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Osteomalacia has been shown to be associated with long-term anticonvulsant therapy. Anticonvulsants modify the hepatic metabolism of vitamin D3 and decrease serum 25-hydroxy-vitamin D3 (25-OH-D3) levels. We have confirmed this and have shown that diphenylhydantoin (DPH) and phenobarbitone (PB) enhance the activity of kidney 25-hydroxy-vitamin D3-1alpha-hydroxylase (1-hydroxylase) in the chicken. Thus, anticonvulsant osteomalacia may not be due to a lack of the active metabolite of vitamin D, 1,25-dihydroxyvitamin D3 (1,25 (OH) 2D3).
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