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Influence of smoking and CYP2C19 genotypes on H. pylori eradication success

Published online by Cambridge University Press:  02 June 2006

T. SUZUKI
Affiliation:
Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, Japan Department of Internal Medicine and Molecular Science, Nagoya City University Graduate School of Medical Science, Japan
K. MATSUO
Affiliation:
Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, Japan
A. SAWAKI
Affiliation:
Department of Gastroenterology, Aichi Cancer Center Research Institute, Japan
K. WAKAI
Affiliation:
Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, Japan
K. HIROSE
Affiliation:
Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, Japan
H. ITO
Affiliation:
Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, Japan
T. SAITO
Affiliation:
Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, Japan
T. NAKAMURA
Affiliation:
Department of Endoscopy, Aichi Cancer Center Research Institute, Japan
K. YAMAO
Affiliation:
Department of Gastroenterology, Aichi Cancer Center Research Institute, Japan
N. HAMAJIMA
Affiliation:
Department of Preventive Medicine/Biostatistics and Medical Decision Making, Nagoya University Graduate School of Medicine, Japan
K. TAJIMA
Affiliation:
Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, Japan
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Abstract

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CYP2C19 polymorphisms and smoking influence the efficacy of H. pylori eradication therapy, but interaction between the two have hitherto not been examined. A total of 142 H. pylori-positive patients who received triple drug therapy with lansoprazole, amoxicillin and clarithromycin were categorized into three groups with regard to diplotypes of CYP2C19: homozygous extensive metabolizer (homEM), heterozygous EM (hetEM), and poor metabolizer (PM). The overall success rate was 61·3%. Smoking was an independent risk factor of eradication failure (OR 2·81, 95% CI 1·14–6·91), whereas CYP2C19 polymorphisms were less influential. Among non-smokers, the homEM and hetEM groups showed worse eradication rates (58·5 and 67·3%) relative to PM (76·2%) as expected; however, an opposite trend was observed among smokers (homEM 50·0%, hetEM 46·7%, PM 20·0%), indicating possible interactions with CYP2C19 polymorphisms. Smoking has a greater influence on H. pylori eradication than the CYP2C19 genotype. Interaction between smoking and CYP2C19 should be examined in the future.

Type
Research Article
Copyright
© 2006 Cambridge University Press