CHRONIC DIPHENYLHYDANTOIN THERAPY DOES NOT REDUCE PLASMA 25‐HYDROXY‐VITAMIN D

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Abstract
The association between osteomalacia or rickets and anticonvulsant drug therapy in epileptic patients has been amply confirmed. Some experimental data have been presented supporting the suggestion that the bone disease is caused by anticonvulsant-induced hepatic enzyme activity, which enhances the metabolism of vitamin D and 25-OHD to inactive products and causes a deficiency of active vitamin D metabolites. A randomized controlled study was performed to investigate the effect of 2 yr monitored diphenylhydantoin (DPH) therapy on plasma 25-hydroxyvitamin D (25-OHD) in non-epileptic, non-institutionalized subjects. Mean .+-. SE plasma 25-OHD of 18 DPH-treated subjects at the end of 2 yr drug treatment was 59 .+-. 8 nM (23.6 .+-. 3.2 ng/ml), which was not decreased compared to that of 18 control subjects (54 .+-. 8 nM, 21.6 .+-. 3.2 ng/ml). In addition, mean plasma 25-OHD had not changed 1 mo. after ceasing DPH. The treated group had a higher mean serum alkaline phosphatase (SAP) during DPH treatment, attributable to hepatic enzyme induction. Therapeutic doses of DPH without other anticonvulsants do not have a clinically significant effect on plasma 25-OHD.