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Presentation of Hypoparathyroidism: Etiologies and Clinical Features
Dolores M Shoback1, John P Bilezikian1, Aline G Costa1
1Endocrine Research Unit (D.M.S.), San Francisco Department of Veterans Affairs Medical Center, University of California, San Francisco, California 94121; Department of Medicine (J.P.B., A.G.C.), Division of Endocrinology, Metabolic Bone Diseases Unit, Columbia University College of Physicians and Surgeons, New York, New York 10032; Department of Medicine (A.G.C.), Division of Endocrinology, São Paulo Federal University, São Paulo 04021-001, Brazil; Department of Pathology and Cell Biology (D.D.), Columbia University College of Physicians and Surgeons, New York, New York 10032; Regional Bone Center (D.D.), Helen Hayes Hospital, Haverstraw, New York 10993; Department of General, Visceral, and Vascular Surgery (H.D.), University Hospital, Medical Faculty, Martin-Luther-University Halle-Wittenberg, 06108 Halle/Saale, Germany; McMaster University Calcium Disorders Clinic (A.A.K.), Hamilton, Canada L8S 4K1; Department of Medicine (M.P.), Indiana University School of Medicine, Indianapolis, Indiana 46202; U.O. di Chirurgica Endocrina e Metabolica, Policlinico A. Gemelli (M.R.), Università Cattolica del Sacro Cuore, 00168 Rome, Italy; Department of Medicine (B.C.S.), University Center of Belo Horizonte, and Division of Endocrinology, Santa Casa de Belo Horizonte, Belo Horizonte 30150-21, Brazil; Academic Endocrine Unit (R.V.T.), Oxford University, Oxford Centre for Diabetes Endocrinology and Metabolism, Churchill Hospital, Headington, Oxford OX3 7LI, United Kingdom; Section of Endocrinology (T.V.), Department of Medicine, University of Chicago, Chicago, Illinois 60637; and Clinic and Laboratory of Experimental Endocrinology (R.B.), Gasthuisberg, KU Leuven, 3000 Leuven, Belgium.
Context:
Understanding the etiology, diagnosis, and symptoms of hypoparathyroidism may help to improve quality of life and long-term disease outcomes. This paper summarizes the results of the findings and recommendations of the Working Group on Presentation of Hypoparathyroidism.
Evidence Acquisition:
Experts convened in Florence, Italy, in May 2015 and evaluated the literature and recent data on the presentation and long-term outcomes of patients with hypoparathyroidism.
Evidence Synthesis:
The most frequent etiology is surgical removal or loss of viability of parathyroid glands. Despite precautions and expertise, about 20-30% of patients develop transient and 1-7% develop permanent postsurgical hypoparathyroidism after total thyroidectomy. Autoimmune destruction is the main reason for nonsurgical hypoparathyroidism. Severe magnesium deficiency is an uncommon but correctable cause of hypoparathyroidism. Several genetic etiologies can result in the loss of parathyroid function or action causing isolated hypoparathyroidism or a complex syndrome with other symptoms apart from those of hypoparathyroidism or pseudohypoparathyroidism. Neuromuscular signs or symptoms due to hypocalcemia are the main characteristics of the disease. Hyperphosphatemia can contribute to major long-term complications such as ectopic calcifications in the kidney, brain, eye, or vasculature. Bone turnover is decreased, and bone mass is increased. Reduced quality of life and higher risk of renal stones, renal calcifications, and renal failure are seen. The risk of seizures and silent or symptomatic calcifications of basal ganglia is also increased.
Conclusions:
Increased awareness of the etiology and presentation of the disease and new research efforts addressing specific questions formulated during the meeting should improve the diagnosis, care, and long-term outcome for patients.
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