Parathyroid Disorders

Description

This book is devoted exclusively to hyper- and hypoparathyroidism with a focus on clinical practice guidelines explained by experts in the field. The clinical, genetic, biochemical, and pharmacological aspects of the most common parathyroid conditions are discussed comprehensively. The 15 chapters review the various forms of hyperparathyroidism and hypoparathyroidism and present data derived from widely diverse sources. New therapeutic approaches for chronic hypoparathyroidism continue to pique interest in parathyroid diseases and show that more research must be done to optimize care. The aim of this book is to serve as a practical guide to clinical management of common parathyroid conditions and to disseminate knowledge useful to the clinic, both for specialists and general practitioners. Also, under- and postgraduates, specialist nurses, and non-experts in the field will find this book to be a valuable source of current information.

Informations

• Publié par: S. Karger AG
• Date de parution: 19 novembre 2018
• Nombre de lectures: 0
• EAN13: 9783318064094
• Langue: English
• Poids de l'ouvrage: 2 Mo

Extrait

Parathyroid Disorders
Frontiers of Hormone Research
Vol. 51
Series Editor
Ezio Ghigo Turin
Co-Editor
Federica Guaraldi Bologna
 
Parathyroid Disorders
Focusing on Unmet Needs
Volume Editor
Maria Luisa Brandi Florence
12 figures, 5 in color, and 14 tables, 2019
Frontiers of Hormone Research Founded 1972 by Tj.B. van Wimersma Greidanus, Utrecht Continued by Ashley B. Grossman, Oxford (1996–2013)
_______________________ Maria Luisa Brandi, MD, PhD Bone Metabolic Diseases Unit, Department of Surgery and Translational Medicine University of Florence Florence (Italy)
Library of Congress Cataloging-in-Publication Data
Names: Brandi, M. L. (Maria Luisa), editor.
Title: Parathyroid disorders : focusing on unmet needs / volume editor, Maria Luisa Brandi.
Other titles: Frontiers of hormone research ; v. 51. 0301-3073
Description: Basel ; New York : Karger, 2019. | Series: Frontiers of hormone research, ISSN 0301-3073 ; vol. 51 | Includes bibliographical references and indexes.
Identifiers: LCCN 2018037624| ISBN 9783318064087 (hard cover : alk. paper) | ISBN 9783318064094 (e-book)
Subjects: | MESH: Hyperparathyroidism | Hypoparathyroidism | Hypercalcemia
Classification: LCC RC656.3 | NLM WK 300 | DDC 616.4/45--dc23 LC record available at
https://lccn.loc.gov/2018037624
Bibliographic Indices. This publication is listed in bibliographic services, including Current Contents ® and PubMed/MEDLINE.
Disclaimer. The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publisher and the editor(s). The appearance of advertisements in the book is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.
Drug Dosage. The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.
© Copyright 2019 by S. Karger AG, P.O. Box, CH–4009 Basel (Switzerland)
www.karger.com
Printed on acid-free and non-aging paper (ISO 9706)
ISSN 0301–3073
e-ISSN 1662–3762
ISBN 978–3–318–06408–7
e-ISBN 978–3–318–06409–4
 
Contents
Preface
Brandi, M.L. (Florence)
Primary Hyperparathyroidism
Masi, L. (Florence)
Asymptomatic Primary Hyperparathyroidism
Clarke, B.L. (Rochester, MN)
Normocalcemic Hyperparathyroidism
Corbetta, S. (Milan)
Familial and Hereditary Forms of Primary Hyperparathyroidism
Cetani, F.; Saponaro, F.; Borsari, S.; Marcocci, C. (Pisa)
Familial Hypocalciuric Hypercalcemia and Neonatal Severe Hyperparathyroidism
Vannucci, L.; Brandi, M.L. (Florence)
Parathyroid Carcinoma
Cetani, F.; Pardi, E.; Marcocci, C. (Pisa)
Nonparathyroid Hypercalcemia
Goltzman, D. (Montreal, QC)
Secondary and Tertiary Hyperparathyroidism
Messa, P.; Alfieri, C.M. (Milan)
Hypoparathyroidism
Hakami, Y.; Khan, A. (Hamilton, ON)
Classification of Hypoparathyroid Disorders
Cianferotti, L. (Florence)
Clinical Presentation of Hypoparathyroidism
Giusti, F.; Brandi, M.L. (Florence)
Inactivating PTH/PTHrP Signaling Disorders
Mantovani, G.; Elli, F.M. (Milan)
Conventional Treatment of Hypoparathyroidism
Marcucci, G.; Brandi, M.L. (Florence)
A New Era for Chronic Management of Hypoparathyroidism: Parathyroid Hormone Peptides
Marcucci, G.; Brandi, M.L. (Florence)
Author Index
Subject Index
Preface
Disorders of the function of parathyroid glands most commonly present with abnormalities of calcium homeostasis. The area of mineral metabolism was not receiving the same attention as diseases affecting other endocrine glands. This was due in part to the lack of targeted medical therapies both in hyperparathyroidism and in hypoparathyroidism. However, recent developments in the medical therapy of hypoparathyroidism has created a renewed interest in parathyroid disorders overall.
Clinical practice guidelines, which describe the consensus of experts in the field, are available for the management of hyperparathyroidism and hypoparathyroidism. Recognition of the need for more research to optimize care in parathyroid disorders has emerged in recent publications.
This book puts together the experiences of specialists in the field, as the demands placed upon a clinician’s time are both unrelenting and enormous. As a busy specialist in this field, I believe there is a genuine need for an up-to-date evidence-based overview that is practically oriented. The aim of this book is to serve as a practical guide to the clinical management of common parathyroid conditions.
The book will be relevant to specialists, general practitioners, undergraduates, postgraduates, and clinical nurse specialists. I am extremely grateful to the contributors who, as experts in their individual areas, have provided authority, experience, and invaluable insight. Finally, we would like to thank Karger for having the trust, determination, and encouragement to carry this project to fruition.
Maria Luisa Brandi , Florence
 
Brandi ML (ed): Parathyroid Disorders. Focusing on Unmet Needs. Front Horm Res. Basel, Karger, 2019, vol 51, pp 1–12 (DOI: 10.1159/000491034)
______________________
Primary Hyperparathyroidism
Laura Masi
Metabolic Bone Diseases Unit, University Hospital of Florence, AOU-Careggi, Florence, Italy
______________________
Abstract
The 4 parathyroid glands derive from the third and fourth pharyngeal pouches and descend caudally to the anterior neck. Through the secretion of parathyroid hormone (PTH), the parathyroid glands are primarily responsible for maintaining extracellular calcium and phosphorus concentrations. Hypercalcemia may be distinguished in parathyroid-hypercalcemia and nonparathyroid hypercalcemia. The most common disorders include primary hyperparathyroidism (PHPT), malignancy, granulomatous diseases, and medications. PHPT is a disease characterized by excessive secretion of PTH. PHPT is most commonly due to a single benign parathyroid adenoma (80%) and with multiglandular disease seen in approximately 15–20% of patients. PHPT is due to multiglandular involvement consisting of either multiple adenomas or hyperplasia of all 4 glands (5–10%), and very rarely parathyroid carcinoma (<1%). In most patients the disease is sporadic, without a personal or family history of PHPT. The genetic syndromes associated with PHPT include multiple endocrine neoplasia type 1 (MEN1), MEN2A, and MEN4, hyperparathyroidism-jaw tumor syndrome, familial isolated PHPT, familial hypocalciuric hypercalcemia, and neonatal severe hyperparathyroidism. The asymptomatic clinical presentation is most common in countries where biochemical screening is routine. Conversely, target organ involvement at presentation dominates the clinical landscape of PHPT in other countries, such as China and India, where biochemical screening is not routine practice.
© 2019 S. Karger AG, Basel
The 4 parathyroid glands derive from the third and fourth pharyngeal pouches and descend caudally to the anterior neck. They are embedded in the posterior thymus, with ectopic locations occurring as well. Through the secretion of parathyroid hormone (PTH), the parathyroid glands are primarily responsible for maintaining extracellular calcium and phosphorus concentrations. PTH has well-described effects on bone, kidney, and intestine, which play a role in controlling serum calcium phosphorus levels [ 1 ]. Hypercalcemia may be distinguished in parathyroid-hypercalcemia and nonparathyroid hypercalcemia. Parathyroid-hypercalcemia is characterized by an overproduction of PTH and causes pathological disorders as seen in primary, secondary, or tertiary hyperparathyroidism. Primary hyperparathyroidism (PHPT) is a disease characterized by excessive secretion of PTH. The increase of serum calcium is the biochemical hallmark of PHPT. It mainly affects women, with a female to male ratio of 3–4:1 [ 2 , 3 ]. A single benign parathyroid adenoma is the cause in most people. However, multiglandular disease is not rare and is typically seen in familial PHPT syndromes. The genetics of PHPT is usually monoclonal when a single gland is involved and polyclonal when multiglandular disease is present. The genes that have been implicated in PHPT include proto-oncogenes and tumor-suppressor genes [ 4 ]. Usually, the concentration of PTH is frankly increased but can remain within the normal range, which is abnormal in the setting of hypercalcemia. Normocal