[ 5 ] De Morais SM, Wilkinson GR, Blaisdell J, et al. The major genetic defect responsible for the polymorphism of S-mephenytoin metabolism in humans[J]. J Biol Chem, 1994, 269(22): 15419-15422.
[2]
[ 6 ] De Morais SM, Wilkinson GR, Blaisdell J, et al. Identification of a new genetic defect responsible for the polymorphism of (S)-mephenytoin metabolism in Japanese[J]. Mol Pharmacol, 1994, 46(4): 594-598.
[3]
Collet JP, Hulot JS, Pena AA, et al. Cytochrome P450 2C19 polymorphism in young patients treated with clopidogrel after myocardial infarction: a cohort study[J]. Lancet, 2009, 373(9660): 309-317.
[4]
Giusti B, Gori AM, Marcucci R, et al. Relation of cytochrome P450 2C19 loss-of-function polymorphism to occurrence of drug-eluting coronary stent thrombosis[J]. Am J Cardiol, 2009, 103(6): 806-811.
[5]
Trenk D, Hochholzer W, Frundi D, et al. Impact of cytochrome P450 3A4-metabolized statins on the antiplatelet effect of a 600-mg loading dose clopidogrel and on clinical outcome in patients undergoing elective coronary stent placement[J]. Thromb Haemost, 2008, 99(1): 174-181.
[6]
Trenk D, Hochholzer W, Fromm MF, et al. Cytochrome P450 2C19 681G＞A polymorphism and high on-clopidogrel platelet reactivity associated with adverse 1-year clinical outcome of elective percutaneous coronary intervention with drug-eluting or bare-metal stents[J]. J Am Coll Cardiol, 2008, 51(20): 1925-1934.
[7]
Mega JL, Close SL, Wiviott SD, et al. Cytochrome p-450 polymorphisms and response to clopidogrel[J]. N Engl J Med, 2009, 360(4): 354-362.
[8]
Bhatt DL, Scheiman J, Abraham NS, et al. ACCF/ACG/AHA 2008 expert consensus document on reducing the gastrointestinal risks of antiplatelet therapy and NSAID use: a report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents[J]. Circulation, 2008, 118(18): 1894-1909.
[9]
Ando Y, Fuse E, Figg WD. Thalidomide metabolism by the CYP2C subfamily[J]. Clin Cancer Res, 2002, 8(6): 1964-1973.
[10]
Li Y, Jiang Z, Xiao Y, et al. Metabolism of Thalidomide by human liver microsome cytochrome CYP2C19 is required for its antimyeloma and antiangiogenic activities in vitro[J]. Hematol Oncol, 2012, 30(1): 13-21.
[11]
Li Y, Hou J, Wang D, et al. Prognostic factors for the efficacy of thalidomide in the treatment of multiple myeloma: a clinical study of 110 patients in China[J]. Leuk Lymphoma, 2006, 47(12): 2593-2600.
[12]
Nakamoto K, Kidd JR, Jenison RD, et al. Genotyping and haplotyping of CYP2C19 functional alleles on thin-film biosensor chips[J]. Pharmacogenet Genomics, 2007, 17(2): 103-114.
[13]
[ 1 ] Wroblewski B, Glenn MB. The cytochrome p-450 drug metabolizing enzyme system: an overview of potential clinically important drug interactions[J]. J Head Trauma Rehabil, 2002, 17(6): 571-574.
[14]
[ 2 ] Wrighton SA, Stevens JC, Becker GW, et al. Isolation and characterization of human liver cytochrome P450 2C19: correlation between 2C19 and S-mephenytoin 4’-hydroxylation[J]. Arch Biochem Biophys, 1993, 306(1): 240-245.
[15]
[ 3 ] He N, Yan FX, Huang SL, et al. CYP2C19 genotype and S-mephenytoin 4’-hydroxylation phenotype in a Chinese Dai population[J]. Eur J Clin Pharmacol, 2002, 58(1): 15-18.
[16]
[ 4 ] Finta C, Zaphiropoulos PG. The human CYP2C locus: a prototype for intergenic and exon repetition splicing events[J]. Genomics, 2000, 63(3): 433-438.
[17]
[ 7 ] Shimizu T, Ochiai H, Asell F, et al. Bioinformatics research on inter-racial difference in drug metabolism I. Analysis on frequencies of mutant alleles and poor metabolizers on CYP2D6 and CYP2C19[J]. Drug Metab Pharmacokinet, 2003, 18(1): 48-70.
[ 9 ] Desta Z, Zhao X, Shin JG, et al. Clinical significance of the cytochrome P450 2C19 genetic polymorphism[J]. Clin Pharmacokinet, 2002, 41(12): 913-958.
[20]
Shu Y, Zhou HH. Individual and ethnic differences in CYP2C19 activity in Chinese populations[J]. Acta Pharmacol Sin, 2000, 21(3): 193-199.
[21]
Malfertheiner P, Mégraud F, O’morain C, et al. Current concepts in the management of Helicobacter pylori infection-the Maastricht 2-2000 Consensus Report[J]. Aliment Pharmacol Ther, 2002, 16(2): 167-180.
[22]
Sahara S, Sugimoto M, Uotani T, et al. Twice-daily dosing of esomeprazole effectively inhibits acid secretion in CYP2C19 rapid metabolisers compared with twice-daily omeprazole, rabeprazole or lansoprazole[J]. Aliment Pharmacol Ther, 2013, 38(9): 1129-1137.
[23]
Furuta T, Ohashi K, Kosuge K, et al. CYP2C19 genotype status and effect of omeprazole on intragastric pH in humans[J]. Clin Pharmacol Ther, 1999, 65(5): 552-561.
[24]
Shirai N, Furuta T, Moriyama Y, et al. Effects of CYP2C19 genotypic differences in the metabolism of omeprazole and rabeprazole on intragastric pH[J]. Aliment Pharmacol Ther, 2001, 15(12): 1929-1937.
[25]
Furuta T, Shirai N, Watanabe F, et al. Effect or cytochrome P4502C19 genotypic differences on cure rates for gastroesophageal reflux disease by lansoprazole[J]. Clin Pharmacol Ther, 2002, 72(4): 453-460.
[26]
Furuta T, Shirai N, Takashima M, et al. Effects of genotypic differences in CYP2C19 status on cure rates for Helicobacter pylori infection by dual therapy with rabeprazole plus amoxicillin[J]. Pharmacogenetics, 2001, 11(4): 341-348.
[27]
Togawa J, Inamori M, Fujisawa N, et al. Efficacy of a triple therapy with rabeprazole, amoxicillin, and faropenem as second-line treatment after failure of initial Helicobacter pylori eradication therapy[J]. Hepatogastroenterology, 2005, 52(62): 645-648.
[28]
Furuta T, Shirai N, Takashima M, et al. Effect of genotypic differences in CYP2C19 on cure rates for Helicobacter pylori infection by triple therapy with a proton pump inhibitor, amoxicillin, and clarithromycin[J]. Clin Pharmacol Ther, 2001, 69(3): 158-168.
Yamamoto Y, Takahashi Y, Imai K, et al. Influence of CYP2C19 polymorphism and concomitant antiepileptic drugs on serum clobazam and N-desmethyl clobazam concentrations in patients with epilepsy[J]. Ther Drug Monit, 2013, 35(3): 305-312.
Van Der Weide J, Steijns LS, Van Weelden MJ, et al. The effect of genetic polymorphism of cytochrome P450 CYP2C9 on phenytoin dose requirement[J]. Pharmacogenetics, 2001, 11(4): 287-291.
Mrazek DA, Biernacka JM, O’ kane DJ, et al. CYP2C19 variation and citalopram response[J]. Pharmacogenet Genomics, 2011, 21(1): 1-9.
[35]
Yu BN, Chen GL, He N, et al. Pharmacokinetics of citalopram in relation to genetic polymorphism of CYP2C19[J]. Drug Metab Dispos, 2003, 31(10): 1255-1259.
[36]
Herrlin K, Yasui-Furukori N, Tybring G, et al. Metabolism of citalopram enantiomers in CYP2C19/CYP2D6 phenotyped panels of healthy Swedes[J]. Br J Clin Pharmacol, 2003, 56(4): 415-421.
[37]
Montgomery SA, Huusom AK, Bothmer J. A randomised study comparing escitalopram with venlafaxine XR in primary care patients with major depressive disorder[J]. Neuropsychobiology, 2004, 50(1): 57-64.
Gurbel PA, Cummings CC, Bell CR, et al. Onset and extent of platelet inhibition by clopidogrel loading in patients undergoing elective coronary stenting: the Plavix Reduction Of New Thrombus Occurrence (PRONTO) trial[J]. Am Heart J, 2003, 145(2): 239-247.
[40]
Matetzky S, Shenkman B, Guetta V, et al. Clopidogrel resistance is associated with increased risk of recurrent atherothrombotic events in patients with acute myocardial infarction[J]. Circulation, 2004, 109(25): 3171-3175.
[41]
Hochholzer W, Trenk D, Bestehorn HP, et al. Impact of the degree of peri-interventional platelet inhibition after loading with clopidogrel on early clinical outcome of elective coronary stent placement[J]. J Am Coll Cardiol, 2006, 48(9): 1742-1750.
[42]
Simon T, Verstuyft C, Mary-Krause M, et al. Genetic determinants of response to clopidogrel and cardiovascular events[J]. N Engl J Med, 2009, 360(4): 363-375.
