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Serum vitamin D metabolites in epileptic patients treated with 2 different anti‐convulsants
Author(s) -
Tjellesen L.,
Christiansen C.
Publication year - 1982
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1982.tb06853.x
Subject(s) - convulsant , phenytoin , medicine , endocrinology , alkaline phosphatase , hypocalcaemia , osteomalacia , vitamin d and neurology , epilepsy , carbamazepine , chemistry , calcium , biochemistry , enzyme , receptor , psychiatry
The serum concentrations of the vitamin D metabolites 25‐hydroxy‐vitamin D (25OHD), 24,25‐dihydroxyvitamin D (24,25(OH) 2 D), and 1,25‐dihydroxyvitamin D (1,25(OH) 2 D) 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 < 0.01). whereas the other serum vitamin D metabolites were normal. Moreover, serum alkaline phosphatase was increased ( P < 0.001) and serum calcium was decreased ( P < 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 < 0.05), but the same degree of hypocalcaemia ( P < 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.