Dihydrotachysterol: a bad choice in the treatment of chronic hypoparathyroidism

Abstract

Hypoparathyroidism is an endocrine disease caused by damage of the parathyroid glands and characterized by underproduction of parathyroid hormone. This can lead to severe hypocalcemia and its associated complications. The chronic hypoparathyroidism requires lifelong therapy including calcium and vitamin D analogues. The goal of treatment is to maintain the target parameters of phosphorus-calcium metabolism. At the same time, there is a risk of iatrogenic hypercalcemia on the standard therapy, up to the hypercalcemic crisis, often complicated by the acute renal failure. Moreover, chronic hypercalcemia acts as a predisposing factor for nephrolithiasis, nephrocalcinosis, chronic renal failure including pre- and dialysis stages.Dihydrotachysterol is a synthetic analogue of vitamin D, which was previously widely prescribed for hypocalcaemic hypoparathyroidism. In accordance with modern Russian and international guidelines, this drug should not be used in the treatment of chronic hypoparathyroidism. The main features in the metabolism of dihydrotachysterol (long elimination period, lack of feedback regulation of the active metabolites, high biological activity) and a narrow therapeutic window cause the frequent development of hypercalcemia and associated disorders.We present several clinical cases of patients with hypoparathyroidism treated with dihydrotachysterol, which was complicated by severe hypercalcemia and acute renal failure.

Keywords

• hypoparathyroidism
• dihydrotachysterol
• parathyroid
• hypocalcemia
• hypercalcemia
• hypercalcemic crisis
• nephrocalcinosis
• renal failure