Abstract
Serum concentrations of 25-hydroxyvitamin D (25-OHD), 24,25-dihydroxyvitamin D [24,25-(OH)2D], and 1 alpha, 25-dihydroxyvitamin D [1, 25-(OH)2D] were measured in 30 ambulatory adult epileptic patients during long-term anticonvulsant treatment with phenytoin, phenobarbital, or carbamazepine. For the entire group, serum 24,25-(OH)2D was decreased (p less than 0.0005) as compared to normal subjects to a mean value of 0.7 +/- 0.1 (SEM) ng/ml. However, serum 1, 25-(OH)2D was increased at 50 +/- 7 pg/ml (p less than 0.025). Serum 25-OHD declined insignificantly to 19 +/- 3 ng/ml. All three drugs caused a significant reduction of serum 24,25-(OH)2D concentrations. A significant decrease in serum 25-OHD was observed only for the phenobarbital-treated patients. Serum 1, 25-(OH)2D was high in patients receiving phenytoin or carbamazepine but not in those taking phenobarbital. The findings suggest that while various anticonvulsant drugs appear to exert different effects on vitamin D metabolism, a universal finding is diminished serum 24,25-(OH)2D. The results support the notion that 24,25-(OH)2D deficiency may play an important role in the pathogenesis of anticonvulsant-induced osteomalacia.
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