hypoparathyroidism

Hypoparathyroidism is a disorder characterized by abnormally low secretion of parathyroid hormone (PTH), leading to low serum calcium and often elevated phosphate. PTH normally maintains calcium homeostasis by increasing bone resorption, promoting renal calcium reabsorption, and stimulating production of 1,25-dihydroxyvitamin D. Without adequate PTH, calcium falls and phosphate rises.

Causes include post-surgical damage or removal of the parathyroid glands (the most common cause in developed countries), autoimmune destruction, genetic mutations (in genes such as PTH, CASR, GCM2), and syndromic conditions such as DiGeorge syndrome. Less commonly, infiltrative diseases or severe magnesium deficiency can suppress PTH secretion.

Clinical features arise from hypocalcemia: tingling around the mouth, numbness in hands and feet, muscle cramps, and seizures in severe cases. Chvostek sign and Trousseau sign may be present. Chronic symptoms include fatigue, irritability, and cognitive changes.

Diagnosis rests on laboratory tests showing hypocalcemia with inappropriately low or normal PTH. Hyperphosphatemia is common; calcitriol may be reduced. Magnesium deficiency can worsen hypocalcemia. Renal function should be checked to exclude kidney disease.

Treatment depends on severity. Acute symptomatic hypocalcemia requires intravenous calcium (often calcium gluconate). Long-term management uses oral calcium supplements plus active vitamin D (calcitriol or alfacalcidol) to improve calcium absorption; magnesium repletion if deficient. Regular monitoring of serum calcium and phosphate is essential to avoid hypercalcemia or nephrocalcinosis. Thiazide diuretics may reduce urinary calcium in some patients. Genetic or autoimmune causes may require specific counseling; surgical patients require endocrinology follow-up.

Prognosis varies; with appropriate treatment most patients manage symptoms, but lifelong monitoring is needed to prevent complications such as calcifications and kidney problems.