Abstract
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.
MeSH terms
-
Adult
-
Aged
-
Antiparkinson Agents / adverse effects*
-
Benzophenones / adverse effects
-
Catechol O-Methyltransferase / metabolism
-
Catechol O-Methyltransferase Inhibitors*
-
Catechols / adverse effects
-
Chemical and Drug Induced Liver Injury*
-
DNA Mutational Analysis
-
Enzyme Inhibitors / adverse effects*
-
Enzyme Inhibitors / metabolism
-
Female
-
Genotype
-
Glucuronates / metabolism
-
Glucuronosyltransferase / genetics*
-
Humans
-
Liver / drug effects
-
Liver / enzymology
-
Liver / physiopathology
-
Liver Diseases / enzymology
-
Liver Diseases / genetics*
-
Middle Aged
-
Mutation / genetics
-
Nitriles
-
Nitrophenols / adverse effects
-
Parkinson Disease / drug therapy
-
Polymorphism, Genetic / genetics
-
Tolcapone
-
UDP-Glucuronosyltransferase 1A9
Substances
-
Antiparkinson Agents
-
Benzophenones
-
Catechol O-Methyltransferase Inhibitors
-
Catechols
-
Enzyme Inhibitors
-
Glucuronates
-
Nitriles
-
Nitrophenols
-
UGT1A9 protein, human
-
entacapone
-
Tolcapone
-
Catechol O-Methyltransferase
-
Glucuronosyltransferase
-
UDP-Glucuronosyltransferase 1A9