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The Parathyroids - 3rd Edition - ISBN: 9780123971661, 9780123977908

The Parathyroids

3rd Edition

Basic and Clinical Concepts

Editors: John P. Bilezikian Robert Marcus Michael A. Levine Claudio Marcocci Shonni J Silverberg John Potts
Hardcover ISBN: 9780123971661
eBook ISBN: 9780123977908
Imprint: Academic Press
Published Date: 5th September 2014
Page Count: 946
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The third edition of The Parathyroids, led by a new stellar editorial team, has been thoroughly updated to reflect the considerable advances in just about every aspect of PTH biology over the past decade. It continues to be the authoritative reference that spans the basic science of parathyroid hormone treatment to major clinical disorders in a superb, single compendium. This translational resource is invaluable to graduate students, fellows, researchers, and research clinicians in the fields of endocrinology, bone biology, osteology, and rheumatology.

Key Features

  • Contains chapters and information on noninvasive imaging, fracture healing, secondary diseases such as CKD, Vitamin D, cell signaling pathways, vascular calcification, as well as advances in genetics/genomics
  • Includes essential updates on the critical importance of Vitamin D insufficiency and its relationship to secondary hyperparathyroidism
  • Offers new insights into the underlying mechanisms of parathyroid hormone actions on osteocytes and sclerostin
  • Examines essential updates in the understanding of secondary hyperparathyroidism associated with chronic kidney disease, facture healing, and vascular disease


Biomedical researchers, research clinicians, graduate students, and fellows in the fields of endocrinology, bone biology, osteology, and rheumatology.

Table of Contents

    <li>Preface to the Third Edition</li> <li>Preface to the Second Edition</li> <li>Preface to the First Edition</li> <li>Section I. Molecular, Cellular, and Physiologic Aspects of The Parathyroids<ul><li>Introduction. A History of the Parathyroid Glands and their Secretory Product, Parathyroid Hormone<ul><li>Prehistoric Development</li><li>Discovery of the Parathyroid Glands</li><li>Discovery of the Parathyroids&#x2019; Active Principle</li><li>The Search for Mechanisms of PTH Action</li><li>Modern Approaches to PTH Structure and Function</li><li>Primary Hyperparathyroidism&#x2014;A New Disease</li><li>Humoral Hypercalcemia of Malignancy and the Discovery of Parathyroid Hormone-Related Protein (PTH<span class="smallcaps">R</i>P)</li><li>Rediscovery of the Anabolic Effect of PTH</li><li>PTH: A Treatment for Osteoporosis</li><li>Conclusion</li></ul></li><li>Chapter 1. Parathyroids<ul><li>Introduction</li><li>Embryology</li><li>Anatomy and Histology</li><li>Hyperparathyroidism</li><li>Familial Hyperparathyroidism</li><li>Unusual Lesions of the Parathyroid</li><li>Intraoperative Assessment of Parathyroid&#x2014;Old and New</li><li>Special Studies and the Parathyroid</li><li>Humoral Hypercalcemia of Malignancy</li><li>Hypoparathyroidism</li></ul></li><li>Chapter 2. Parathyroid Hormone Gene<ul><li>Introduction</li><li>preproPTH</li><li>Gene Structure</li><li>Evolution</li><li>Regulation</li></ul></li><li>Chapter 3. Parathyroid Hormone-related Protein<ul><li>Introduction</li><li>Isolation and Cloning of PTHrP</li><li>Gene Structure</li><li>Transcriptional Regulation and mRNA Splicing</li><li>Protein Structure and Posttranslational Processing</li><li>Nuclear Import and Intracrine Function of PTHrP</li><li>Tissue Distribution and Paracrine Function</li><li>Conclusion</li></ul></li><li>Chapter 4. Interactions of PTH with Receptors and Signaling<ul><li>Introduction</li><li>Parathyroid Hormone&#x2014;Ligand Determinants of Biological Activity</li><li>The PTHR1 Cloning, Gene Characterization, and Evolution</li><li>Structural Features of the PTHR1 and Mode of Ligand Binding</li><li>Ligand Interactions to the Receptor&#x2019;s N-Terminal Extracellular Domain (ECD)</li><li>The PTHR1 Transmembrane Domain (TMD) Region, Structure, and Mode of Action</li><li>Mechanisms of Signaling Transduction and Signal Regulation</li><li>Mechanism of Conformational Change and Prolonged Signaling at the PTHR1</li><li>Small Molecule Ligands for the PTHR</li></ul></li><li>Chapter 5. Interactions of PTHrP with Receptors and Signaling<ul><li>Introduction</li><li>Structures of the PTHrP Gene, <span class="smallcaps">M</i>RNA, and Peptides</li><li>N-terminal PTH<span class="smallcaps">R</i>P and Receptors</li><li>Mid-Molecular PTHrP and Receptors</li><li>Nuclear/Nucleolar PTHrP and its Receptors</li><li>C-terminal PTHrP and its Receptors</li><li>Conclusions</li></ul></li><li>Chapter 6. Control of Parathyroid Hormone Secretion by its Key Physiological Regulators<ul><li>Introduction</li><li>Importance of PTH in Maintaining Mineral Ion Homeostasis <i>in Vivo</i></li><li>General Mechanisms Determining the Overall Rate of PTH Secretion</li><li>Cellular and Molecular Mechanisms by which Cao2+ Regulates the Various Aspects of Parathyroid Function Determining the Overall Rate of PTH Release</li><li>Regulation of Overall Parathyroid Function by 1,25(OH)<sub>2</sub>D<sub>3</sub></li><li>Regulation of Overall Parathyroid Secretory Function by Phosphate</li><li>Effects of FGF23 on Overall Parathyroid Function</li><li>Conclusions</li></ul></li><li>Chapter 7. Molecular Actions of Parathyroid Hormone<ul><li>Introduction</li><li>PTH Signal Transduction</li><li>PTH Regulation of Gene Transcription</li><li>Control of Cell Proliferation and Survival by PTH</li><li>Regulation of Ion Transport By PTH</li></ul></li><li>Chapter 8. Cellular Actions of PTH<ul><li>Introduction</li><li>Cellular Actions of PTH on Bone</li><li>Conclusion</li></ul></li><li>Chapter 9. Physiologic Actions of PTH I<ul><li>Introduction</li><li>Physiologic, Pharmacologic, and Pathologic Interactions of PTH with the Skeleton</li><li>Molecular and Cellular Mechanisms of Action</li><li>Contributions to Modeling and Remodeling of the Skeleton</li><li>Summary</li></ul></li><li>Chapter 10. Physiological Actions of PTH II<ul><li>Introduction</li><li>Nephron Sites of PTH Action</li><li>PTH Actions on Ion Transport</li><li>PTH Effects on Metabolism</li><li>PTH Metabolism by the Kidney</li></ul></li><li>Chapter 11. Physiological Actions of PTH and PTHrP III<ul><li>Endochondral Bone Formation</li><li>The PTHrP&#x2014;Indian Hedgehog Pathway in the Growth Plate</li><li>Actions of PTHrP During Bone Development</li><li>Actions of Indian Hedgehog During Bone Development</li><li>Roles of Ihh, PTHrP, and PTHR1 in the Postnatal Skeleton</li><li>Conclusion</li></ul></li><li>Chapter 12. Physiological Actions of PTH and PTHrP IV<ul><li>Introduction</li><li>PTH/PTHrP Biology in Cardiovascular Development</li><li>PTHR Signaling in Arterial Biology: Vascular Smooth Muscle Cell and Endothelial Responses to PTH and PTHrP</li><li>TIP39 in Vascular Pharmacology and Potential Contributions of CNS TIP39 and PTHrP to Cardiovascular Medicine</li><li>Impact of Hyperparathyroidism on Cardiovascular Mortality, Coronary Flow Reserve, and Vascular Stiffness: An Emerging Concern in Cardiovascular Endocrinology</li><li>Secondary Hyperparathyroidism of Chronic Kidney Disease (CKD); The Metabolic &#x201C;Perfect Storm&#x201D; of Cardiovascular Risk</li><li>Impact of PTH and Hyperparathyroidism on Calcific Aortic Valve Disease (CAVD): A Sclerotic Conundrum</li><li>Chronic PTH1R Activation and the Renin&#x2013;Angiotensin&#x2013;Aldosterone (RAA) Axis in Cardiovascular Disease: A Feed-Forward Vicious Cycle</li><li>PTH/PTHrP Signaling and the Bone&#x2013;Vascular Axis</li><li>Conclusions and Future Directions</li></ul></li><li>Chapter 13. Physiological Actions of Parathyroid Hormone (PTH) and PTH-related Protein<ul><li>Introduction</li><li>Skin</li><li>Mammary Gland</li><li>Reproductive Tissues</li><li>Endocrine Pancreas</li><li>Conclusion</li></ul></li><li>Chapter 14. PTH and T-cell Biology<ul><li>Effects of PTH in Bone</li><li>T-Cell Subsets and their Role in Bone Homeostasis</li><li>T cells and PTH-Induced Bone Loss</li><li>Role of T cells in the Anabolic Activity of Intermittent PTH Treatment</li><li>Role of T cells on the Expansion of HSCs Induced by PTH</li><li>Conclusions</li></ul></li><li>Chapter 15. Anabolic and Catabolic Pathways of Parathyroid Hormone on the Skeleton<ul><li>Introduction</li><li>PTH Signaling</li><li>Actions of PTH that Contribute to Increased Bone Resorption: Catabolic</li><li>Actions of PTH Contributing to Increased Bone Formation: Anabolic</li><li>Gene Profile in Catabolic and Anabolic PTH Regimes</li><li>The Role of T Cells on the Anabolic and Catabolic Actions of PTH</li><li>The Influence of Bone Resorption on PTH-Induced Bone Anabolism</li><li>Summary</li></ul></li><li>Chapter 16. Metabolism and Measurement of Parathyroid Hormone<ul><li>The Circulating Parathyroid Hormone (PTH) Paradox</li><li>First-Generation PTH Assays: Circulating PTH Immunoheterogeneity</li><li>Second-Generation PTH Assays: Immunoradiometric (IRMA) Assays</li><li>Third-Generation PTH Assay: Improved IRMA</li><li>Origin of Circulating PTH Molecular Forms</li><li>Regulation of Circulating PTH Molecular Forms</li><li>Molecular Forms of PTH Associated with Specific Clinical Conditions</li><li>Conclusion</li></ul></li></ul></li> <li>Section II. Clinical Aspects of Primary Hyperparathyroidism<ul><li>Chapter 17. Parathyroid Growth<ul><li>Introduction and Background</li><li>Abnormal Parathyroid Growth</li><li>Integration of Parathyroid Growth and Hormone Secretion</li></ul></li><li>Chapter 18. Molecular Basis of Primary Hyperparathyroidism<ul><li>Introduction</li><li>Clonality of Parathyroid Tumors</li><li>Specific Genetic Abnormalities in Benign Parathyroid Tumors</li><li>Other Genetic Abnormalities in Sporadic Parathyroid Tumors</li><li>Molecular Pathogenesis of Parathyroid Carcinoma</li><li>Epigenetics and Gene Expression Alterations in Sporadic Parathyroid Adenomas</li><li>Ectopic Secretion of PTH</li><li>Summary</li></ul></li><li>Chapter 19. Epidemiology of Primary Hyperparathyroidism<ul><li>Introduction</li><li>Incidence and Prevalence</li><li>Special Population Considerations in Sporadic Primary Hyperparathyroidism</li><li>Clinical Features</li><li>Mortality</li><li>Cost of Primary Hyperparathyroidism</li><li>Summary and Conclusion</li></ul></li><li>Chapter 20. Clinical Presentation of Primary Hyperparathyroidism<ul><li>Introduction</li><li>Presentation in The United States</li><li>Presentation in Europe</li><li>Presentation in Latin America</li><li>Presentation in Asia</li><li>Bone Disease in Primary Hyperparathyroidism</li><li>Nephrolithiasis in Primary Hyperparathyroidism</li><li>Non-Classical Manifestations of Primary Hyperparathyroidism</li><li>Diagnosis of Primary Hyperparathyroidism</li></ul></li><li>Chapter 21. Asymptomatic Primary Hyperparathyroidism<ul><li>Introduction</li><li>Incidence and Pathogenesis of Primary Hyperthyroidism</li><li>Clinical Presentation of Primary Hyperparathyroidism: Then and Now</li><li>Diagnosis and Biochemical Characterization of Asymptomatic Primary Hyperparathyroidism</li><li>Classical Organ Involvement in Asymptomatic Primary Hyperparathyroidism</li><li>Non-Classical Organ Involvement in Asymptomatic PHPT</li><li>Primary Hyperparathyroidism: Yesterday, Today, and Tomorrow</li></ul></li><li>Chapter 22. Normocalcemic PHPT<ul><li>Introduction</li><li>Pathophysiology</li><li>Diagnosis</li><li>Epidemiology</li><li>Clinical Presentation</li><li>Natural History</li><li>Management</li><li>Summary and Conclusions</li></ul></li><li>Chapter 23. Familial and Hereditary Forms of Primary Hyperparathyroidism<ul><li>Introduction</li><li>Syndromic Forms of PHPT</li><li>Non-Syndromic (Isolated) Forms of PHPT</li><li>Gene Testing in Clinical Practice for PHPT Patients</li><li>Conclusions</li></ul></li><li>Chapter 24. Familial Hypocalciuric Hypercalcemia and Neonatal Severe Hyperparathyroidism<ul><li>Historical Perspective and Nomenclature</li><li>Clinical Characteristics of FHH</li><li>Laboratory and Dynamic Studies in FHH</li><li>Genetics and Molecular Genetics of FHH</li><li>Genotype&#x2013;Phenotype Associations</li><li>Diagnosis and Management of FHH</li><li>Clinical Characteristics of Neonatal Hyperparathyroidism</li><li>Genetics and Molecular Genetics of Neonatal Hyperparathyroidism, Including Neonatal Severe Hyperparathyrodism</li><li>Diagnosis and Management of NHPT and NSHPT</li><li>Conclusions</li></ul></li><li>Chapter 25. Primary Hyperparathyroidism in Children and Adolescents<ul><li>Introduction</li><li>Etiology of Pediatric Primary Hyperparathyroidism</li><li>Pathology</li><li>Clinical Features and Complications</li><li>Ascertainment and Diagnosis</li><li>Management and Outcome</li><li>Outcomes</li><li>Summary</li></ul></li><li>Chapter 26. Acute Primary Hyperparathyroidism<ul><li>Acute Primary Hyperparathyroidism</li><li>Risk of Developing Acute Primary Hyperparathyroidism</li><li>Demographics</li><li>Laboratory Evaluation</li><li>Target Organ Manifestations</li><li>Pathology</li><li>Pathophysiology</li><li>Acute Parathyroid Crisis Associated with Pregnancy</li><li>Other Associations with Acute Primary Hyperparathyroidism</li><li>Animal Models of Acute Primary Hyperparathyroidism</li><li>Treatment</li><li>Outcomes</li><li>Summary</li></ul></li><li>Chapter 27. Parathyroid Carcinoma<ul><li>Introduction</li><li>Epidemiology</li><li>Etiology</li><li>Pathogenesis</li><li>Pathology</li><li>Clinical Features</li><li>Imaging Studies</li><li>Natural History and Surveillance</li><li>Management</li><li>Management of Hypercalcemia</li><li>Prognosis</li><li>Closing Remarks</li></ul></li><li>Chapter 28. Bone Turnover Markers in Primary Hyperparathyroidism<ul><li>Introduction</li><li>Bone Turnover Markers</li><li>Management of PHPT and Effects on Bone Turnover Markers</li><li>Conclusion</li></ul></li><li>Chapter 29. Bone Histomorphometry and Bone Quality in Primary Hyperparathyroidism<ul><li>Introduction</li><li>Bone Histomorphometry: Static and Dynamic Indices</li><li>Bone Turnover in Primary Hyperparathyroidism</li><li>Bone Mass in Primary Hyperparathyroidism</li><li>Bone Structure in Primary Hyperparathyroidism</li><li>Mechanism of Maintenance of Cancellous Bone Volume and Structure at the Iliac Crest</li><li>Effects of Parathyroidectomy on Bone Structure and Remodeling Activity in the Iliac Crest</li><li>Effects of Primary Hyperparathyroidism on Material Properties of Bone Matrix</li><li>Conclusion</li></ul></li><li>Chapter 30. Skeletal Imaging in Primary Hyperparathyroidism<ul><li>Introduction</li><li>Dual-Energy X-Ray Absorptiometry</li><li>High-Resolution Peripheral Quantitative Computed Tomography (HRpQCT)</li><li>Trabecular Bone Score</li><li>Conclusion</li></ul></li><li>Chapter 31. Primary Hyperparathyroidism and the Kidney<ul><li>Introduction</li><li>Co-Evolution of the Parathyroid Gland and Kidney: from Water to Land</li><li>Renal Calcium Reabsorption</li><li>Clinical Assessment of Calcium Processing by the Kidney</li><li>Renal Phosphate Reabsorption</li><li>Clinical Assessment of Phosphate Processing by the Kidney</li><li>Renal Bicarbonate Reabsorption</li><li>Renal Production of 1,25-Dihydroxyvitamin D</li><li>Role of Kidney in Setting the Serum Level of Calcium and Phosphate in PHPT</li><li>Effect of Renal Failure and Drugs Acting on the Kidney</li><li>Effect of Treatment of PHPT on the Kidney</li><li>Urinary Stone Disease</li><li>Nephrocalcinosis</li></ul></li><li>Chapter 32. Non-traditional Manifestations of Primary Hyperparathyroidism<ul><li>Introduction</li><li>Psychological and Cognitive Symptoms and Quality of Life</li><li>Cardiovascular Disease</li><li>Rheumatic Disease</li><li>Gastrointenstinal Disease</li><li>Cancer</li><li>Conclusions</li></ul></li><li>Chapter 33. Vitamin D and Primary Hyperparathyroidism<ul><li>Cross-Sectional Studies</li><li>Why are Primary Hyperparathyroidism and Low Vitamin D Levels so Consistently Associated?</li><li>Vitamin D Supplementation Studies</li><li>General Conclusions</li></ul></li><li>Chapter 34. Guidelines for the Management of Asymptomatic Primary Hyperparathyroidism<ul><li>Introduction</li><li>Methods</li><li>Workshop Group #1: Diagnosis of Primary Hyperparathyroidism</li><li>Clinical Presentations of Primary Hyperparathyroidism</li><li>Management</li><li>Blueprint for Future Research (Adapted from Reference 1)</li><li>Conclusion</li><li>Acknowledgments</li></ul></li><li>Chapter 35. Preoperative Localization of Abnormal Parathyroid Glands<ul><li>Introduction</li><li>Ultrasound</li><li>Parathyroid Scintigraphy</li><li>Computed Tomography</li><li>Magnetic Resonance Imaging (MRI)</li><li>Radioguided Surgery</li><li>Concluding Remarks</li></ul></li><li>Chapter 36. Surgical Management of Primary Hyperparathyroidism<ul><li>Introduction</li><li>Clinical Presentation to the Surgeon and Diagnostic Considerations</li><li>Indications for Surgery</li><li>Preoperative Preparation</li><li>Operative Approaches</li><li>Postoperative Management</li><li>Outcomes of Parathyroid Surgery</li><li>Special Considerations</li><li>Summary</li></ul></li><li>Chapter 37. Medical Management of Primary Hyperparathyroidism<ul><li>Introduction</li><li>General Measures</li><li>Pharmacologic Therapy</li><li>Specific Situations</li></ul></li></ul></li> <li>Section III. Non-Parathyroid Hypercalcemic States<ul><li>Chapter 38. Hypercalcemia Due to PTHrP<ul><li>PTHrP Discovery and Molecular Identification</li><li>Metabolism of PTHrP</li><li>Circulating Forms of PTHrP</li><li>PTHrP as a Clinical Target</li><li>Summary</li></ul></li><li>Chapter 39. Hypercalcemia Associated with Local and Ectopic Hormone Production<ul><li>1&#x3B1;-Hydroxylase</li><li>25-Hydroxyvitamin D-24-Hydroxylase</li><li>Systemic Elevations of Cytokines in Malignancy-Associated Hypercalcemia</li><li>Breast Cancer</li><li>Multiple Myeloma</li></ul></li><li>Chapter 40. Genetic Disorders Caused by Mutations in the PTH/PTHrP Receptor and Downstream Effector Molecules<ul><li>Introduction</li><li>The PTH/PTHrP Receptor System</li><li>Human Disorders caused by Mutations in the PTH/PTHrP Signaling Pathway</li><li>Mutations in Genes Downstream of the PTH/PTHrP Receptor</li><li>Conclusions</li></ul></li><li>Chapter 41. The Differential Diagnosis of Hypercalcemia<ul><li>Introduction</li><li>Parathyroid Hormone-Mediated Hypercalcemia</li><li>Parathyroid Hormone-Related Protein-Mediated Hypercalcemia</li><li>Mixed PTHrP and Cytokine-Mediated Hypercalcemia</li><li>1,25-Dihydroxyvitamin D-Induced Hypercalcemia</li><li>Other Causes of Excessive Bone Resorption</li><li>Supplement and Drug-Induced Hypercalcemia</li><li>Other Causes of Hypercalcemia, Mechanism Unknown</li><li>An Approach to the Patient with Hypercalcemia</li></ul></li><li>Chapter 42. Acute Management of Hypercalcemia<ul><li>Introduction</li><li>Differental Diagnosis of Hypercalcemia</li><li>Pathophysiology of Acute Hypercalcemia</li><li>Clinical Features of Hypercalcemia</li><li>Therapy of Acute Hypercalcemia</li></ul></li></ul></li> <li>Section IV. Secondary and Tertiary Hyperparathyroid States<ul><li>Chapter 43. Vitamin D and Parathyroid Hormone<ul><li>Introduction</li><li>The Vitamin D&#x2013;Calcium Homeostatic System</li><li>PTH and Vitamin D Interactions in Calcium Balance</li><li>PTH and Vitamin D Adequacy</li><li>PTH and Vitamin D&#x2014;Reciprocal Influences</li><li>Magnesium, PTH, and Vitamin D</li></ul></li><li>Chapter 44. The Parathyroids in Renal Disease<ul><li>Introduction</li><li>Pathogenesis of CKD-MBD</li><li>Systemic Consequences of Abnormal Mineral Metabolism in CKD</li><li>Summary</li></ul></li><li>Chapter 45. Clinical Skeletal Syndromes Associated with Parathyroid Disorders in Chronic Kidney Disease<ul><li>Introduction and Evolution of Secondary Hyperparathyroidism</li><li>Skeletal Diseases Associated with Parathyroid Hormone in Chronic Renal Failure</li><li>Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD)</li><li>Osteoporosis</li><li>Bone Mineral Density and Use of FRAX at Different Stages of CKD</li><li>Biochemical Markers of Bone Turnover Combined with PTH in the Management of Skeletal Abnormalities in CKD</li><li>Bone Biopsy for Quantitative Histomorphometry in Skeletal Disorders of CKD</li><li>Treatment of Skeletal Fractures in Chronic Kidney Disease</li><li>Conclusions</li></ul></li><li>Chapter 46. Other Secondary Hyperparathyroid States<ul><li>Disorders of Calcium Balance</li><li>Phosphate-Wasting Disorders</li><li>Post-Renal Transplant</li><li>Acid&#x2013;Base Disorders</li><li>Medications</li></ul></li></ul></li> <li>Section V. The Hypoparathyroid States<ul><li>Chapter 47. Hypoparathyroidism in the Differential Diagnosis of Hypocalcemia<ul><li>Definition of the Problem</li><li>Differential Diagnosis of Hypocalcemia</li><li>Clinical Evaluation</li><li>Laboratory Evaluation</li><li>Gene and Antibody Testing</li></ul></li><li>Chapter 48. Magnesium Depletion and Parathyroid Function<ul><li>Introduction</li><li>The Calcium-Sensing Receptor</li><li>The Role of Magnesium in CaSR Function</li><li>Clinical Manifestations of Magnesium Deficiency</li><li>Conditions that Produce Magnesium Deficiency</li><li>Homeostasis and Functions of Magnesium</li><li>Diagnosis of Magnesium Deficiency</li><li>The Magnesium Tolerance Test</li><li>Treatment of Magnesium Deficiency and its Effect on the Parathyroid Calcium-Sensing Receptor</li><li>Magnesium Depletion and Vitamin D Status</li><li>Summary</li></ul></li><li>Chapter 49. Epidemiology of Hypoparathyroidism<ul><li>Introduction</li><li>Incidence and Risk Factors</li><li>Prevalence</li><li>Cost</li><li>Hospitalization</li><li>Morbidity</li><li>Mortality</li><li>Conclusion</li></ul></li><li>Chapter 50. The Molecular Genetics of Hypoparathyroidism<ul><li>Introduction</li><li>Isolated Hypoparathyroidism</li><li>Hypoparathyroidism Associated with Complex Disorders</li><li>Diagnostic Work-Up in Non-Surgical, Idiopathic Hypoparathyroidism, Prenatal Diagnosis, and Genetic Counseling</li><li>Conclusion</li></ul></li><li>Chapter 51. Surgical Hypoparathyroidism<ul><li>Introduction</li><li>Hypopara After Thyroid Surgery</li><li>Hypopara After Parathyroid Surgery</li><li>Clinical Manifestations</li><li>Predicting and Preventing Surgical Hypoparathyroidism</li><li>Parathyroid Autotransplantation</li><li>Management of Immediate Postoperative Hypocalcemia: Our Protocol</li><li>Summary</li></ul></li><li>Chapter 52. Autoimmune Hypoparathyroidism<ul><li>Introduction</li><li>History</li><li>Clinical Features of APS1</li><li>Pathogenesis</li><li>Etiology</li><li>Treatment</li></ul></li><li>Chapter 53. Clinical Manifestations of Hypoparathyroidism<ul><li>Introduction</li><li>Neurologic Manifestations</li><li>Cardiac Manifestations</li><li>Ophthalmic Manifestations</li><li>Cutaneous Manifestations</li><li>Dental Manifestions</li><li>Hypoparathyroidism-Associated Myopathy</li><li>Gastrointestinal Manifestations</li><li>Skeletal Manifestations</li><li>Renal Manifestations</li><li>Latent and Subclinical Hypoparathyroidism</li><li>Presenting Signs and Symptoms</li></ul></li><li>Chapter 54. Skeletal Manifestations of Hypoparathyroidism<ul><li>Introduction</li><li>Skeletal Manifestations of Hypoparathyroidism</li><li>Skeletal Effects of PTH Treatment in Hypoparathyroidism</li><li>Summary</li></ul></li><li>Chapter 55. Molecular and Clinical Aspects of Pseudohypoparathyroidism<ul><li>History and Nosology</li><li>PTH Signal Transduction and the Role of G-Proteins</li><li>Molecular Biology of the <i>GNAS</i> Gene</li><li>Tissue-Specific Imprinting of <i>GNAS</i></li><li>Pathophysiology of PTH Resistance in Pseudohypoparathyroidism</li><li>Molecular Classes of Pseudohypoparathyroidism</li><li>Multiple Hormone Resistance in Pseudohypoparathyroidism Type 1A</li><li>Clinical Features</li><li>Diagnosis of Pseudohypoparathyroidism</li><li>Treatment</li><li>Conclusion</li></ul></li><li>Chapter 56. Treatment of Hypoparathyroidism with Calcium and Vitamin D<ul><li>Treatment</li><li>Conclusion</li></ul></li><li>Chapter 57. Treatment of Hypoparathyroidism with Parathyroid Hormone<ul><li>Introduction</li><li>Treatment of Hypoparathyroidism with PTH(1&#x2013;34)</li><li>Treatment of Hypoparathyroidism with PTH(1&#x2013;84)</li><li>Summary, Areas of Uncertainty, and Future Directions</li></ul></li></ul></li> <li>Section VI. The Parathyroids and Osteoporosis<ul><li>Chapter 58. Parathyroid Hormone in the Pathophysiology of Osteoporosis<ul><li>Introduction</li><li>Early Postmenopausal Bone Loss</li><li>Age-Related Changes in PTH Secretion</li><li>Relationship of Age-Related Increases in Serum PTH to Increased Bone Turnover and Bone Loss</li><li>Etiology of the Secondary Hyperparathyroidism of Aging</li><li>Summary and Conclusions</li></ul></li><li>Chapter 59. Parathyroid Hormone and Glucocorticoid-induced Osteoporosis<ul><li>Introduction</li><li>Mechanism of Glucocorticoid- Induced Bone Loss</li><li>Mechanism of Anabolic Action of PTH on Bone in GIOP</li><li>Role of PTH in the Pathogenesis of GIOP</li><li>Treatment of GIOP with Parathyroid Hormone</li><li>Conclusion</li></ul></li><li>Chapter 60. Parathyroid Hormone as Monotherapy for the Treatment of Osteoporosis<ul><li>Introduction</li><li>Indications for PTH Therapy in Osteoporosis</li><li>Mode of Action</li><li>Persistence of Effect</li><li>Rechallenge with PTH</li><li>Cost Effectiveness of TPTD</li><li>PTH Treatment in Glucocorticoid-Treated Patients</li><li>Other Potential Applications for PTH Treatment</li><li>Conclusion Regarding Osteoporosis Treatment</li></ul></li><li>Chapter 61. Combination Osteoporosis Therapy with Parathyroid Hormone<ul><li>Introduction</li><li>Combination Osteoporosis Therapy</li><li>Parathyroid Hormone and Estrogen or Selective Estrogen-Receptor Modulator Therapy in Postmenopausal Osteoporosis</li><li>Parathyroid Hormone and Bisphosphonates in Postmenopausal Osteoporosis</li><li>Parathyroid Hormone and Denosumab in Postmenopausal Osteoporosis</li><li>Combination Therapy in Male Osteoporosis</li><li>Parathyroid Hormone After Antiresorptive Therapy</li><li>Antiresorptive Therapy After Parathyroid Hormone</li><li>Hypercalcemia and Hypercalciuria with Combination Therapy</li><li>Summary</li></ul></li><li>Chapter 62. The Role of Parathyroid Hormone in Fracture Healing<ul><li>The Biology of Fracture Repair</li><li>The Role of PTH in Pre-clinical Models of Fracture Healing</li><li>The Role of PTH in Clinical Models of Fracture Healing</li><li>The Effect of PTH with Additional Adjuvants</li><li>Conclusions</li></ul></li><li>Chapter 63. Parathyroid Function and Disease during Pregnancy, Lactation, and Fetal/Neonatal Development<ul><li>Introduction</li><li>Mineral Physiology During Pregnancy</li><li>Mineral Physiology During Fetal Development</li><li>Mineral Physiology During Lactation</li><li>Mineral Physiology in the Neonate</li><li>Parathyroid Disorders during Pregnancy</li><li>Parathyroid Disorders during Lactation</li><li>Parathyroid Disorders during Fetal and Neonatal Development</li><li>Conclusions</li></ul></li></ul></li> <li>Index</li>


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© Academic Press 2015
5th September 2014
Academic Press
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About the Editors

John P. Bilezikian

John P. Bilezikian

Dr. John P. Bilezikian, the Dorothy L. and Daniel H. Silberberg Professor of Medicine and Professor of Pharmacology at the College of Physicians & Surgeons, Columbia University is Chief of the Division of Endocrinology and Director of the Metabolic Bone Diseases Program at Columbia University Medical Center. Dr. Bilezikian received his undergraduate training at Harvard College and his medical training at the College of Physicians & Surgeons. He completed four years of house staff training (internship, residency and Chief Residency) on the Medical Service at Columbia Presbyterian Medical Center. Dr. Bilezikian received his training in Metabolic Bone Diseases and in Endocrinology at the NIH in the Mineral Metabolism Branch under the tutelage of Dr. Gerald Aurbach.

Affiliations and Expertise

Professor of Medicine and Pharmacology; Chief, Division of Endocrinology; Director, Metabolic Bone Diseases Program, Departments of Medicine and Pharmacology, College of Physicians and Surgeons, Columbia University, New York, NY, USA

Robert Marcus

Robert Marcus

Dr. Marcus is Professor-Emeritus, Stanford University, where he served on the full-time medical faculty for almost 25 years, before joining the Emeritus faculty in 2001. At Stanford, he was located at the Veterans Affairs Medical Center, Palo Alto California, where he served as Director of the Aging Study Unit of the Geriatrics Research, Education, & Clinical Center from 1982-2001. Dr. Marcus enjoyed a long career as a clinical investigator in the fields of bone and mineral metabolism and osteoporosis medicine. His own research interests included diagnosis and therapy of primary hyperpara-thyroidism, interactions of the parathyroid-vitamin D axis with estrogen, age-related changes in the growth hormone-IGF axis, effects of growth hormone replacement for older men and women, metabolic and musculoskeletal effects of resistance exercise in older men and women, adolescent bone acquisition, and osteoporosis therapeutics. Dr. Marcus’ laboratory was a study site for many of the pivotal clinical trials in the osteoporosis field. These include the NIH Post-menopausal Estrogen/Progestin Interventions Trial (PEPI), Merck’s Fracture Intervention Trial (FIT), Lilly’s Multiple Outcomes of Raloxifene Intervention (MORE), and Lilly’s registration trial of recombinant PTH(1-34) in the treatment of postmenopausal women with osteoporosis. In 2001. Dr. Marcus joined the US Affiliate of Eli Lilly & Company to support Lilly’s program in Osteoporosis and Skeletal Medicine. From 2003 until his retirement from Lilly in 2008, Dr. Marcus was the lead physician for the Forteo team at Lilly. He has published more than 150 research papers, editorials, and reviews. Dr. Marcus served as President of the American Society for Bone & Mineral Research in 2000-2001.

Affiliations and Expertise

Emeritus, Department of Medicine, Stanford University School of Medicine, CA, USA

Michael A. Levine

Michael A. Levine

Dr. Michael A. Levine is Chief of Endocrinology and Diabetes and Director of the Center for Bone Health at The Children’s Hospital of Philadelphia. Dr. Levine holds the Lester Baker Endowed Chair and is Professor of Pediatrics and Medicine at the University of Pennsylvania Perelman School of Medicine. Dr. Levine’s research focuses on the genetic basis of disorders of bone and mineral metabolism and complements his clinical expertise in endocrine diseases that affect bone and mineral metabolism. His approach is to apply molecular and genetic tools to analyze the basis of altered hormone action, particularly in G protein-coupled signal transduction systems that affect growth and development. He has identified or contributed to the molecular basis of several inherited disorders of bone and mineral metabolism, including familial hypoparathyroidism, pseudohypoparathyroidism, cherubism, and the McCune Albright syndrome. His research interests now extend to the molecular events that control embryological development of the parathyroid glands and genetic modifiers of vitamin D action.

Affiliations and Expertise

The Children’s Hospital of Philadelphia, Philadelphia, PA, USA

Claudio Marcocci

Claudio Marcocci

Claudio Marcocci, MD, is Professor of Endocrinology at the Department of Clinical and Experimental Medicine, Director of the Postgraduate School in Endocrinology and Metabolism, University of Pisa and Director of the Endocrine Unit 2, University Hospital of Pisa. Over the years he has combined its clinical appointments with basic, translational and clinical research in the fields of parathyroid and thyroid diseases and vitamin D. Over the last 10 years he has contributed original work on the management of Graves’ orbitopathy, the calcium sensing receptor, clinical aspects of primary hyperparathyroidism and hypoparathyroidism and the molecular mechanisms of parathyroid tumorigenesis. Member of several Scientific Associations: Italian Society of Endocrinology, Italian Society of Osteoporosis, Mineral Metabolism and Skeletal Diseases, European Thyroid Association, American Thyroid Association, Endocrine Society, American Society of Bone and Mineral Research, American Association of Clinical Endocrinologists.

Affiliations and Expertise

Professor of Endocrinology, Department of Endocrinology, Metabolism, and Orthopaedics, University of Pisa, Pisa, Italy

Shonni J Silverberg

Shonni J. Silverberg, MD, is an endocrinologist in New York and is affiliated with New York-Presbyterian Hospital-Columbia and Cornell. She received her medical degree from Weill Cornell Medical College of Cornell University and has been in practice for more than 20 years. She is Professor of Clinical Medicine, Division of Endocrinology, Departments of Medicine and Pharmacology, College of Physicians and Surgeons, Columbia University, New York, NY, USA.

Affiliations and Expertise

Professor of Clinical Medicine, Division of Endocrinology, Departments of Medicine and Pharmacology, College of Physicians and Surgeons, Columbia University, New York, NY, USA

John Potts

John T. Potts, Jr., MD, is currently the Jackson Distinguished Professor of Clinical Medicine at Harvard Medical School. After medical training at the University of Pennsylvania, he completed his internship and residency at Massachusetts General Hospital. He went on to work at the National Institutes of Health (NIH), studying protein chemistry with Nobel laureate Christian Anfinsen. Dr. Potts remained at the NIH from 1959 until 1968, when he returned to the MGH as chief of endocrinology. The author or co-author of more than 500 scientific publications, he is a member of the National Academy of Sciences, the Institute of Medicine, and the American Academy of Arts and Sciences. He is also a director of ReceptorBase, Inc. and Zeltiq Aesthetics, a founder of Radius Health, Inc., and a member of the Scientific Advisory Boards of MPM Capital and HealthCare Ventures, as well as the Medical Advisory Board of Cell Genesys

Affiliations and Expertise

Distinguished Jackson Professor of Clinical Medicine, Harvard Medical School and The Massachusetts General Hospital, Endocrine Unit, Boston, MA, USA


"...a comprehensive source of information that most endocrinologists will want to have on their bookshelves." --Trends in Endocrinology And Metabolism, 2003

"It represents a significant contribution to the field, and likely will continue to do so for many editions." --Bart L. Clarke, Mayo Clinic, for Doody Publishing Reviews, 2002

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