Helicobacter pylori infection on the risk of stomach cancer and chronic atrophic gastritis

Citation
Zf. Zhang et al., Helicobacter pylori infection on the risk of stomach cancer and chronic atrophic gastritis, CANCER DET, 23(5), 1999, pp. 357-367
Citations number
52
Categorie Soggetti
Oncology
Journal title
CANCER DETECTION AND PREVENTION
ISSN journal
0361090X → ACNP
Volume
23
Issue
5
Year of publication
1999
Pages
357 - 367
Database
ISI
SICI code
0361-090X(1999)23:5<357:HPIOTR>2.0.ZU;2-H
Abstract
Helicobacter pylori infection is associated with gastric adenocarcinoma. Ho wever, the mechanisms of this interaction are still unclear. This study was conducted to explore the effects of H. pylori infection on early and late stage gastric carcinogenesis. This study included 134 patients with adenoca rcinoma of the stomach (ACS), 67 patients with chronic atrophic gastritis ( CAG), and 65 normal controls recruited at Memorial Sloan-Kettering Cancer C enter (MSKCC) from November 1, 1992 to November 1, 1994. Epidemiologic data were collected by a modified National Cancer Institute Health Habits Histo ry Questionnaire. H. pylori infection was diagnosed by pathological evaluat ion. Risk factors were analyzed using logistic regression. The odds ratio ( OR) associated with H. pylori infection was 10.4 [95% confidence interval ( CI): 2.6-41.6] for CAG and 11.2 (95% CI: 2.5-50.3) for gastric cancer in co mparison with normal controls, with adjustment for pack-years of smoking, a lcohol drinking, body mass index, total caloric intake, dietary fat and fib er intake, and Barrett's esophagus. But H. pylori infection was not associa ted with risk of stomach cancer when patients with stomach cancer were comp ared with patients with CAG (OR = 0.6, 95% CI: 0.3-1.3) after controlling f or potential confounding variables. This association was persistent when on ly patients with both gastric cancer and chronic gastritis were considered as cases and patients with CAG were considered as controls (OR = 0.7, 95% C I: 0.3-2.0) in the multivariate analysis. Our results suggest that H. pylor i infection may be involved in the early stage of development of GAG, but n ot in the development of stomach cancer from GAG, and indicate that strateg ies for prevention of stomach cancer should target the early stage to elimi nate H. pylori infection in high-risk populations.