HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

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

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 4655 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, 126/100000 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.
AuthorsHiroshi Ohata, Shintaro Kitauchi, Noriko Yoshimura, Kouichi Mugitani, Masataka Iwane, Hideya Nakamura, Akiyoshi Yoshikawa, Kimihiko Yanaoka, Kenji Arii, Hideyuki Tamai, Yasuhito Shimizu, Tatsuya Takeshita, Osamu Mohara, Masao Ichinose
JournalInternational journal of cancer (Int J Cancer) Vol. 109 Issue 1 Pg. 138-43 (Mar 2004) ISSN: 0020-7136 [Print] United States
PMID14735480 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright 2003 Wiley-Liss, Inc.
Chemical References
  • Pepsinogen A
Topics
  • Adult
  • Chronic Disease
  • Cohort Studies
  • Disease Progression
  • Follow-Up Studies
  • Gastritis, Atrophic (microbiology)
  • Helicobacter pylori (metabolism)
  • Humans
  • Male
  • Middle Aged
  • Pepsinogen A (blood)
  • Risk Factors
  • Stomach (microbiology)
  • Stomach Neoplasms (diagnosis, etiology, microbiology)
  • Time Factors

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: