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J Clin Endocrinol Metab. 2016 Jun;101(6):2313-24. doi: 10.1210/jc.2015-3910. Epub 2016 Mar 3.

Management of Hypoparathyroidism: Present and Future.

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Columbia University College of Physicians & Surgeons (J.P.B., N.E.C., M.R.R.), New York, New York 10032; Department of Surgery and Translational Medicine (M.L.B.), University of Florence, 50121 Florence, Italy; Massachusetts General Hospital (M.M., J.T.P.), Boston, Massachusetts 02114; Aarhus University Hospital (L.R.), 8000 Aarhus, Denmark; Geneva University Hospitals and Faculty of Medicine (R.R.), 1205 Geneva, Switzerland; Eunice Kennedy Shriver National Institute of Child Health and Human Development (K.K.W.), National Institutes of Health, Bethesda, Maryland 20892; and Sackler School of Medicine (U.A.L.), Tel Aviv University, Tel Aviv 6997801, Israel.



Conventional management of hypoparathyroidism has focused upon maintaining the serum calcium with oral calcium and active vitamin D, often requiring high doses and giving rise to concerns about long-term consequences including renal and brain calcifications. Replacement therapy with PTH has recently become available. This paper summarizes the results of the findings and recommendations of the Working Group on Management of Hypoparathyroidism.


Contributing authors reviewed the literature regarding physiology, pathophysiology, and nutritional aspects of hypoparathyroidism, management of acute hypocalcemia, clinical aspects of chronic management, and replacement therapy of hypoparathyroidism with PTH peptides. PubMed and other literature search engines were utilized.


Under normal circumstances, interactions between PTH and active vitamin D along with the dynamics of calcium and phosphorus absorption, renal tubular handing of those ions, and skeletal responsiveness help to maintain calcium homeostasis and skeletal health. In the absence of PTH, the gastrointestinal tract, kidneys, and skeleton are all affected, leading to hypocalcemia, hyperphosphatemia, reduced bone remodeling, and an inability to conserve filtered calcium. Acute hypocalcemia can be a medical emergency presenting with neuromuscular irritability. The recent availability of recombinant human PTH (1-84) has given hope that management of hypoparathyroidism with the missing hormone in this disorder will provide better control and reduced needs for calcium and vitamin D.


Hypoparathyroidism is associated with abnormal calcium and skeletal homeostasis. Control with calcium and active vitamin D can be a challenge. The availability of PTH (1-84) replacement therapy may usher new opportunities for better control with reduced supplementation requirements.

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