CYP2C19*2 polymorphism is not the sole determinant of the response to clopidogrel: implications for its monitoring.
Aleil
B
B
Léon
C
C
Cazenave
J-P
JP
Gachet
C
C
D000368:Aged; D001189:Aryl Hydrocarbon Hydroxylases / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D001835:Body Weight; D000077144:Clopidogrel; D015897:Comorbidity; D065731:Cytochrome P-450 CYP2C19; D004347:Drug Interactions; D016903:Drug Monitoring; D005260:Female; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000493:pharmacokinetics / Q000494:pharmacology*; D011110:Polymorphism, Genetic; D019338:Polypharmacy; D012907:Smoking / Q000453:epidemiology; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000493:pharmacokinetics / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
D010975:Platelet Aggregation Inhibitors; D014665:Vasodilator Agents; D000077144:Clopidogrel; D001189:Aryl Hydrocarbon Hydroxylases; C045793:CYP2C19 protein, human; D065731:Cytochrome P-450 CYP2C19; D013988:Ticlopidine