• Shizuka Sasazuki, Manami Inoue, Motoki Iwasaki, Tetsuya Otani, Seiichiro Yamamoto, Shinobu Ikeda, Tomoyuki Hanaoka, Shoichiro Tsugane, and Japan Public Health Center Study Group.
• Epidemiology and Prevention Division, Research Center for Cancer Prevention and Screening, National Cancer Center, Chuo-ku, Tokyo, Japan. ssasazuk@gan2.res.ncc.go.jp
• Cancer Epidemiol. Biomarkers Prev. 2006 Jul 1; 15 (7): 1341-7.

BackgroundAlthough accumulating evidence suggests that Helicobacter pylori plays a role in gastric carcinogenesis, the magnitude of the risk remains uncertain.AimWe aimed to estimate the magnitude of the risk of gastric cancer associated with H. pylori infection by a large case-control study nested within a prospective cohort. Possible effect modification by CagA status, and serum pepsinogen status, as a marker of atrophic gastritis, was also considered to see its effect on developing gastric cancer.Subjects And MethodsSubjects (n = 123,576) were followed up from 1990 to 2004; 511 gastric cancer cases matched to 511 controls were used in the analysis. Plasma immunoglobulin G antibody to H. pylori, CagA, and pepsinogen I and II were measured.ResultsThe adjusted odds ratio (95% confidence interval) of gastric cancer associated with H. pylori infection was 5.1 (3.2-8.0). Assuming all CagA-positive subjects are true H. pylori positives doubled this risk. Atrophic gastritis was also associated with an elevated risk of gastric cancer and the risk increased further with pepsinogen levels.ConclusionsSubjects with pepsinogen levels indicative of severe atrophic gastritis may need careful examination regularly regardless of H. pylori infection. Those who have other pepsinogen levels but who are H. pylori seropositive are likely to benefit from H. pylori eradication therapy. Considering both the cost and the potential for misclassification that may occur using multiple serologic tests, caution is needed in interpreting or extrapolating these findings into a screening strategy.

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