Hypocalcemia: Diagnosis and Treatment

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


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.

Publication types

  • Review