Abstract
There is ample evidence for genetic polymorphisms of drug-metabolizing enzymes showing distinct subgroups in a population with or without the ability to transform certain drugs into polar metabolites before elimination. The polymorphic alleles lead to altered activity of these isoenzymes causing absent, decreased, or increased metabolism. An individual carrying two defective mutation alleles is categorized as a poor metabolizer (PM) and an individual carrying one or two wild-type alleles as an extensive metabolizer (EM). Like most other agents, many antiepileptic drugs (AED) are metabolized by a variety of enzymatic reactions, and the polymorphisms in the CYP family have attracted considerable attention. The CYP2D6, 2C9, and 2C19 polymorphisms account for the most frequent variations in phase I metabolism of drugs [1, 2].
