Long-term anticonvulsant therapy and vitamin D metabolism in ambulatory pubertal children

Parameters of calcium metabolism were thoroughly examined in 28 adolescents with long-term (over 6 years) anticonvulsant therapy (phenytoin, carbamazepine or combination) and in 10 normal controls in September and in March. The adolescents did not receive any vitamin D supplementation during the study. Serum calcium, inorganic phosphorus, parathyroid hormone and alkaline phosphatase levels in the anticonvulsant group did not differ from those of the control group. Serum 25(OH)D and 24,25(OH)2D levels were in all groups consistently higher in September than in March, but no seasonal variation was found in the 1,25(OH)2D levels in any group. The serum 25(OH)D levels in the phenytoin group in March were the lowest among the three groups treated with anticonvulsants, but the levels in the anticonvulsant groups did not differ significantly from each other or from the control group in the same season. The 24,25(OH)2D and 1,25(OH)2D levels in the anticonvulsant groups did not differ significantly from those of control group in September or in March. There was no correlation between anticonvulsant serum free fraction levels and vitamin D metabolites. The bone mineral content in the distal radius was not significantly decreased in the epileptic patients. In conclusion, the long-term anticonvulsant therapy did not induce the so-called "anticonvulsant rickets" in this ambulatory adolescent material. Our data do not indicate that anticonvulsant drugs alter significantly the vitamin D metabolism. Thus, routine vitamin D supplementation does not appear to be indicated in children on anticonvulsant therapy.