Chlorothiazide-Induced Hypercalcemia in Juvenile Osteoporosis and Hyperparathyroidism

Thiazide diuretic administration was followed within three to four days by symptomatic hypercalcemia (calcium level of 12.6 mg per 100 ml) and elevation of blood urea nitrogen in a patient with idiopathic juvenile osteoporosis treated with calciferol. Pre-existing hypercalcemia was exacerbated in two patients with primary hyperparathyroidism. Restoration of previous plasma calcium levels and disappearance of symptoms rapidly followed discontinuation of the drug. There was little change in plasma calcium (corrected for change in plasma protein) in eight other patients. The change in plasma level did not correlate with the magnitude of the fall in urine calcium, so that effects of thiazides other than hypocalciuria may contribute to the hypercalcemia. Thiazide diuretics should be given with caution to actually or potentially hypercalcemic patients, and those with diseases causing accelerated bone resorption, in whom increased excretion of calcium by the kidney may be preventing or delaying the onset of hypercalcemia.