Hypocalcemia: Diagnosis and Treatment - PubMed (original) (raw)

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Kenneth R Feingold 1, S. Faisal Ahmed 2, Bradley Anawalt 3, Marc R Blackman 4, Alison Boyce 5, George Chrousos [ 6](#full-view-book-affiliation-6 "Professor of Pediatrics and Endocrinology, Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, National and Kapodistrian University of Athens Medical School, "Aghia Sophia" Children's Hospital, Athens, Greece"), Emiliano Corpas 7, Wouter W de Herder 8, Ketan Dhatariya 9, Kathleen Dungan 10, Johannes Hofland 11, Sanjay Kalra 12, Gregory Kaltsas 13, Nitin Kapoor 14, Christian Koch 15, Peter Kopp 16, Márta Korbonits 17, Christopher S Kovacs 18, Wendy Kuohung 19, Blandine Laferrère 20, Miles Levy 21, Elizabeth A McGee 22, Robert McLachlan 23, Radhika Muzumdar 24, Jonathan Purnell 25, Rodolfo Rey 26, Rakesh Sahay 27, Amy S Shah 28, Frederick Singer 29, Mark A Sperling 30, Constantine A Stratakis 31, Dace L Trence 32, Don P Wilson 33

, editors.

In: Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000.

2016 Jan 3.

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Hypocalcemia: Diagnosis and Treatment

Anne L Schafer et al.

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Excerpt

Hypocalcemia is an electrolyte derangement commonly encountered on surgical and medical services. This derangement can result from a vast spectrum of disorders. The condition may be transient, reversing with addressing the underlying cause expeditiously, or chronic and even lifelong, when due to a genetic disorder or the result of irreversible damage to the parathyroid glands after surgery or secondary to autoimmune destruction. Adult and pediatric endocrinologists must carefully assess patients with hypocalcemia, factoring into that assessment clinical presentation and symptomatology, concomitant laboratory abnormalities, past medical and family histories, recent medications, and even genetic sequencing analysis on the patient or affected family members. Critical initial laboratory testing involves measuring serum phosphate, magnesium, intact parathyroid hormone (PTH), 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D levels. Further evaluation is directed by the clinical and laboratory profiles that emerge. Significant fundamental insights into the molecular pathogenesis of several disorders that cause hypocalcemia have been made. These insights involve the molecular etiologies for PTH resistance (i.e., the different subtypes of pseudohypoparathyroidism); the role of the AIRE (autoimmune regulator) protein in autoimmune hypoparathyroidism and in mediating central tolerance to self-antigens; and the molecular bases for different genetic forms of magnesium wasting (that in turn causes hypocalcemia) and hypoparathyroidism. Genetic etiologies for hypoparathyroidism involve mutations in the calcium-sensing receptor, the G protein subunit alpha 11 that couples the receptor to downstream signaling molecules in parathyroid cells, transcription factors essential for parathyroid gland development, and the PTH molecule itself. Treatment of hypocalcemia depends on severity and chronicity. A calcium infusion is indicated for severe acute and or symptomatic hypocalcemia, while the standard mainstays of oral therapy are calcium supplements and activated vitamin D metabolites. Finally, and importantly, despite the rarity of chronic hypoparathyroidism, there have been several clinical trials supporting the use of recombinant human PTH (1-84) in the management of patients not well controlled on standard treatment. These trials have led to the approval of PTH (1-84) by the US Food and Drug Administration for adults with this disorder not well regulated on the usual therapy. Future research is being directed toward designing ideal treatment regimens with PTH (1-84) as well as developing a better understanding of the risks for post-surgical hypoparathyroidism, the most common etiology of hypoparathyroidism in adult patients. For complete coverage of this and all related ares of Endocrinology, please see our FREE web-book www.endotext.org.

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