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.