Treatment of hypocalcemia depends on severity and chronicity. 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. 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.
Significant fundamental insights into the molecular pathogenesis of several disorders that cause hypocalcemia have been made. Further evaluation is directed by the clinical and laboratory profiles that emerge.
Critical initial laboratory testing involves measuring serum phosphate, magnesium, intact parathyroid hormone (PTH), 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D levels. 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. 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. This derangement can result from a vast spectrum of disorders.
Hypocalcemia is an electrolyte derangement commonly encountered on surgical and medical services.
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