Serum vitamin D metabolites in epileptic patients treated with 2 different anti-convulsants.
The serum concentrations of the vitamin D metabolites 25-hydroxyvitamin D (25OHD), 24,25-dihydroxyvitamin D (24,25(OH)2D), and 1,25-dihydroxyvitamin D (1,25(OH)2D) were measured in 18 epileptic patients and 10 controls. The patients were divided according to the anti-convulsant treatment they had been receiving for at least 1 year: 9 patients had received phenytoin and 9 patients carbamazepine, as the sole anti-convulsant therapy. The serum 25OHD was decreased in the patients on phenytoin (P less than 0.01), whereas the other serum vitamin D metabolites were normal. Moreover, serum alkaline phosphatase was increased (P less than 0.001) and serum calcium was decreased (P less than 0.001) in this patient group. In the patient group treated with carbamazepine (a negligible, liver inductor), changes in serum 25OHD and serum alkaline phosphatase were less pronounced (P less than 0.05), but the same degree of hypocalcaemia (P less than 0.001) was present. Our data suggest that liver induction in epileptic patients on anti-convulsant drugs cannot explain the pathophysiology behind anti-convulsant osteomalacia.
D015650:24,25-Dihydroxyvitamin D 3; D000328:Adult; D000368:Aged; D000469:Alkaline Phosphatase / Q000097:blood; D002112:Calcifediol / Q000097:blood*; D002117:Calcitriol / Q000097:blood*; D002118:Calcium / Q000097:blood; D002220:Carbamazepine / Q000009:adverse effects*; D004100:Dihydroxycholecalciferols / Q000097:blood*; D004827:Epilepsy / Q000097:blood / Q000188:drug therapy; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010018:Osteomalacia / Q000097:blood / Q000139:chemically induced*; D010672:Phenytoin / Q000009:adverse effects*
D004100:Dihydroxycholecalciferols; D002220:Carbamazepine; D015650:24,25-Dihydroxyvitamin D 3; D010672:Phenytoin; D000469:Alkaline Phosphatase; D002117:Calcitriol; D002112:Calcifediol; D002118:Calcium