plasminogen Activators: A heterogeneous group of proteolytic enzymes that convert plasminogen to plasmin. They are concentrated in the lysosomes of most cells and in the vascular endothelium, particularly in the vessels of the microcirculation. EC 3.4.21.-. [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] 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] Polyarteritis Nodosa: A form of necrotizing vasculitis involving small- and medium-sized arteries. The signs and symptoms result from infarction and scarring of the affected organ system. [NIH] Polymorphism: The occurrence together of two or more distinct forms in the same population. [NIH] Polypeptide: A peptide which on hydrolysis yields more than two amino acids; called tripeptides, tetrapeptides, etc. according to the number of amino acids contained. [EU] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Polyunsaturated fat: An unsaturated fat found in greatest amounts in foods derived from plants, including safflower, sunflower, corn, and soybean oils. [NIH] 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] 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] Prednisone: A synthetic anti-inflammatory glucocorticoid derived from cortisone. It is biologically inert and converted to prednisolone in the liver. [NIH] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] Prognostic factor: A situation or condition, or a characteristic of a patient, that can be used to estimate the chance of recovery from a disease, or the chance of the disease recurring (coming back). [NIH]

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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] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Prophylaxis: An attempt to prevent disease. [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] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein Kinase C: An enzyme that phosphorylates proteins on serine or threonine residues in the presence of physiological concentrations of calcium and membrane phospholipids. The additional presence of diacylglycerols markedly increases its sensitivity to both calcium and phospholipids. The sensitivity of the enzyme can also be increased by phorbol esters and it is believed that protein kinase C is the receptor protein of tumor-promoting phorbol esters. EC 2.7.1.-. [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] Protein-Serine-Threonine Kinases: A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors. EC 2.7.10. [NIH] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [NIH] Proteoglycans: Glycoproteins which have a very high polysaccharide content. [NIH] Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] 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

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pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]

Purpura: Purplish or brownish red discoloration, easily visible through the epidermis, caused by hemorrhage into the tissues. [NIH] Pyelonephritis: Inflammation of the kidney and its pelvis, beginning in the interstitium and rapidly extending to involve the tubules, glomeruli, and blood vessels; due to bacterial infection. [EU] 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] Random Allocation: A process involving chance used in therapeutic trials or other research endeavor for allocating experimental subjects, human or animal, between treatment and control groups, or among treatment groups. It may also apply to experiments on inanimate objects. [NIH] Randomization: Also called random allocation. Is allocation of individuals to groups, e.g., for experimental and control regimens, by chance. Within the limits of chance variation, random allocation should make the control and experimental groups similar at the start of an investigation and ensure that personal judgment and prejudices of the investigator do not influence allocation. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Randomized clinical trial: A study in which the participants are assigned by chance to separate groups that compare different treatments; neither the researchers nor the participants can choose which group. Using chance to assign people to groups means that the groups will be similar and that the treatments they receive can be compared objectively. At the time of the trial, it is not known which treatment is best. It is the patient's choice to be in a randomized trial. [NIH] Reactive Oxygen Species: Reactive intermediate oxygen species including both radicals and non-radicals. These substances are constantly formed in the human body and have been shown to kill bacteria and inactivate proteins, and have been implicated in a number of diseases. Scientific data exist that link the reactive oxygen species produced by inflammatory phagocytes to cancer development. [NIH] 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] Reconstitution: 1. A type of regeneration in which a new organ forms by the rearrangement of tissues rather than from new formation at an injured surface. 2. The restoration to original form of a substance previously altered for preservation and storage, as the restoration to a liquid state of blood serum or plasma that has been dried and stored. [EU] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH]

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Refer: To send or direct for treatment, aid, information, de decision. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [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] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [NIH] Retrospective: Looking back at events that have already taken place. [NIH] Retrovirus: A member of a group of RNA viruses, the RNA of which is copied during viral replication into DNA by reverse transcriptase. The viral DNA is then able to be integrated into the host chromosomal DNA. [NIH] Rheumatism: A group of disorders marked by inflammation or pain in the connective tissue structures of the body. These structures include bone, cartilage, and fat. [NIH] Rheumatoid: Resembling rheumatism. [EU] 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] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] 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] Scrotum: In males, the external sac that contains the testicles. [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] Segmental: Describing or pertaining to a structure which is repeated in similar form in successive segments of an organism, or which is undergoing segmentation. [NIH] Segmentation: The process by which muscles in the intestines move food and wastes through the body. [NIH] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as epilepsy or "seizure disorder." [NIH] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [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]

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Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [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]

Shunt: A surgically created diversion of fluid (e.g., blood or cerebrospinal fluid) from one area of the body to another area of the body. [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] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] 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]

Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Soybean Oil: Oil from soybean or soybean plant. [NIH] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] Sperm: The fecundating fluid of the male. [NIH] Spermatic: A cord-like structure formed by the vas deferens and the blood vessels, nerves and lymphatics of the testis. [NIH] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Stenosis: Narrowing or stricture of a duct or canal. [EU] Sterility: 1. The inability to produce offspring, i.e., the inability to conceive (female s.) or to induce conception (male s.). 2. The state of being aseptic, or free from microorganisms. [EU] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this

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group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] 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] Streptococcal: Caused by infection due to any species of streptococcus. [NIH] Streptococcus: A genus of gram-positive, coccoid bacteria whose organisms occur in pairs or chains. No endospores are produced. Many species exist as commensals or parasites on man or animals with some being highly pathogenic. A few species are saprophytes and occur in the natural environment. [NIH] 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] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH] Submaxillary: Four to six lymph glands, located between the lower jaw and the submandibular salivary gland. [NIH] 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] Supplementation: Adding nutrients to the diet. [NIH] Support group: A group of people with similar disease who meet to discuss how better to cope with their cancer and treatment. [NIH] Systemic: Affecting the entire body. [NIH] Systemic disease: Disease that affects the whole body. [NIH] Systemic lupus erythematosus: SLE. A chronic inflammatory connective tissue disease marked by skin rashes, joint pain and swelling, inflammation of the kidneys, inflammation of the fibrous tissue surrounding the heart (i.e., the pericardium), as well as other problems. 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] Terminalis: A groove on the lateral surface of the right atrium. [NIH] Testicles: The two egg-shaped glands found inside the scrotum. They produce sperm and male hormones. Also called testes. [NIH] Testicular: Pertaining to a testis. [EU] Testis: Either of the paired male reproductive glands that produce the male germ cells and the male hormones. [NIH] Thalidomide: A pharmaceutical agent originally introduced as a non-barbiturate hypnotic, but withdrawn from the market because of its known tetratogenic effects. It has been

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reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppresive and anti-angiogenic activity. It inhibits release of tumor necrosis factor alpha from monocytes, and modulates other cytokine action. [NIH] Thorax: A part of the trunk between the neck and the abdomen; the chest. [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] Thrombolytic: 1. Dissolving or splitting up a thrombus. 2. A thrombolytic agent. [EU] Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation. [NIH]

Thrombopenia: Reduction in the number of platelets in the blood. [NIH] Thromboses: The formation or presence of a blood clot within a blood vessel during life. [NIH]

Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thromboxanes: Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase. [NIH] Thrombus: An aggregation of blood factors, primarily platelets and fibrin with entrapment of cellular elements, frequently causing vascular obstruction at the point of its formation. Some authorities thus differentiate thrombus formation from simple coagulation or clot formation. [EU] Thymus: An organ that is part of the lymphatic system, in which T lymphocytes grow and multiply. The thymus is in the chest behind the breastbone. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Plasminogen Activator: A proteolytic enzyme in the serine protease family found in many tissues which converts plasminogen to plasmin. It has fibrin-binding activity and is immunologically different from urinary plasminogen activator. The primary sequence, composed of 527 amino acids, is identical in both the naturally occurring and synthetic proteases. EC 3.4.21.68. [NIH] Torsion: A twisting or rotation of a bodily part or member on its axis. [NIH] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] 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] Transcriptase: An enzyme which catalyses the synthesis of a complementary mRNA molecule from a DNA template in the presence of a mixture of the four ribonucleotides

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(ATP, UTP, GTP and CTP). [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transfer Factor: Factor derived from leukocyte lysates of immune donors which can transfer both local and systemic cellular immunity to nonimmune recipients. [NIH] Transferases: Transferases are enzymes transferring a group, for example, the methyl group or a glycosyl group, from one compound (generally regarded as donor) to another compound (generally regarded as acceptor). The classification is based on the scheme "donor:acceptor group transferase". (Enzyme Nomenclature, 1992) EC 2. [NIH] Translocation: The movement of material in solution inside the body of the plant. [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] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tuberculosis: Any of the infectious diseases of man and other animals caused by species of Mycobacterium. [NIH] 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] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH] 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] 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] Ureter: One of a pair of thick-walled tubes that transports urine from the kidney pelvis to the bladder. [NIH] Ureteritis: Inflammation of the ureter. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]

Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary Plasminogen Activator: A proteolytic enzyme that converts plasminogen to plasmin where the preferential cleavage is between arginine and valine. It was isolated originally from human urine, but is found in most tissues of most vertebrates. EC 3.4.21.73. [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] Vaccination: Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis. [NIH] Vaccines: Suspensions of killed or attenuated microorganisms (bacteria, viruses, fungi,

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protozoa, or rickettsiae), antigenic proteins derived from them, or synthetic constructs, administered for the prevention, amelioration, or treatment of infectious and other diseases. [NIH]

Varicella: Chicken pox. [EU] Vas Deferens: The excretory duct of the testes that carries spermatozoa. It rises from the scrotum and joins the seminal vesicles to form the ejaculatory duct. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasculitis: Inflammation of a blood vessel. [NIH] Vasodilators: Any nerve or agent which induces dilatation of the blood vessels. [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] 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] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] 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] 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]

X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] Zoster: A virus infection of the Gasserian ganglion and its nerve branches, characterized by discrete areas of vesiculation of the epithelium of the forehead, the nose, the eyelids, and the cornea together with subepithelial infiltration. [NIH]

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INDEX A Abdomen, 13, 49, 93, 97, 108, 109, 113, 114, 120, 121 Abdominal, 22, 35, 38, 87, 93, 110, 113, 114 Abdominal Pain, 22, 93 Aberrant, 7, 93 Abortion, 93, 95 Abscess, 45, 93 Acetylcholine, 93, 112 Acetylgalactosamine, 7, 93 Acute renal, 13, 93, 106 Adrenal Cortex, 93, 106, 115 Aetiology, 41, 93 Algorithms, 93, 96 Alkaloid, 93, 99 Allografts, 93, 106 Alopecia, 93, 101 Alternative medicine, 93 Amino acid, 94, 95, 99, 103, 106, 113, 115, 116, 118, 120, 121, 122 Amino Acid Sequence, 94 Ampulla, 94, 102 Anal, 94, 112 Anaphylatoxins, 94, 100 Anatomical, 94, 96, 107, 118 Anemia, 94, 112 Angiitis, 28, 94 Antibacterial, 94, 119 Antibiotic, 94, 99, 103, 119 Antibodies, 7, 8, 22, 23, 36, 49, 50, 64, 91, 94, 95, 96, 103, 106, 107, 110, 114 Antibodies, Anticardiolipin, 94, 95 Antibody, 7, 34, 59, 64, 65, 66, 91, 94, 95, 99, 107, 117, 119 Anticoagulant, 94, 95, 116 Antigen, 7, 9, 10, 43, 59, 64, 91, 94, 95, 98, 100, 103, 105, 107 Antigen-Antibody Complex, 95, 100, 105 Anti-inflammatory, 95, 105, 115 Anti-Inflammatory Agents, 95 Antineoplastic, 95, 101, 104 Antiphospholipid Syndrome, 43, 94, 95 Anus, 94, 95, 99, 108 Apolipoproteins, 95, 109 Apoptosis, 8, 51, 95 Appendicitis, 30, 95 Applicability, 9, 95 Arachidonic Acid, 51, 95, 116

Arginine, 94, 95, 112, 122 Arterial, 95, 98, 107, 116, 120 Arteries, 95, 97, 100, 110, 115, 121 Arterioles, 95, 97, 111 Artery, 95, 100, 102, 116 Ascites, 19, 95 Aspirin, 49, 95 Assay, 54, 96 Asymptomatic, 4, 96 Atmospheric Pressure, 96, 107 Atrium, 96, 120, 123 Attenuated, 6, 96, 122 Autoantibodies, 96 Autoantigens, 39, 96 Autoimmune disease, 6, 96 B Bacteria, 94, 96, 99, 102, 111, 117, 119, 120, 122 Bacterium, 96, 106 Barbiturate, 96, 120 Basement Membrane, 64, 96, 103, 105, 109 Basophils, 96, 109 Bilateral, 16, 52, 96 Bile, 96, 104, 106, 109, 120 Biochemical, 96, 105, 109 Biopsy, 5, 18, 21, 23, 65, 66, 89, 90, 96 Biosynthesis, 5, 6, 95, 96, 118 Biotechnology, 11, 73, 96 Bladder, 97, 122 Blood Coagulation, 97, 121 Blood Platelets, 97, 121 Blood pressure, 88, 89, 97, 107, 111 Blood vessel, 33, 97, 102, 105, 110, 112, 117, 119, 121, 123 Bone Marrow, 97, 107, 110, 111 Bowel, 12, 48, 51, 94, 97, 102, 108, 114 Bradykinin, 97, 112 Buccal, 97, 110 C Calcium, 97, 99, 102, 116 Capillary, 40, 97, 104, 105, 123 Capsules, 97, 104 Carbohydrate, 7, 97, 105, 115 Carcinogenic, 97, 120 Cardiac, 12, 16, 28, 97, 102, 112, 120 Cardiolipins, 95, 97 Case report, 14, 17, 29, 38, 47, 50, 54, 60, 98 Catabolism, 6, 98

126


Causal, 66, 98 Cell Death, 95, 98, 112 Cell Lineage, 10, 98 Cell motility, 98, 106 Cellulose, 98, 114 Central Nervous System, 38, 93, 98, 104 Cerebrospinal, 98, 119 Cerebrospinal fluid, 98, 119 Character, 10, 98, 101 Chemotactic Factors, 98, 100 Cholesterol, 96, 98, 109, 110, 120 Cholesterol Esters, 98, 109 Chromatin, 95, 98, 103 Chromosomal, 98, 118 Chromosome, 5, 98 Chronic, 4, 6, 12, 17, 28, 39, 49, 65, 66, 98, 99, 102, 108, 109, 110, 120 Chronic Disease, 98, 99 Chronic renal, 28, 98, 110 Chylomicrons, 98, 109 Clarithromycin, 29, 99 Clinical Medicine, 33, 99, 115 Clinical trial, 4, 9, 73, 99, 101, 117 Cloning, 96, 99 Codon, 42, 99 Cofactor, 99, 116, 121 Colchicine, 18, 49, 99 Colitis, 44, 99 Collagen, 64, 68, 94, 96, 99, 100, 104, 106, 115, 116 Collagen disease, 68, 99, 106 Colon, 99 Complement, 7, 19, 33, 39, 48, 50, 94, 99, 100 Complementary and alternative medicine, 59, 62, 100 Complementary medicine, 59, 100 Computational Biology, 73, 100 Connective Tissue, 78, 95, 97, 99, 100, 104, 105, 110, 118, 120 Connective Tissue Diseases, 95, 100 Consultation, 5, 100 Contraindications, ii, 100 Corn Oil, 6, 100 Cornea, 100, 123 Coronary, 100, 110 Coronary Thrombosis, 100, 110 Corpus, 100, 113, 115 Cortisone, 100, 115 Cutaneous, 20, 26, 28, 31, 33, 34, 56, 61, 101, 110 Cyclic, 101, 105, 112

Cyclophosphamide, 3, 52, 101 Cytokine, 8, 10, 101, 121 Cytoplasm, 95, 96, 101, 102, 103, 111 D Data Collection, 5, 101 Degenerative, 101, 106 Deletion, 21, 95, 101 Density, 101, 109 Dermal, 36, 56, 101 Dermatologist, 15, 101 Diagnostic Imaging, 18, 101 Diagnostic procedure, 63, 101 Diastolic, 101, 107 Digestion, 96, 97, 101, 108, 109, 120 Direct, iii, 9, 99, 101, 118 Discrete, 101, 123 Distal, 101, 114 Double-blind, 9, 101 Duodenal Ulcer, 24, 101 Duodenum, 96, 101, 102, 120 E Edema, 13, 88, 101, 112 Effector, 93, 99, 102 Efficacy, 3, 8, 102 Elastin, 99, 100, 102 Elective, 11, 102 Electrolytes, 96, 102, 109 Embolus, 102, 107 Embryo, 93, 98, 102 Endemic, 102, 119 Endocarditis, 31, 68, 102 Endocardium, 102 Endoscope, 102 Endoscopic, 24, 33, 102 Endoscopy, 18, 24, 26, 27, 33, 37, 102 Endothelial cell, 49, 50, 102, 121 Endothelium, 102, 112, 115 Endothelium-derived, 102, 112 Endotoxins, 100, 102 End-stage renal, 8, 9, 61, 67, 98, 102, 110 Enteritis, 18, 102 Enterocolitis, 102 Environmental Health, 72, 74, 103 Enzymatic, 94, 97, 100, 103, 104 Enzyme, 21, 102, 103, 105, 114, 116, 120, 121, 122, 123 Eosinophils, 103, 109 Epidemic, 103, 119 Epidemiological, 19, 103 Epidermal, 25, 103 Epidermal Growth Factor, 25, 103 Epidermis, 103, 117

127

Epithelial, 103, 105, 106, 109 Epithelial Cells, 103, 106, 109 Epithelium, 96, 102, 103, 123 Epitopes, 7, 103 Erectile, 103, 113 Erythromycin, 99, 103 Excrete, 103, 109 Extracellular, 8, 100, 103, 104, 105, 111 Extracellular Matrix, 8, 100, 103, 104, 105 Extracellular Space, 103 Extrarenal, 64, 103 F Family Planning, 73, 103 Fat, 95, 97, 102, 104, 109, 115, 118 Fibrinogen, 104, 115, 121 Fibrinolysis, 34, 104 Fibrinolytic, 34, 104 Fibroblasts, 104, 108 Fibronectin, 40, 48, 64, 104 Fibrosis, 104, 118 Fold, 104, 110 Forearm, 97, 104 G Gallbladder, 53, 93, 104 Gamma-interferon, 104, 108 Ganglion, 104, 123 Gas, 104, 106, 112 Gastric, 39, 103, 104 Gastrointestinal, 18, 21, 24, 26, 27, 33, 37, 42, 44, 64, 97, 104, 120 Gastrointestinal Hemorrhage, 37, 104 Gastrointestinal tract, 104 Gene, 6, 21, 34, 35, 42, 43, 96, 104, 113 Gene Expression, 6, 104 Genotype, 93, 104, 114 Glomerular, 4, 7, 8, 23, 48, 49, 64, 66, 67, 104, 105, 108, 109, 118 Glomerular Filtration Rate, 4, 104, 109 Glomerular Mesangium, 7, 8, 64, 104 Glomeruli, 105, 110, 117 Glomerulonephritis, 4, 5, 6, 7, 9, 10, 13, 15, 17, 21, 27, 44, 52, 60, 65, 67, 68, 105 Glomerulonephritis, Membranous, 67, 105 Glomerulus, 65, 104, 105, 112 Glucocorticoid, 105, 106, 115 Glycoprotein, 104, 105, 109, 121, 122 Glycosidic, 7, 105 Glycosylation, 5, 6, 7, 10, 12, 15, 105 Gonadal, 105, 120 Gout, 99, 105 Governing Board, 105, 115 Guanylate Cyclase, 105, 112

H Habitual, 98, 105 Haematoma, 14, 105 Haemorrhage, 13, 44, 93, 105 Hematuria, 4, 13, 66, 88, 105, 110 Hemodialysis, 105, 109 Hemolytic, 68, 105 Hemorrhage, 22, 26, 39, 44, 53, 65, 66, 106, 117 Hemostasis, 24, 106 Hepatic, 106, 109 Hepatitis, 29, 67, 106 Hepatocyte, 48, 106 Hepatocyte Growth Factor, 48, 106 Heredity, 104, 106 Histocompatibility, 38, 106 Hormones, 105, 106, 120 Humoral, 10, 106 Humour, 106 Hybridomas, 106, 108 Hydrocortisone, 34, 54, 106 Hydrogen, 97, 106, 111 Hydrophobic, 106, 109 Hydroxylysine, 99, 106 Hydroxyproline, 94, 99, 107 Hyperbaric, 60, 107 Hyperbaric oxygen, 60, 107 Hypersensitivity, 15, 19, 107, 118 Hypertension, 48, 107 Hypnotic, 96, 107, 120 I Idiopathic, 22, 33, 107 Ileum, 33, 107 Immune response, 9, 10, 94, 96, 101, 107, 120, 122, 123 Immune Sera, 107 Immune system, 9, 107, 110, 123 Immunization, 9, 10, 107 Immunoglobulin, 6, 11, 21, 25, 33, 34, 35, 39, 66, 94, 107 Immunologic, 98, 107 Immunosuppressive, 43, 101, 105, 107 Impairment, 107, 108 In vitro, 5, 8, 107 In vivo, 6, 107, 121 Infancy, 107 Infantile, 13, 34, 107 Infarction, 26, 40, 100, 107, 110, 115 Infection, 28, 29, 31, 32, 36, 40, 49, 51, 60, 68, 98, 107, 110, 112, 117, 118, 120, 123 Infiltration, 105, 108, 123

128


Inflammation, 3, 94, 95, 99, 102, 104, 106, 108, 110, 112, 115, 117, 118, 120, 122, 123 Ingestion, 6, 108 Insight, 43, 108 Intercellular Adhesion Molecule-1, 42, 108 Interferon, 26, 104, 108 Interferon-alpha, 108 Interleukin-6, 6, 108 Intermittent, 108, 114 Interstitial, 8, 13, 103, 108, 112, 118 Intestinal, 18, 26, 35, 60, 61, 102, 108 Intestinal Obstruction, 26, 108 Intestine, 97, 102, 108, 119 Intracellular, 107, 108, 112 Intravenous, 35, 54, 108 Intrinsic, 96, 108 Intussusception, 18, 35, 53, 108 Inulin, 104, 108 Invasive, 108, 110 K Kb, 72, 109 Kidney Failure, 68, 78, 102, 109 Kidney Failure, Acute, 109 Kidney Failure, Chronic, 109 L Labile, 99, 109 Laminin, 96, 109 Lectin, 7, 19, 109 Lesion, 31, 37, 89, 109, 122 Leukocytes, 65, 96, 97, 98, 103, 108, 109, 111, 122 Leukopenia, 38, 109 Lipid, 95, 109 Lipoprotein, 22, 109, 110 Liver, 44, 93, 95, 96, 101, 104, 106, 109, 115 Liver Cirrhosis, 44, 109 Localization, 7, 109 Localized, 93, 105, 107, 109, 114, 122 Low-density lipoprotein, 109, 110 Lupus, 78, 94, 95, 110, 120 Lymph, 38, 94, 102, 106, 110, 120 Lymphatic, 102, 108, 110, 121 Lymphocyte, 95, 110 Lymphoid, 9, 68, 94, 110 M Macrophage, 6, 110 Magnetic Resonance Imaging, 17, 110 Malignancy, 14, 68, 110 Malignant, 95, 110, 111 Malignant tumor, 110, 111 MEDLINE, 73, 110

Membrane, 39, 100, 104, 105, 109, 110, 111, 113, 114, 116 Membranoproliferative, 4, 17, 67, 110 Meninges, 98, 110 Mesenchymal, 103, 110 Mesenteric, 49, 110 Mesentery, 110, 114 Methylprednisolone, 49, 110 MI, 92, 110 Mice Minute Virus, 111, 113 Microcirculation, 109, 111, 115 Microorganism, 99, 111, 113, 123 Migration, 108, 111 Mitochondrial Swelling, 111, 112 Mitogen-Activated Protein Kinase Kinases, 111 Mitogen-Activated Protein Kinases, 6, 111 Mitosis, 95, 111 Molecular, 6, 7, 73, 75, 96, 100, 104, 111, 114, 115, 122 Molecular mass, 7, 111 Molecule, 52, 95, 97, 100, 102, 105, 109, 111, 117, 121 Monitor, 111, 113 Monocytes, 10, 108, 109, 111, 121 Mononuclear, 111, 122 Mucosa, 102, 110, 111 Multiple Myeloma, 34, 111 Multivariate Analysis, 46, 112 Muscle, Smooth, Vascular, 105, 112 Myeloma, 32, 60, 112 Myocardium, 110, 112 Myositis, 78, 112 N Necrosis, 52, 95, 107, 110, 112 Neoplastic, 106, 112 Nephrosis, 112 Nephrotic, 4, 33, 46, 67, 105, 112 Nephrotic Syndrome, 4, 33, 46, 67, 105, 112 Nerve, 104, 112, 114, 118, 123 Nervous System, 98, 112, 120 Neural, 106, 112 Neuropathy, 112, 114 Neutrophil, 22, 43, 50, 108, 112 Nitric Oxide, 36, 112 Nitrogen, 93, 101, 109, 111, 112, 122 Nuclear, 6, 104, 112, 113 Nuclei, 110, 111, 113 Nucleus, 95, 96, 98, 101, 103, 111, 113 O Oliguria, 109, 113

129

Oncogene, 106, 113 Orbit, 113 Orbital, 16, 113 Organelles, 101, 111, 113 P Pancreas, 93, 113 Paroxysmal, 15, 113 Parvovirus, 36, 41, 111, 113 Pathogen, 9, 10, 113 Pathogenesis, 5, 7, 8, 9, 10, 16, 47, 51, 113 Pathologic, 4, 95, 96, 100, 107, 113 Pathologic Processes, 95, 113 Patient Compliance, 9, 113 Pelvis, 93, 113, 117, 122 Penis, 30, 113 Peptide, 65, 66, 94, 99, 113, 115, 116 Peptide Chain Elongation, 99, 113 Peripheral Neuropathy, 16, 114 Peritoneal, 20, 95, 114 Peritoneal Cavity, 95, 114 Peritoneal Dialysis, 20, 114 Peritoneum, 110, 114 Petechiae, 45, 89, 105, 114 Pharmacologic, 114, 121 Phenotypes, 5, 114 Phospholipids, 95, 97, 104, 109, 114, 116 Phosphorylation, 111, 114, 116 Physiologic, 96, 101, 108, 114, 117 Physiology, 43, 112, 114 Pilot study, 8, 114 Plant Oils, 5, 114 Plants, 93, 108, 109, 114, 115, 118, 121 Plasma, 40, 42, 51, 60, 94, 97, 98, 104, 106, 109, 111, 112, 114, 115, 117 Plasma cells, 94, 111, 112, 114 Plasmapheresis, 17, 42, 114 Plasmin, 114, 115, 121, 122 Plasminogen, 52, 114, 115, 121, 122 Plasminogen Activators, 114, 115 Platelet Aggregation, 94, 112, 115, 121 Platelets, 112, 115, 121 Pneumonia, 36, 37, 100, 115 Polyarteritis Nodosa, 38, 42, 115 Polymorphism, 21, 34, 35, 42, 115 Polypeptide, 94, 99, 103, 104, 114, 115 Polysaccharide, 95, 98, 115, 116 Polyunsaturated fat, 5, 115, 121 Practice Guidelines, 74, 115 Precursor, 95, 101, 102, 103, 115, 122 Prednisolone, 110, 115 Prednisone, 5, 8, 23, 115 Progesterone, 115, 120

Prognostic factor, 46, 115 Progression, 6, 33, 116 Progressive, 42, 44, 68, 98, 109, 112, 116, 118 Proline, 99, 107, 116 Prophylaxis, 116, 122 Prostaglandins, 47, 51, 95, 116 Protease, 116, 121 Protein C, 94, 95, 99, 109, 116 Protein Kinase C, 111, 116 Protein S, 96, 99, 103, 116 Proteins, 26, 94, 95, 98, 99, 103, 105, 111, 112, 113, 114, 116, 117, 119, 121, 123 Protein-Serine-Threonine Kinases, 111, 116 Proteinuria, 4, 5, 20, 21, 23, 46, 66, 105, 110, 112, 116 Proteoglycans, 96, 116 Proteolytic, 99, 104, 114, 115, 116, 121, 122 Public Policy, 73, 116 Publishing, 11, 116 Pulmonary, 26, 29, 43, 44, 97, 109, 116, 123 Pulmonary Artery, 97, 116, 123 Pulmonary Edema, 109, 116 Pulse, 49, 111, 116 Pyelonephritis, 45, 117 R Radiation, 107, 117, 123 Radiation therapy, 107, 117 Radioactive, 106, 113, 117 Random Allocation, 117 Randomization, 5, 117 Randomized, 3, 9, 102, 117 Randomized clinical trial, 9, 117 Reactive Oxygen Species, 8, 117 Receptor, 21, 34, 49, 95, 106, 116, 117 Reconstitution, 10, 117 Red blood cells, 105, 117, 118 Refer, 1, 97, 99, 109, 118 Refraction, 118, 119 Refractory, 12, 50, 118 Regeneration, 117, 118 Regimen, 102, 113, 118 Renal failure, 6, 13, 22, 29, 61, 65, 66, 118 Retrospective, 50, 118 Retrovirus, 36, 118 Rheumatism, 14, 19, 29, 30, 50, 118 Rheumatoid, 46, 51, 99, 118 Rheumatoid arthritis, 46, 99, 118 S Saponins, 118, 120 Sclerosis, 8, 78, 99, 118

130


Screening, 99, 118 Scrotum, 14, 15, 118, 120, 123 Secretion, 103, 106, 118 Secretory, 7, 118 Segmental, 60, 118 Segmentation, 118 Seizures, 47, 113, 118 Semisynthetic, 99, 118 Serine, 111, 116, 118, 121 Serum, 7, 21, 33, 34, 35, 38, 48, 52, 94, 99, 107, 109, 110, 117, 119, 122 Shock, 106, 119, 122 Shunt, 68, 119 Side effect, 101, 119, 121 Signs and Symptoms, 115, 119 Skeletal, 112, 119 Small intestine, 99, 101, 102, 107, 108, 119 Smooth muscle, 94, 105, 119, 120 Somatic, 106, 111, 114, 119 Soybean Oil, 115, 119 Specialist, 79, 119 Species, 93, 99, 111, 113, 117, 119, 120, 122, 123 Specificity, 7, 8, 119 Spectrum, 50, 119 Sperm, 98, 119, 120 Spermatic, 12, 119 Spinal cord, 98, 104, 110, 112, 119 Sporadic, 5, 6, 119 Stenosis, 119, 120 Sterility, 101, 119 Steroid, 20, 22, 39, 100, 118, 119 Stomach, 93, 104, 114, 119, 120 Streptococcal, 28, 32, 51, 120 Streptococcus, 120 Stress, 89, 111, 118, 120 Stricture, 25, 48, 119, 120 Subacute, 31, 108, 120 Subclinical, 108, 118, 120 Subcutaneous, 49, 101, 120 Submaxillary, 103, 120 Substance P, 103, 117, 118, 120 Substrate, 64, 120 Supplementation, 5, 120 Support group, 91, 120 Systemic, 6, 7, 11, 21, 45, 52, 61, 68, 94, 95, 97, 99, 108, 115, 117, 120, 122 Systemic disease, 68, 120 Systemic lupus erythematosus, 11, 21, 52, 68, 94, 95, 99, 120 Systolic, 107, 120

T Terminalis, 33, 120 Testicles, 118, 120 Testicular, 25, 44, 120 Testis, 119, 120 Thalidomide, 12, 120 Thorax, 93, 121 Threshold, 107, 121 Thrombin, 104, 115, 116, 121 Thrombocytopenia, 16, 38, 121 Thrombolytic, 115, 121 Thrombomodulin, 49, 52, 116, 121 Thrombopenia, 95, 121 Thromboses, 95, 121 Thrombosis, 12, 116, 121 Thromboxanes, 95, 121 Thrombus, 100, 107, 115, 121 Thymus, 107, 110, 121 Tissue Plasminogen Activator, 52, 121 Torsion, 25, 107, 121 Toxic, iv, 112, 121 Toxicology, 74, 121 Toxins, 94, 102, 107, 121 Transcriptase, 118, 121 Transfection, 96, 122 Transfer Factor, 107, 122 Transferases, 105, 122 Translocation, 99, 103, 122 Transplantation, 12, 13, 16, 26, 31, 37, 38, 43, 44, 45, 47, 60, 78, 98, 107, 109, 122 Trauma, 112, 122 Tryptophan, 99, 122 Tuberculosis, 29, 54, 110, 122 Tumor Necrosis Factor, 21, 121, 122 U Ulcer, 101, 122 Ultrasonography, 47, 51, 53, 122 Uremia, 109, 118, 122 Ureter, 122 Ureteritis, 52, 122 Urethra, 113, 122 Urinary, 4, 48, 54, 113, 121, 122 Urinary Plasminogen Activator, 121, 122 Urine, 4, 5, 88, 90, 97, 103, 105, 109, 113, 116, 122 V Vaccination, 29, 122 Vaccines, 122, 123 Varicella, 15, 123 Vas Deferens, 119, 123 Vascular, 48, 54, 61, 64, 68, 102, 105, 107, 108, 109, 111, 112, 115, 121, 123

131

Vasculitis, 15, 16, 17, 19, 26, 28, 33, 34, 37, 38, 46, 49, 56, 61, 68, 78, 87, 94, 115, 123 Vasodilators, 112, 123 Vein, 50, 108, 113, 123 Venous, 95, 116, 123 Ventricle, 116, 117, 120, 123 Venules, 97, 111, 123 Veterinary Medicine, 73, 123 Viral, 9, 10, 118, 123 Virulence, 96, 123

Virus, 9, 10, 108, 123 Vitro, 8, 123 Vivo, 6, 123 W White blood cell, 94, 109, 110, 112, 114, 123 X X-ray, 90, 113, 117, 123 Z Zoster, 15, 123

132


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