Nonnutritional Rickets and Osteomalacia

Induction of cytochrome P450 enzymes by barbiturates and other anticonvulsants can result in increased catabolism of calcidiol, and hence secondary, drug-induced osteomalacia. The antituberculosis drug isoniazid inhibits cholecalciferol 25-hydroxylase, and again prolonged administration can cause osteomalacia.

Three conditions associated with defective 1-hydroxylation of calcidiol can all be treated by the administration of either calcitriol itself or 1a-hydroxycholecalciferol, which is a substrate for 25-hydroxylation in the liver forming calcitriol:

1. Strontium intoxication can cause vitamin D-resistant rickets because strontium is a potent inhibitor of calcidiol 1-hydroxylase (Omdahl and DeLuca, 1971).

2. Renal failure is associated with an osteomalacia-like syndrome, renal osteodystrophy, as a result of the loss of calcidiol 1-hydroxylase activity. The condition may be complicated by defective reabsorption of calcium and phosphate from the urine. Furthermore, the half-life of parathyroid hormone is increased, because the principal site of its catabolism is the kidney, so there is increased parathyroid hormone-stimulated osteoclastic action without the compensatory action of calcitriol (Mawer etal., 1973).

3. Hypoparathyroidism is also associated with a failure of calcidiol 1-hydroxylation, in this case because the major stimulus for induction of 1-hydroxylase is parathyroid hormone.

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