Epidemiology

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Progression of chronic atrophic gastritis associated with Helicobacter pylori infection increases risk of gastric cancer

  1. Hiroshi Ohata1,3,
  2. Shintaro Kitauchi1,
  3. Noriko Yoshimura2,
  4. Kouichi Mugitani3,
  5. Masataka Iwane3,
  6. Hideya Nakamura3,
  7. Akiyoshi Yoshikawa3,
  8. Kimihiko Yanaoka1,
  9. Kenji Arii1,
  10. Hideyuki Tamai1,
  11. Yasuhito Shimizu1,
  12. Tatsuya Takeshita2,
  13. Osamu Mohara3,
  14. Masao Ichinose1,†,*

Article first published online: 11 DEC 2003

DOI: 10.1002/ijc.11680

Issue

International Journal of Cancer

International Journal of Cancer

Volume 109, Issue 1, pages 138–143, 10 March 2004

Additional Information

How to Cite

Ohata, H., Kitauchi, S., Yoshimura, N., Mugitani, K., Iwane, M., Nakamura, H., Yoshikawa, A., Yanaoka, K., Arii, K., Tamai, H., Shimizu, Y., Takeshita, T., Mohara, O. and Ichinose, M. (2004), Progression of chronic atrophic gastritis associated with Helicobacter pylori infection increases risk of gastric cancer. International Journal of Cancer, 109: 138–143. doi: 10.1002/ijc.11680

Author Information

  1. 1

    Second Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan

  2. 2

    Department of Public Health, Wakayama Medical University, Wakayama, Japan

  3. 3

    Wakayama Wellness Foundation, Wakayama, Japan

  1. †

    Fax: +81-734-45-3616, +81-734-47-1335

*Second Department of Internal Medicine, Wakayama Medical University, 811-1 Kimiidera, Wakayama-shi, Wakayama 641-0012, Japan

Publication History

  1. Issue published online: 15 JAN 2004
  2. Article first published online: 11 DEC 2003
  3. Manuscript Accepted: 7 OCT 2003
  4. Manuscript Revised: 29 SEP 2003
  5. Manuscript Received: 3 JUL 2003

Funded by

  • Ministry of Health, Labor, and Welfare of Japan
  • Japan Society for the Promotion of Science. Grant Number: 13670548

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Keywords:

  • atrophic gastritis;
  • gastric cancer;
  • Helicobacter pylori;
  • cohort study;
  • pepsinogen

Abstract

We conducted a longitudinal cohort study to determine the association of Helicobacter pylori infection and the progression of chronic atrophic gastritis (CAG) with gastric cancer. A cohort of 4,655 healthy asymptomatic subjects was followed for a mean period of 7.7 years. H. pylori infection was established by serum specific antibodies and the presence of CAG was confirmed by serum pepsinogen. During the follow-up period, 45 gastric cancer cases were detected (incidence rate, 126/100,000 person-years). A univariate analysis after adjustment for age showed that both H. pylori and CAG were significantly associated with gastric cancer. To clarify the interaction between H. pylori and CAG, an analysis stratified by H. pylori- and CAG–status was performed. No cancer developed in the H. pylori(−)/CAG(−) group during the study period. This supports the theory that it is quite rare for any type of gastric cancer to develop in an H. pylori-free healthy stomach. With the progression of H. pylori-induced gastritis, the risk of gastric cancer increased in a stepwise fashion from CAG-free gastritis [H. pylori(+)/CAG(−) group] (HR=7.13, 95%CI=0.95-53.33) to CAG [H. pylori(+)/CAG(+) group] (HR=14.85, 95%CI=1.96–107.7) and finally to severe CAG with extensive intestinal metaplasia [H. pylori(−)/CAG(+) group] (HR=61.85, 95%CI=5.6–682.64) in which loss of H. pylori from the stomach is observed. Therefore, it is probable that H. pylori alone is not directly associated with stomach carcinogenesis. Instead, H. pylori appears to influence stomach carcinogenesis through the development of CAG. The observed positive correlation between the extent of H. pylori-induced gastritis and the development of cancer was strong, especially for the intestinal type. These results are compelling evidence that severe gastritis with extensive intestinal metaplasia is a major risk factor for gastric cancer, and they confirm the previously described model of stomach carcinogenesis: the gastritis-metaplasia-carcinoma sequence. © 2003 Wiley-Liss, Inc.

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