DOCSLIB.ORG

Pituitary-Thyroid Relationships James A

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Pituitary-Thyroid Relationships James A Molecular and Cellular Endocrinology PRINCIPLES OF MEDICAL BIOLOGY A Multi-Volume Work, Volume 10A Editors: E. EDWARD BITTAR, Department of Physiology, University of Wisconsin, Madison NEVILLE BITTAR, Department of Medicine, University of Wisconsin, Madison This Page Intentionally Left Blank Principles of Medical Biology A Multi-Volume Work Edited by 15. Edward Bittar, Department of Physiology, University of Wisconsin, Madison and Neville Bittar, Department of Medicine, University of Wisconsin, Madison This work provides: * A holistic treatment of the main medical disciplines. The basic sci- ences including most of the achievements in cell and molecular biology have been blended with pathology and clinical medicine. Thus, a special feature is that departmental barriers have been overcome. * The subject matter covered in preclinical and clinical courses has been reduced by almost one-third without Sacrificing any of the essentials of a sound medical education. This information base thus represents an integrated core curriculum. * The movement towards reform in medical teaching calls for the adoption of an integrated core curriculum involving small-group teach- ing and the recognition of the student as an active learner. * There are increasing indications that the traditional education system in which the teacher plays the role of expert and the student that of a passive learner is undergoing reform in many medical schools. The trend can only grow. * Medical biology as the new profession has the power to simplify the problem of reductionism. * Over 700 internationally acclaimed medical scientists, pathologists, clinical investigators, clinicians and bioethicists are participants in this undertaking. This Page Intentionally Left Blank Molecular and Cellular Endocrinology Edited by E. EDWARD BITTAR Department of Physiology University of Wisconsin Madison, Wisconsin NEVILLE BITTAR Department of Medicine University of Wisconsin Madison, Wisconsin @ JAI PRESS INC. Greenwich, Connecticut London, England Library of Congress Cataloging-in-Publication Data Molecular and cellular endocrinology / edited by E. Edward Bittar, Neville Bittar. p. cm.- - (Principles of medical biology ; v. 10A, 10B) Includes bibliographical references and index. ISBN 1-55938-815-3 1. Molecular endocrinology. 2. Endocrine glands. 3. Hormones. I. Bittar, E. Edward. II. Bittar, Neville. III. Series. QP 187.3.M64M616 1997 616.4'07 - - dc21 97-41660 CIP Copyright 9 1997 by JAI PRESS INC. 55 Old Post Road, No. 2 Greenwich, Connecticut 06836 JAI PRESS LTD. 38 Tavistock Street Covent Garden London WC2E 7PB England All rights reserved. No part of this publication may be reproduced, stored on a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, filming, recording or otherwise without prior permission in writing from the publisher. ISBN." 1-55938-815-3 Library of Congress Catalog No.: 97-41660 Manufactured in the United States of America CONTENTS (Volume IOA) List of Contributors Preface E. Edward Bittar and Neville Bittar xvii Chapter 1 Endocrine Feedback Control in Health and Disease Terence J. Wilkin Chapter 2 Mechanisms of Negative and Positive Feedback of Steroids in the Hypothalamic-Pituitary System George Fink 29 Chapter 3 Corticotropin-Releasing Hormone Neurosecretory Cells: Regulation of Peptide Expression and Release Mark H. Whitnall 101 Chapter 4 Functional Morphology of Hypophysiotropic Hormone-Synthesizing Neurons: Identification, Connectivity, and Plasticity Istv~n Merchenthaler 119 Chapter 5 The Pineal Gland Russel J. Reiter 145 Chapter 6 Pituitary-Thyroid Relationships James A. Magner 165 .o VII viii CONTENTS Chapter 7 The Parathyroid Gland: Regulation of Production of Parathyroid Hormone Hitoshi Miki, Jonathan A. van Heerden, and Lorraine A. Fitzpatrick 191 Chapter 8 The Adrenal Medulla Stephen W. Carmichael 207 Chapter 9 The Adrenal Cortex Louisa Laue* and Gordon B. Cutler, Jr. 227 Chapter 10 Steroid Hormone and Related Receptors Hansj6rg Keller and Walter Wahli 255 Chapter 11 Enzyme Modulation of Access to Corticosteroid Receptors Brian R. Walker, Paul M. Stewart, and Christopher R. W. Edwards 297 Chapter 12 Control of Steroid Receptor Function and Gene Expression: The Glucocorticoid Receptor Jeffrey C. Webster and John A. Cidlowski 311 Chapter 13 Molecular Mechanisms of Thyroid Hormone Action Kelly D. Davis and Mitchell A. Lazar 321 * Deceased CONTENTS (Volume lOB) xiii List of Contributors Preface E. Edward Bittar and Neville Bittar xix Chapter 14 Insulin and the insulinlike Growth Factors in Health and Disease M. Adamo, C.T. Roberts, Jr., and D. LeRoith 339 Chapter 15 Molecular Mechanisms in the Pathophysiology of Noninsulin-Dependent Diabetes Mellitus: Insulin Resistance and Insulin Deficiency Simeon I. Taylor 365 Chapter 16 Glucagon: Molecular Biology and Structure-Activity Victor J. Hruby 387 Chapter 17 Somatostatin S.W.J. Lamberts, J-C. Reubi, and E.P. Krenning 403 Chapter 18 The Vasopressin-Oxytocin Systems of the Neurohypophysis Gareth Leng and Simon M. Luckman 421 Chapter 19 Prolactin Julian R.E. Davis 439 Chapter 20 Growth Hormone Jens Otto Lunde J1argensen 451 ix CONTENTS Chapter 21 Neuropeptide Y: Its Central and Peripheral Significance to Molecular and Cellular Endocrinology Janet M. Allen 467 Chapter 22 Natriuretic Peptides Rudolf E. Lang 485 Chapter 23 Natriuretic Hormone as a Circulating Inhibitor of Na§247 Branislav Lichardus and L~szl6 Kov~cs 501 Chapter 24 Vasoactive Intestinal Polypeptide Edwin E. Daniel and Jo-Ann E. T. Fox-Threlkeld 517 Chapter 25 The Mechanisms of Parathyroid Hormone Action Diarmuid S. O'Riordain and Lorraine A. Fitzpatrick 531 Chapter 26 The Endothelins William G. Haynes and David J. Webb 543 Chapter 27 Genetic Engineering in the Study of Hormones Michael Wallis 573 Chapter 28 Genetics and Cell Biology of Calcitonin Action Mone Zaidi, Baljit S. Moonga, Michael Pazianas, Vijai S. Shankar, and Christopher L.H. Huang 601 Chapter 29 The Genetics and Biology of Vitamin D Hector F. Deluca 617 Chapter 30 The Tissue Matrix: Cell Signaling and Hormone Regulation Robert H. Getzenberg 643 Index 663 LIST OF CONTRIBUTORS M. Adamo Department of Biochemistry University of Texas Health Science Center San Antonio, Texas Janet M. Allen Division of Biochemistry and Molecular Biology University of Glasgow Glasgow, Scotland Stephen W. Carmichael Department of Anatomy Mayo Clinic/Foundation Rochester, Minnesota John A. Cidlowski National Institute of Environmental Health Sciences National Institutes of Health Research Triangle Park, North Carolina Gordon B. Cutler, Jr. Child Health and Human Development National Institutes of Health Bethesda, Maryland Edwin E. Daniel Department of Biomedical Sciences McMaster University Hamilton, Ontario, Canada Julian R.E. Davis Department of Medicine University Of Manchester Manchester, England Kelly D. Davis Departments of Medicine and Genetics University of Pennsylvania School of Medicine Philadelphia, Pennsylvania xi oo XII LIST OF CONTRIBUTORS Hector F. DeLuca Department of Biochemistry University of Wisconsin Madison, Wisconsin Christopher R. W. Edwards Department of Medicine University of Edinburgh Edinburgh, Scotland George Fink Department of Pharmacology University of Edinburgh Edinburgh, Scotland Lorraine A. Fitzpatrick Departments of Internal Medicine and Surgery Mayo Clinic/Foundation Rochester, Minnesota Jo-Ann E.T. Fox-Threlkeld Department of Biomedical Sciences McMaster University Hamilton, Ontario, Canada Robert H. Getzenberg Pittsburgh Cancer Institute University of Pittsburgh Pittsburgh, Pennsylvania William G. Haynes Department of Medicine University of Edinburgh Edinburgh, Scotland Victor J. Hruby Department of Chemistry University of Arizona Tucson, Arizona Christopher L.H. Huang The Physiological Laboratory University of Cambridge Cambridge, England Jens Otto Lunde Je~rgensen Endocrinology and Diabetes Department Aarhus Kommunehospital Aarhus, Denmark List of Contributors xiii Hansj6rg Keller Institut de Biologie Animale Universit~ de Lausanne Lausanne, Switzerland L~szl6 Kov~cs Department of Pediatrics Comenius University Medical School Bratislava, Slovak Republic E.P. Krenning Departments of Medicine and Nuclear Medicine Erasmus University Rotterdam, The Netherlands S. W.J. Lamberts Departments of Medicine and Nuclear Medicine Erasmus University Rotterdam, The Netherlands Rudolf E. Lang Department of Physiology and Pathophysiology Philipps-Universit~t Marburg Marburg, Germany Louisa Laue* Georgetown University Children's Medical Center Washington, District of Columbia Mitchell A. Lazar Departments of Medicine and Genetics University of Pennsylvania School of Medicine Philadelphia, Pennsylvania Gareth Leng Department of Neurobioiogy The Babraham Institute Cambridge, England D. LeRoith Section on Molecular and Cellular Physiology-Diabetes Branch National Institutes of Health Bethesda, Maryland * Deceased xiv LIST OF CONTRIBUTORS Branislav Lichardus Institute of Experimental Endocrinology Siovak Academy of Sciences Bratislava, Slovak Republic Simon M. Luckman Department of Neurobiology The Babraham Institute Cambridge, England James A. Magner Bayer Corp. Pharmaceutical Division West Haven, Connecticut Hitoshi Miki Departments of Internal Medicine and Surgery Mayo Clinic/Foundation Rochester, Minnesota Istv~n Merchenthaler Women's Health Research Institute Wyeth-Ayerst Research Radnor, Pennsylvania Baljit S. Moonga VA Medical Center Philadelphia, Pennsylvania Diarmuid S. O'Riordain St. Vincent's Hospital Dublin, Ireland Michael
Load more

Recommended publications
  • Hyperthyroidism with an FSH- and TSH-Secreting Pituitary Adenoma
    • Hyperthyroidism with an FSH- and TSH-secreting pituitary adenoma JOHN BERMINGHAM, DO LOUIS C. HAENEL, DO A 34-year-old man was found noma is rare. The combined secretion of follicle- to have elevated thyroxine (T 4 ), triiodothy- stimulating hormone (FSH) and TSH by a pi- ronine (T3 ), calculated free T4 , thyroid- tuitary adenoma is rarer. But with current stimulating hormone (TSH), follicle-stimu- widespread use of TSH assays, plus the future lating hormone (FSH), and alpha subunits clinical availability of more sensitive TSH as- of TSH and FSH. A computed tomography says as well as TSH bioactivity testing, more scan of the head showed a 16-mm mac- patients will have pituitary-induced hyperthy- roadenoma of the pituitary gland. There roidism correctly diagnosed, and the disorder was no evidence of loss or excess secre- will be better understood. tion of other pituitary hormones. The large As illustrated in the following case study, chromophobe adenoma was removed via making the correct diagnosis of primary ver- a transphenoidal approach. The patient sus secondary hyperthyroidism is imperative has been taken off all medication. Thyroid because the treatment and potential conse- function has returned to normal and there quences of each of these diseases are totally has been no loss of pituitary secretory ca- different. pacity of other pituitary hormones. The oc- currence of a combined TSH- and FSH- Report of case secreting pituitary adenoma is rare; to the In August 1985, a 34-year-old man was seen with authors knowledge, only one case has complaints that were initially vague and nonspe- been documented in the literature.
    [Show full text]
  • A Case of Cushing Syndrome with Both Secondary Hypothyroidism and Hypercalcemia Due to Postoperative Adrenal Insufficiency
    Endocrine Journal 2004, 51 (1), 105–113 NOTE A Case of Cushing Syndrome with Both Secondary Hypothyroidism and Hypercalcemia Due to Postoperative Adrenal Insufficiency MASAHITO KATAHIRA, TSUTOMU YAMADA* AND MASAHIKO KAWAI* Department of Internal Medicine, Kyoritsu General Hospital, Nagoya 456-8611, Japan *Division of Endocrinology, Department of Internal Medicine, Okazaki City Hospital, Okazaki 444-8553, Japan Abstract. A 48-year-old woman was referred to our hospital because of secondary hypothyroidism. Upon admission a left adrenal tumor was also detected using computed tomography. Laboratory data and adrenal scintigraphy were compatible with Cushing syndrome due to the left adrenocortical adenoma, although she showed no response to the TRH stimulation test. Hypercortisolism resulting in secondary hypothyroidism was diagnosed. After a left adrenalectomy, hydrocortisone administration was begun and the dose was reduced gradually. After discharge on the 23rd postoperative day, she began to suffer from anorexia. ACTH level remained low, and serum cortisol, free thyroxine and TSH levels were within the normal range. Since her condition became worse, she was re-admitted on the 107th postoperative day at which time serum calcium level was high (15.6 mg/dl). Both ACTH response to the CRH stimulation test and TSH response to the TRH stimulation test were restored to almost normal levels, but there was no response of cortisol to CRH stimulation test. We diagnosed that the hypercalcemia was due to adrenal insufficiency. Although the serum calcium level decreased to normal after hydrocortisone was increased (35 mg/day), secondary hypothyroidism recurred. It was suggested that sufficient glucocorticoids suppressed TSH secretion mainly at the pituitary level, which resulted in secondary (corticogenic) hypothyroidism.
    [Show full text]
  • Clinical Research Protocol
    CLINICAL RESEARCH PROTOCOL NCT02399475 The Thyroid Axis in Older Individuals with Persistent Subclinical Hypothyroidism: a Mechanistic, Randomized, Double-Blind, Cross-Over Study of Levothyroxine and Liothyronine Administration Regulatory Sponsor: Anne R. Cappola, MD, ScM Division of Endocrinology, Diabetes, and Metabolism 12-136 Translational Research Center 3400 Civic Center Blvd, Bldg 421 Philadelphia, PA 19104-5160 (215) 573 5359 Funding Sponsor: National Institute on Aging, NIH Medications Used: Thyrotropin Releasing Hormone (TRH) Levothyroxine (LT4) Liothyronine (LT3) Protocol Number: 821564 IND Number: 125167 Initial version:[11/26/2014] Amended [7/22/2015] Amended: [12/18/2014] Amended [9/9/2015] Amended: [1/2/2015] Amended [8/25/2016] Amended: [3/26/2015] Amended [12/23/2016] Amended: [5/13/2015] Amended [3/24/2017] Amended: [06/04/2015] Amended [9/26/2017] Amended: [6/10/2015] Amended [12/18/2017] (additional next page) Amended [12/18/18] CONFIDENTIAL This material is the property of the University of Pennsylvania. Do not disclose or use except as authorized in writing by the study sponsor LT4 and LT3 in Subclinical Hypothyroidism Page ii Version 12/18/2018 Table of Contents STUDY SUMMARY ......................................................................................................... 1 1 INTRODUCTION ...................................................................................................... 3 1.1 BACKGROUND ....................................................................................................
    [Show full text]
  • Kaplan & Sadock's Study Guide and Self Examination Review In
    Kaplan & Sadock’s Study Guide and Self Examination Review in Psychiatry 8th Edition ← ↑ → © 2007 Lippincott Williams & Wilkins Philadelphia 530 Walnut Street, Philadelphia, PA 19106 USA, LWW.com 978-0-7817-8043-8 © 2007 by LIPPINCOTT WILLIAMS & WILKINS, a WOLTERS KLUWER BUSINESS 530 Walnut Street, Philadelphia, PA 19106 USA, LWW.com “Kaplan Sadock Psychiatry” with the pyramid logo is a trademark of Lippincott Williams & Wilkins. All rights reserved. This book is protected by copyright. No part of this book may be reproduced in any form or by any means, including photocopying, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this book prepared by individuals as part of their official duties as U.S. government employees are not covered by the above-mentioned copyright. Printed in the USA Library of Congress Cataloging-in-Publication Data Sadock, Benjamin J., 1933– Kaplan & Sadock’s study guide and self-examination review in psychiatry / Benjamin James Sadock, Virginia Alcott Sadock. —8th ed. p. cm. Includes bibliographical references and index. ISBN 978-0-7817-8043-8 (alk. paper) 1. Psychiatry—Examinations—Study guides. 2. Psychiatry—Examinations, questions, etc. I. Sadock, Virginia A. II. Title. III. Title: Kaplan and Sadock’s study guide and self-examination review in psychiatry. IV. Title: Study guide and self-examination review in psychiatry. RC454.K36 2007 616.890076—dc22 2007010764 Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices. However, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents of the publication.
    [Show full text]
  • Society for Endocrinology National Clinical Cases 2021
    Endocrine Abstracts June 2021 Volume 74 ISSN 1479-6848 (online) Society for Endocrinology National Clinical Cases 2021 22 June 2021, Online published by Online version available at bioscientifica www.endocrine-abstracts.org Volume 74 Endocrine Abstracts June 2021 Society for Endocrinology National Clinical Cases 2021 Tuesday 22 June 2021 Online Meeting Chairs Dr Anna Crown (Brighton) Dr Miles Levy (Leicester) Dr Annice Mukherjee (Manchester) Dr Michael O’Reilly (Dublin) Abstract Marking Panel Dr Kristien Boelart (Birmingham) Dr Karin Bradley (Bristol) Dr Simon Howell (Preston) Dr Andrew Lansdown (Cardiff) Dr Miles Levy (Leicester) Dr Daniel Morganstein (London) Dr Michael O’Reilly (Dublin) Professor Robert Semple (Edinburgh) Dr Peter Taylor (Cardiff) Dr Helen Turner (Oxford) Professor Bijay Vaidya (Exeter) Dr Nicola Zammitt (Edinburgh) Society for Endocrinology National Clinical Cases 2021 CONTENTS Society for Endocrinology National Clinical Cases 2021 Oral Communications ................................................. OC1–OC10 Highlighted Cases ................................................. NCC1–NCC71 AUTHOR INDEX Endocrine Abstracts (2021) Vol 74 Society for Endocrinology National Clinical Cases 2021 Oral Communications Endocrine Abstracts (2021) Vol 74 Society for Endocrinology National Clinical Cases 2021 OC1 lupus-anticoagulant. 5 days post-admission, in view of sudden onset lower A rare heterozygous IGFI variant causing postnatal growth failure and backache & worsening infection markers, repeat CT CAP was done which offering novel insights into IGF-I physiology revealed new bilateral adrenal haemorrhages. MRI adrenals revealed B/l adrenal 1 1 2 1 haemorrhages with fat stranding ,no underlying adrenal mass noted. Her 9am Emily Cottrell , Sumana Chatterjee , Vivian Hwa & Helen L. Storr ! 1 cortisol was 25, therefore she was started on IV hydrocortisone for acute Centre for Endocrinology, William Harvey Research Institute, Barts and adrenal insufficiency.
    [Show full text]
  • Central Hypothyroidism in Miniature Schnauzers
    J Vet Intern Med 2016;30:85–91 Central Hypothyroidism in Miniature Schnauzers Annemarie M.W.Y. Voorbij, Peter A.J. Leegwater, Jenny J.C.W.M. Buijtels, Sylvie Daminet, and Hans S. Kooistra Background: Primary hypothyroidism is a common endocrinopathy in dogs. In contrast, central hypothyroidism is rare in this species. Objectives: The objective of this article is to describe the occurrence and clinical presentation of central hypothyroidism in Miniature Schnauzers. Additionally, the possible role of the thyroid-stimulating hormone (TSH)-releasing hormone recep- tor (TRHR) gene and the TSHb (TSHB) gene was investigated. Animals: Miniature Schnauzers with proven central hypothyroidism, based on scintigraphy, and the results of a 3-day- TSH-stimulation test, or a TSH-releasing hormone (TRH)-stimulation test or both, presented to the Department of Clinical Sciences of Companion Animals at Utrecht University or the Department of Medicine and Clinical Biology of Small Animals at Ghent University from 2008 to 2012. Methods: Retrospective study. Pituitary function tests, thyroid scintigraphy, and computed tomography (CT) of the pitui- tary area were performed. Gene fragments of affected dogs and controls were amplified by polymerase chain reaction (PCR). Subsequently, the deoxyribonucleic acid (DNA) sequences of the products were analyzed. Results: Central hypothyroidism was diagnosed in 7 Miniature Schnauzers. Three dogs had disproportionate dwarfism and at least one of them had a combined deficiency of TSH and prolactin. No disease-causing mutations were found in the TSHB gene and the exons of the TRHR gene of these Schnauzers. Conclusions and clinical importance: Central hypothyroidism could be underdiagnosed in Miniature Schnauzers with hypothyroidism, especially in those of normal stature.
    [Show full text]
  • Hypothyroidism in Patients with Pseudohypoparathyroidism Type Ia
    European Journal of Endocrinology (2008) 159 431–437 ISSN 0804-4643 CLINICAL STUDY Hypothyroidism in patients with pseudohypoparathyroidism type Ia: clinical evidence of resistance to TSH and TRH Anne-Sophie Balavoine1, Miriam Ladsous1, Fritz-Line Velayoudom1, Virginie Vlaeminck1, Catherine Cardot-Bauters1, Miche`le d’Herbomez2 and Jean-Louis Wemeau1 1Clinique Endocrinologique Marc Linquette and 2Laboratoire de Me´decine Nucle´aire, CHU, 59037 Lille-Cedex, France (Correspondence should be addressed to A-S Balavoine who is now at Service d’Endocrinologie et Maladies Me´taboliques, Clinique Endocrinologique Marc Linquette, CHRU, 59037 Lille Cedex, France; Email: [email protected]) Abstract Objective: Hypothyroidism is a manifestation of multi-hormonal resistance in pseudohypoparathyroid- ism type Ia (PHP Ia). The objective of the study was to determine the mechanisms of hypothyroidism in PHP Ia. Design: A prospective study. Patients: Ten patients with PHP Ia. Measurements: The serum concentrations of TSH, free triiodothyronine (FT3), free thyroxine (FT4), and prolactin (PRL) were measured at baseline and after stimulation with TRH (200 mg i.v). Results: The median basal serum TSH concentration was 4.92 mU/l. Basal serum TSH concentration was slightly elevated in eight patients (4.22–7.0 mU/l; normal range, 0.4–3.6 mU/l), normal in one patient (2.5 mU/l), and high in one patient (13.1 mU/l). After the TRH test, TSH concentrations increased to 13.4–36.0 mU/l (normal range, 4.0–20.0 mU/l). The absolute values after the test were normal in three patients and high in seven patients. However, TSH responses relative to the baseline value (stimulated/basal TSH and expressed as a fold increase), which reflect the relative increases after TRH stimulation, were low in seven patients (2.3- to 4.3-fold TSH) and normal in three patients.
    [Show full text]
  • An Update on the Pathophysiology and Diagnosis of Inappropriate Secretion of Thyroid-Stimulating Hormone
    International Journal of Molecular Sciences Review An Update on the Pathophysiology and Diagnosis of Inappropriate Secretion of Thyroid-Stimulating Hormone Kenji Ohba 1,2 1 Medical Education Center, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka 431-3192, Japan; [email protected]; Tel./Fax: +81-53-435-2843 2 Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka 431-3192, Japan Abstract: Inappropriate secretion of thyroid-stimulating hormone (IST), also known as central hy- perthyroidism, is a clinical condition characterized by elevated free thyroxine and triiodothyronine concentrations concurrent with detectable thyroid-stimulating hormone (TSH) concentrations. Simi- larly, the term syndrome of IST (SITSH) is widely used in Japan to refer to a closely related condition; however, unlike that for IST, an elevated serum free triiodothyronine concentration is not a requisite criterion for SITSH diagnosis. IST or SITSH is an important indicator of resistance to thyroid hormone β (RTHβ) caused by germline mutations in genes encoding thyroid hormone receptor β (TRβ) and TSH-secreting pituitary adenoma. Recent evidence has accumulated for several conditions associated with IST, including RTH without mutations in the TRβ gene (non-TR-RTH), the phenomenon of hysteresis involving the hypothalamus-pituitary-thyroid axis (HPT-axis), methodological interfer- ence, and Cushing’s syndrome after surgical resection. However, little information is available on the systematic pathophysiological aspects of IST in previous review articles. This report presents an overview of the recent advances in our understanding of the etiological aspects of IST that are relevant for diagnosis and treatment.
    [Show full text]
  • Endocrine Test Selection and Interpretation
    The Quest Diagnostics Manual Endocrinology Test Selection and Interpretation Fourth Edition The Quest Diagnostics Manual Endocrinology Test Selection and Interpretation Fourth Edition Edited by: Delbert A. Fisher, MD Senior Science Officer Quest Diagnostics Nichols Institute Professor Emeritus, Pediatrics and Medicine UCLA School of Medicine Consulting Editors: Wael Salameh, MD, FACP Medical Director, Endocrinology/Metabolism Quest Diagnostics Nichols Institute San Juan Capistrano, CA Associate Clinical Professor of Medicine, David Geffen School of Medicine at UCLA Richard W. Furlanetto, MD, PhD Medical Director, Endocrinology/Metabolism Quest Diagnostics Nichols Institute Chantilly, VA ©2007 Quest Diagnostics Incorporated. All rights reserved. Fourth Edition Printed in the United States of America Quest, Quest Diagnostics, the associated logo, Nichols Institute, and all associated Quest Diagnostics marks are the trademarks of Quest Diagnostics. All third party marks − ®' and ™' − are the property of their respective owners. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, and information storage and retrieval system, without permission in writing from the publisher. Address inquiries to the Medical Information Department, Quest Diagnostics Nichols Institute, 33608 Ortega Highway, San Juan Capistrano, CA 92690-6130. Previous editions copyrighted in 1996, 1998, and 2004. Re-order # IG1984 Forward Quest Diagnostics Nichols Institute has been
    [Show full text]
  • NACB LMPG Thyroid Disease
    Volume 13/2002 The National Academy of Clinical Biochemistry Presents LABORATORY MEDICINE PRACTICE GUIDELINES LABORATORY SUPPORT FOR THE DIAGNOSIS OF THYROID DISEASE ARCHIVED NACB: Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease Laurence M. Demers, Ph.D., F.A.C.B.and Carole A. Spencer Ph.D., F.A.C.B. LABORATORY MEDICINE PRACTICE GUIDELINES Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease Table of Contents Section I. Foreword and Introduction Section 2. Pre-analytic factors Section 3. Thyroid Tests for the Laboratorian and Physician A. Total Thyroxine (TT4) and Total Triiodothyronine (TT3) methods B. Free Thyroxine (FT4) and Free Triiodothyronine (FT3) tests C. Thyrotropin/ Thyroid Stimulating Hormone (TSH) measurement D. Thyroid Autoantibodies: • Thyroid Peroxidase Antibodies (TPOAb) • Thyroglobulin Antibodies (TgAb) • Thyrotrophin Receptor Antibodies (TRAb) E. Thyroglobulin (Tg) Measurement F. Calcitonin (CT) and ret Proto-oncogene G. Urinary Iodide Measurement H. Thyroid Fine Needle Aspiration (FNA) and Cytology I. Screening for Congenital Hypothyroidism Section 4. The Importance of the Laboratory - Physician Interface Appendices and Glossary References Editors: Laurence M. Demers, Ph.D., F.A.C.B. Carole A. Spencer Ph.D., F.A.C.B. Guidelines Committee: The preparation of this revised monograph was achieved with the expert input of the editors, members of the guidelines committee, experts who submitted manuscripts for each section and many expert reviewers, who are listed in Appendix A. The material in this monograph represents the opinions of the editors and does not represent the official position of the National Academy of Clinical Biochemistry or any of the co-sponsoring organizations. The National Academy of Clinical Biochemistry is the official academy of the American Association of Clinical Chemistry.
    [Show full text]
  • TRH Stimulation Test in Patients with Repeatedly Elevated TSH
    ORIGINAL ARTICLE J Bras Patol Med Lab. 2020; 56: 1-4. TRH stimulation test in patients with repeatedly elevated TSH and normal FT4 Teste de estímulo com TRH em pacientes com TSH repetidamente elevado e T4L normal 10.5935/1676-2444.20200043 Pedro Weslley Rosario Santa Casa de Belo Horizonte, Minas Gerais, Brazil. ABSTRACT Subclinical hypothyroidism (SCH) is defined by elevated thyroid-stimulating hormone (TSH) with normal free thyroxine (FT4). We aimed to evaluate the thyrotropin-releasing hormone (TRH) stimulation test in patients with repeatedly elevated TSH (up to 10 mIU/l) and normal FT4, but without apparent thyroid disease. Women with TSH > 4.5 and ≤ 10 mIU/l (in two measurements) and normal FT4 were selected. Women with a known non-thyroid cause of TSH elevation, those treated with anti-thyroid drugs, amiodarone, lithium, and those with a history of thyroidectomy, neck radiotherapy and 131I treatment were excluded. Seventy women had negative antithyroperoxidase antibodies. Ultrasonography revealed a eutopic thyroid, usual echogenicity, and a volume ≤ 15 ml, and they underwent the TRH stimulation test during initial evaluation. After stimulation with TRH, TSH > 30 mIU/l was observed in 38 women (expected response), while 32 women had TSH < 20 mIU/l (inadequate response). Age, basal TSH or thyroid volume did not differ between both groups, but FT4 concentrations were significantly lower in the first group. Follow-up was available for 66/70 women. Seven women developed a need for levothyroxine, all of them in the group with an adequate response to TRH [7/36 (19.4%) versus 0/30]. The results suggest that some cases of TSH elevation (even persistent) do not represent the early stage of thyroid insufficiency.
    [Show full text]
  • Scientific Proceedings 2018 CVMA Convention
    Scientific Proceedings 2018 CVMA Convention Table of Contents THURSDAY, JULY 5, 2018. .................................................................................................................................................... 5 Business Management Track .............................................................................................................................................. 5 How to Train Your Millennial ................................................................................................................................................... 5 Show Me the Money! ................................................................................................................................................................ 7 Don’t Fear the Feedback .......................................................................................................................................................... 11 It’s All in the Family: Creating a Team Culture ...................................................................................................................... 15 Becoming a Loving Leader ..................................................................................................................................................... 17 FRIDAY, JULY 6, 2018. ......................................................................................................................................................... 22 Companion Animal: Dentistry ........................................................................................................................................
    [Show full text]