Altered vitamin D metabolism has been implicated as a cause of anticonvulsant-induced osteomalacia. Previous studies have demonstrated accelerated biotransformation of vitamin D3 to 25-hydroxycholecalciferol (25-OHD3). However, it is not known whether the 25-OHD3 is metabolized to 1,25-dihydroxycholecalciferol (1,25-(OH)2D3), the tissue-active metabolite of vitamin D3. This study using rats was undertaken to study the influence of phenobarbital on the biotransformation of 25-OHD3 to 1,25-(OH)2D3. The disappearance rate of 25-OHD3 was virtually the same in the pheno-barbital-treated group (re = 0.0615 pmole/min) and the control group (re - 0.0549 pmole/min). Similarly, the appearance rate of 1,25-(OH)2D3 was virtually the same in the treated group (ra = 0.0133 pmole/min) and the control group (ra = 0.0134 pmole/min). These data suggest that phenobarbital does not affect the biotransformation of 25-OHD3 to 1,25-(OH)2D3. The implication of this observation is that altered vitamin D metabolism does not account for phenobarbital-induced osteomalacia.

Animals↗

PubMedDate not supplied

Absorption and biotransfomation of cholecalciferol in drug-induced osteomalacia.

The gastrointestinal absorption of vitamin D3 and its biotransformation to 25-hydroxycholecalciferol was studied in patients with drug-induced osteomalacia. The mean coefficient of absorption was virtually identical in the drug-treated group (82.8%) and the control (83.8%). The biotransformation of vitamin D3 to 25-hydroxycholecalciferol was significantly accelerated (P less than 0.03) in the drug-treated group compared to the control group. These data suggest that vitamin D absorption is not significantly altered but that biotransformation of vitamin D3 to 25-hydroxycholecalciferol is accelerated in drug-induced osteomalacia.

Adolescent↗