Anticonvulsant induced increase in 25-hydroxy-vitamin D3-1alpha-hydroxylase.
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).
D015090:25-Hydroxyvitamin D3 1-alpha-Hydroxylase / Q000378:metabolism*; D000469:Alkaline Phosphatase / Q000097:blood; D000818:Animals; D002118:Calcium / Q000097:blood; D002645:Chickens; D004789:Enzyme Activation / Q000187:drug effects; D007668:Kidney / Q000201:enzymology; D008297:Male; D010634:Phenobarbital / Q000494:pharmacology*; D010672:Phenytoin / Q000494:pharmacology*; D013250:Steroid Hydroxylases / Q000378:metabolism*
D010672:Phenytoin; D013250:Steroid Hydroxylases; D015090:25-Hydroxyvitamin D3 1-alpha-Hydroxylase; D000469:Alkaline Phosphatase; D002118:Calcium; D010634:Phenobarbital