Abstract
Hyperhomocysteinemia, a possible risk factor for vascular disease can result from
folate deficiency due to anticonvulsant therapy. A reaction catalyzed by 5,10-methylenetetrahydrofolate
reductase (MTHFR) supplies 5-methyltetrahydrofolate, needed to remethylate homocysteine
to methionine. MTHFR gene mutation (C677T) also can lead to hyperhomocysteinemia.
We examined interaction between anticonvulsant therapy, C677T homozygosity, serum
folate concentration, and plasma total homocysteine (tHcy) concentration in 81 epileptic
patients. Patients receiving monotherapy showed no difference in occurrence of hyperhomocysteinemia
(tHcy>90th percentile for controls) between homozygotes for C677T and heterozygotes
or patients with no mutant MTHFR. No monotherapy patient was folate deficient (<3 ng/ml). Among patients receiving multidrug therapy, hyperhomocysteinemia in homozygotes
for C677T occured significantly more often than in heterozygotes or patients with
no mutant enzyme (88.9 vs. 21.1%). The same was true for folate deficiency (44.4 vs.
0%). The C677T mutation is closely related to hyperhomocysteinemia and folate deficiency
in epileptic patients taking multiple anticonvulsants.
Keywords
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Article info
Publication history
Accepted:
December 13,
2001
Received in revised form:
December 4,
2001
Received:
April 9,
2001
Identification
Copyright
© 2002 Elsevier Science B.V. Published by Elsevier Inc. All rights reserved.
