We hypothesized that elevated plasma
homocysteine concentrations (
hyperhomocysteinemia) exist in patients receiving
antiepileptic drugs (AED), and a long-term administration of AED may result in an increased risk of occlusive
vascular disease in these patients. A total of 62 patients who received AED monotherapy (
phenytoin,
lamotrigine,
carbamazepine or
valproate) participated in this study. Blood concentrations of
homocysteine,
folate,
vitamin B-12 and pyridoxal-5'-phosphate (PLP, a
coenzyme form of
vitamin B-6) were measured, and thermolabile genotypes of 5, 10-methylenetetrahydrofolate
reductase (MTHFR) were also determined. Of 62 patients, only seven (11.4%) had
hyperhomocysteinemia. Of 20 patients who received
phenytoin, three (15.0%) had
hyperhomocysteinemia, whereas 85% of these had plasma
folate concentrations below the normal range. However, erythrocyte
folate concentrations were abnormally low in only 25% of the patients who received
phenytoin.
Valproate administration increased serum
vitamin B-12 concentrations. Over 55% of the entire patients had PLP concentrations below the normal range, although the reason is unknown. Only three patients had the homozygous thermolabile genotype of MTHFR; therefore, meaningful statistical analysis was not possible in this study. However, one patient with homozygous genotype who received
phenytoin therapy had
hyperhomocysteinemia with poor
folate nutritional status, and the other two had normal
homocysteine concentrations with normal
folate status. Our data suggest that
hyperhomocysteinemia is not a serious clinical concern in epileptic patients when
folate nutriture is adequate.