Background: Rabeprazole is a new, potent, proton pump inhibitor. The metabolism of rabeprazole is less dependent on CYP2C19 genetic polymorphism. Methods: A total of 102 Helicobacter pylori‐positive patients with gastric ulcer were randomly allocated to three groups: rabeprazole 10 mg (RAC10), rabeprazole 20 mg (RAC20) or rabeprazole 40 mg (RAC40) plus amoxicillin 750 mg and clarithromycin 200 mg twice daily for 7 days. CYP2C19 genotype was determined by the polymerase chain reaction‐restriction fragment length polymorphism method. Results: All‐patients‐treated‐based eradication rates in patients treated with RAC10, RAC20 and RAC40 were 83%, 77% and 90%, respectively, and per protocol‐based eradication rates were 83%, 80% and 90%, respectively. The eradication rates in the three groups were not significantly different. There was also no significant difference between the all‐patients‐treated‐based eradication rate in CYP2C19 extensive metabolizers and that in poor metabolizers (86% vs. 77%). Adverse events were 12% in extensive metabolizers and 23% in poor metabolizers, and the difference in these incidence rates was also not statistically significant. Conclusions: Triple therapy with 10 mg of rabeprazole combined with amoxicillin/clarithromycin is effective for Japanese patients with H. pylori infection, and the H. pylori eradication rate is not affected by CYP2C19 genetic polymorphism.

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Genotypic variation of Helicobacter pylori is speculated to associate with different clinical outcomes. In Western countries, the gene encoding blood group antigen-binding adhesin (BabA), babA2, is of high clinical relevance and is a useful marker to identify patients who are at higher risk for peptic ulceration and gastric adenocarcinoma, as are vacA and cagA. We investigated the presence of babA2 and cagA in 179 Japanese clinical isolates by PCR and Southern blot analysis and looked for correlations with various clinical outcomes (nonulcer dyspepsia, duodenal ulcers, gastric ulcers gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma). The prevalence of the babA2 genotype was 84.9% and that of the cagA genotype was 96.1%. There was no correlation between the babA2 and cagA genotypes, and there was no association between the babA2 or cagA status and clinical outcome. These results indicate that babA2 status is not of high clinical relevance in Japan and that Japanese strains are different from those infecting Western populations.Helicobacter pylori infection in the stomach activates a mucosal inflammatory response and leads to diverse clinical outcomes in humans (3). Most infected persons are asymptomatic with histologic gastritis (22), or they may develop a gastric or duodenal ulcer (1), adenocarcinoma (13), or mucosa-associated lymphoid tissue (MALT) lymphoma (27, 32) of the stomach.Numerous studies indicate that both bacterial and host factors may be important in leading to particular clinical and pathological sequelae of the infection. Among the bacterial factors, the role of the ability to adhere to epithelial cells is crucial in the initiation of a gastric inflammatory response (17,24,28). The blood group antigen-binding adhesin BabA has been shown to mediate adherence of H. pylori to human Lewis b (␣-1,3/4-difucosylated) blood group antigens on gastric epithelial cells (5). In vitro adherence assays revealed that H. pylori bound in a lineage-specific manner to gastric surface mucous cells mediated by fucosylated blood group antigens (11). Furthermore, a study using transgenic mice expressing the human Lewis b epitope in gastric epithelial cells indicated that Lewis b antigens function as receptors for an H. pylori adhesin and mediate its attachment to gastric pit and surface mucous cells (12). The attachment of H. pylori to gastric epithelial cells in such transgenic mice resulted in the development of chronic gastritis and gastric atrophy (15). In a recent study, the gene encoding BabA was cloned (and named babA2), thus allowing the identification of H. pylori strains harboring the babA2 genotype by PCR (18).The cag pathogenicity island is one of the major virulence factors of H. pylori, and there is a high frequency of the presence of the cagA gene in the cag pathogenicity island in patients with duodenal ulcers (16), atrophic gastritis (21, 22), gastric carcinomas (4), and MALT lymphomas (9) in Western countries. However, in Japan H. pylori strains harboring the cagA gene have not be...