Nonnutritional Rickets and Osteomalacia

Induction of cytochrome P450 enzymes by bMbiturates and other emticonvul-stmts Ctm result in increeised catabolism of cedcidiol, and hence secondeuy. 

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

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

Rentd ftiilure is associated with an osteomedacia-like syndrome, rened 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 htdf-Ufe of parathyroid hormone is increased, because the principeil site of its catabolism is the kidney, so there is increased ptuathyroid hormone-stimulated osteoclastic action without the compensatory action of calcitriol (Mawer etal., 1973). 

Hypoparathyroidism is also tissociated with a failure of cedcidiol 1-hydroxylation, in this case because the major stimulus for induction of 1-hydroxylase is peuathyroid hormone. 

Induction of cytochrome P450 enzymes by barbiturates and other anticonvulsants can result in increased catabolism of calcidiol, and hence secondary. 

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