[Homocysteine and asymmetric dimethylarginine (ADMA) in epilepsy]

Abstract

Homocysteine (Hcy) is a thyol amino acid resulting from demethylation of methionine. It is metabolized through two pathways: remethylation and trassulfuration, which use as cofactors folate, vitamin B6 and vitamin B12. Hyperhomocysteinemia (hHcy) is a risk factor for cerebrovascular disease, dementia, inborn defects, impaired cognitive function. Several drugs may change metabolic pathways of Hcy, leading to an alteration of plasma Hcy levels. HHcy has been documented in epileptic patients after chronic treatment with antiepileptic drugs (carbamazepine, valproate). HHcy may lead to increase of the level of asymmetric dimethylarginine (ADMA). ADMA has been identified as a potential risk factor for cardiovascular disease and endothelial dysfunction. ADMA is a product of methylation of L-arginine and endogenous nitric oxide (NO) synthase inhibitor, and regulator of NO production. NO plays a role in the convulsant effect. Supplementation of B vitamins, folate and L-arginine is a strategy to reduce Hcy levels in patients with epilepsy treatment antiepileptic drugs.