Hypoparathyroidism can occur due to aplasia or hypoplasia of parathyroid glands, (as in DiGeorge syndrome, Shprintzen syndrome), Parathyroid hormone gene mutations, autoimmune parathyroiditis (in isolation or with Addison’s disease & mucocutaneous candidiasis), hemosiderosis, Wilson’s disease, familial congenital variant with dysmorphic features or surgical removal or damage to the parathyroid glands during thyroidectomy.

Autoimmune hypoparathyroidism is suggested by the finding of parathyroid antibodies and by frequent association with other autoimmune disorders. It is often seen as a part of polyglandular autoimmune disease type I (At least 2 of the following are required – autoimmune hypoparathyroidism, Addison’s disease and chronic mucocutaneous candidiasis). In this polyglandular endocrinopathy candidiasis precedes the other disorders followed by hypoparathyroidism and then Addison’s disease.

Patients present with muscle pain and cramps, stiffness, tingling of hands and feet with laryngeal or carpopedal spasms. Convulsions and cataracts may occur in long standing untreated cases. Investigations reveal hypocalcemia with hyperphosphatemia. Serum alkaline phosphatase is normal or low but high levels may be seen in patients with severe hypocalcemia. Serum parathyroid levels are low. Treatment consists of intravenous calcium gluconate (10% solution – 5 to 10 ml rate of 0.5-1 mL/min) for emergency treatment of tetany. Supplementation with 1, 25 dihydroxycholecalciferol in a dose of 0.01 to 0.1 ug/kg/day to maximum of 1-2 ug/day is required. Once normocalcemia is achieved, one can continue therapy with Vitamin D2 (50,000 – 1,00,000 IU) daily to make therapy economically feasible. Vitamin D3 has the advantage of rapid onset of action and rapid reversal of hypercalcemia after discontinuation in the event of overdosage. Calcium supplement should be ensured. High phosphorus containing food such as milks, eggs and cheese should be avoided.