PRIMARY HYPERPARATHYROIDISM MASKED BY ANTITUBERCULOUS THERAPY-INDUCEDVITAMIN-D DEFICIENCY

Antituberculous chemotherapy agents, particularly rifampicin and isoni azid, affect vitamin D metabolism and can create biochemical evidence of vitamin D deficiency. Vitamin D deficiency induces a state of resis tance to parathyroid hormone. This study sought to explain the tempora ry resolution of hypercalcaemia and hyper-calciuria, during antituberc ulous chemotherapy with rifampicin and isoniazid, in a subject with a surgically proven parathyroid adenoma and coincidental spinal tubercul osis. Serum ionized calcium, 25-hydroxyvitamin D and 1,25-dihydroxyvit amin D, plasma parathyroid hormone, and 24-hour urine excretions of ca lcium, inorganic phosphorus and hydroxyproline were sequentially measu red over a 3-year interval that included 18 months of antituberculous chemotherapy. Initial serum ionized calcium was 1.52 mmol/l (normal 1. 20-1.35 mmol/l), 24-hour urine calcium excretion was 9.40 mmol/day (no rmal 1.25 to 7.50 mmol/day) and plasma intact PTH was 9.2 pmol/l (norm al 0.0-4.5 pmol/l). During antituberculous chemotherapy the serum ioni zed calcium and 24-hour urine calcium excretion were normal but the pl asma PTH rose to higher levels. Following completion of the chemothera py, hypercalcaemia and hypercalciuria returned with levels similar to those observed pretreatment. Serum 25-hydroxyvitamin D was low at 6.25 nmol/l (normal 20 to 90 nmol/l) during antituberculous chemotherapy, but was normal before and after. Serum 1,25-dihydroxyvitamin D was nor mal throughout the 3-year interval. We conclude that the antituberculo us chemotherapy induced relative vitamin D deficiency and resistance t o parathyroid hormone action, thereby masking the hyperparathyroidism and hypercalcaemia until the chemotherapy was completed.