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. 2010 Aug 20;3(8):2709–2732. doi: 10.3390/ph3082709

Table 3.

The clinical impact of genetic polymorphisms of drug-metabolizing enzymes on AED therapy.

AED Genetic polymorphisms Associated pharmacokinetic or pharmacodynamic parameters References
Carbamazepine CYP3A5*3/*3 genotype Oral clearance [12,43,44]
EPHX1 Try113His and His139Arg Maintenance dose [84]
GSTM1 null genotype Mild hepatotoxicity [88]
Clobazam CYP2C19 hetero EMs and PMs Serum N-desmethylclobazam concentration, responder rate [35]
Lamotrigine UGT2B7 -161C>T Concentration to daily dose ratio [97]
Phenobarbital CYP2C19 PMs Oral clearance [37]
CYP2C9 hetero EMs Oral clearance, ethnic differences in tolerability (?) [12,36]
Phenytoin CYP2C9 hetero EMs/PMs and/or CYP2C19 PMs Plasma concentration, maintenance dose, CNS toxicity [12]
CYP2C9*1B haplotype Maintenance dose [104]
EPHX1 113Try/139His haplotype Risk of craniofacial abnormalities [58]
Valproic acid CYP2C9 hetero EMs and CYP2C19 PMs Oral clearance [120]
GSTM1 and GSTT1 null genotypes Mild elevation of γ-glutamyltransferase [125]
Zonisamide CYP2C19 hetero EMs and PMs Oral clearance, zonisamide-specific adverse reactions [12,38]

AED, antiepileptic drug; CYP, cytochrome P450; EPHX1, microsomal epoxide hydrolase gene; UGT, UDP-glucuronosyltransferase; GST, Glutathione S-transferase; CNS, central nervous system.