Effects of CYP2C19 and MDR1 genotype on the eradication rate of Helicobacter pylori infection by triple therapy with pantoprazole, amoxycillin and clarithromycin.
BACKGROUND
CYP2C19 polymorphism plays an important role in the metabolism of proton pump inhibitors. The multidrug resistance (MDR)1 genotype is associated with the successful eradication of Helicobacter pylori. The aim of the present study was to investigate the effects of CYP2C19 and MDR1 genotypes on the eradication rate of H. pylori using a pantoprazole-based triple therapy.


METHODS
A total of 210 patients infected with H. pylori were treated with 40 mg pantoprazole, 500 mg clarithromycin and 1000 mg amoxicillin twice daily for 7 days. The CYP2C19 genotype was determined with polymerase chain reaction (PCR)-restriction fragment length polymorphism analysis. The MDR1 C3435T polymorphism was identified by PCR-based allele-specific amplification (PCR-ASA).


RESULTS
Of the 210 patients who completed the study, 174 (82.9%, 95.0% confidence interval [CI], 77.8-88.0%) achieved successful eradication after the first cycle of therapy. The eradication rates for H. pylori were 86.7%, 81.1% and 82.1% in the homozygous extensive, heterozygous extensive and poor metabolizer groups, respectively (P = 0.65). Moreover, the cure rates in the CC, CT, and TT groups were 82.7%, 84.4% and 76.9%, respectively (P = 0.66). Multiple logistic regression analysis revealed that endoscopic diagnosis was a significant independent risk factor for treatment failure.


CONCLUSIONS
The eradication rates of H. pylori by pantoprazole, amoxicillin and clarithromycin were not significantly different among the CYP2C19 and MDR1 genotypes. Hence, the cure rate of H. pylori in the Korean population was no different for the CYP2C19 and MDR1 genotypes.
Oh
Jung-Hwan
JH
Division of Gastroenterology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Dong
Mi-Sook
MS
Choi
Myung-Gyu
MG
Yoo
Hae-Won
HW
Lee
Sang-Bum
SB
Park
Young In
YI
Chung
In-Sik
IS
D053799:2-Pyridinylmethylsulfinylbenzimidazoles / Q000627:therapeutic use*; D018435:ATP Binding Cassette Transporter, Subfamily B; D020168:ATP Binding Cassette Transporter, Subfamily B, Member 1 / Q000235:genetics* / Q000378:metabolism; D000328:Adult; D000658:Amoxicillin / Q000627:therapeutic use*; D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D001189:Aryl Hydrocarbon Hydroxylases / Q000235:genetics* / Q000378:metabolism; D017291:Clarithromycin / Q000627:therapeutic use*; D065731:Cytochrome P-450 CYP2C19; D024881:Drug Resistance, Bacterial; D004359:Drug Therapy, Combination; D005260:Female; D005756:Gastritis / Q000188:drug therapy / Q000235:genetics / Q000382:microbiology / Q000473:pathology; D005773:Gastroscopy; D005787:Gene Frequency; D005838:Genotype; D016481:Helicobacter Infections / Q000188:drug therapy* / Q000201:enzymology / Q000235:genetics / Q000382:microbiology; D016480:Helicobacter pylori / Q000187:drug effects* / Q000472:pathogenicity; D006801:Humans; D007723:Korea; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D000077402:Pantoprazole; D010641:Phenotype; D011110:Polymorphism, Genetic; D054328:Proton Pump Inhibitors / Q000627:therapeutic use*; D018570:Risk Assessment; D012307:Risk Factors; D012737:Sex Factors; D017211:Treatment Failure
D053799:2-Pyridinylmethylsulfinylbenzimidazoles; C513055:ABCB1 protein, human; D018435:ATP Binding Cassette Transporter, Subfamily B; D020168:ATP Binding Cassette Transporter, Subfamily B, Member 1; D000900:Anti-Bacterial Agents; D054328:Proton Pump Inhibitors; D000658:Amoxicillin; D000077402:Pantoprazole; D001189:Aryl Hydrocarbon Hydroxylases; C045793:CYP2C19 protein, human; D065731:Cytochrome P-450 CYP2C19; D017291:Clarithromycin