Two patients with COMT inhibitor–induced hepatic dysfunction and UGT1A9 genetic polymorphism
Copyright policy )Two patients with COMT inhibitor–induced hepatic dysfunction and UGT1A9 genetic polymorphism
The authors report two cases of catechol-O-methyltransferase (COMT) inhibitor-induced asymptomatic hepatic dysfunction in women with Parkinson disease. The patients were genotyped for the UDP-glucuronosyltransferase (UGT) 1A9 gene (which encodes the main COMT inhibitor-metabolizing enzyme), and found to carry mutations leading to defective glucuronidation activity. This suggests that UGT1A9 poor metabolizer genotype(s) may be a predisposing factor for COMT inhibitor-induced hepatotoxicity.
Adult, Genotype, Liver Diseases, DNA Mutational Analysis, Catechols, Catechol O-Methyltransferase Inhibitors, Glucuronates, Middle Aged, Catechol O-Methyltransferase, Antiparkinson Agents, Benzophenones, Liver, Mutation, Nitriles, Humans, Female, Chemical and Drug Induced Liver Injury, Enzyme Inhibitors, Glucuronosyltransferase, Aged
Adult, Genotype, Liver Diseases, DNA Mutational Analysis, Catechols, Catechol O-Methyltransferase Inhibitors, Glucuronates, Middle Aged, Catechol O-Methyltransferase, Antiparkinson Agents, Benzophenones, Liver, Mutation, Nitriles, Humans, Female, Chemical and Drug Induced Liver Injury, Enzyme Inhibitors, Glucuronosyltransferase, Aged
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