Background: Although many studies have found an association between Helicob
acter pylori infection and the development of gastric cancer, many aspects
of this relation remain uncertain.
Methods: We prospectively studied 1526 Japanese patients who had duodenal u
lcers, gastric ulcers, gastric hyperplasia, or nonulcer dyspepsia at the ti
me of enrollment; 1246 had H. pylori infection and 280 did not. The mean fo
llow-up was 7.8 years (range, 1.0 to 10.6). Patients underwent endoscopy wi
th biopsy at enrollment and then between one and three years after enrollme
nt. H. pylori infection was assessed by histologic examination, serologic t
esting, and rapid urease tests and was defined by a positive result on any
of these tests.
Results: Gastric cancers developed in 36 (2.9 percent) of the infected and
none of the uninfected patients. There were 23 intestinal-type and 13 diffu
se-type cancers. Among the patients with H. pylori infection, those with se
vere gastric atrophy, corpus-predominant gastritis, and intestinal metaplas
ia were at significantly higher risk for gastric cancer. We detected gastri
c cancers in 21 (4.7 percent) of the 445 patients with nonulcer dyspepsia,
10 (3.4 percent) of the 297 with gastric ulcers, 5 (2.2 percent) of the 229
with gastric hyperplastic polyps, and none of the 275 with duodenal ulcers
.
Conclusions: Gastric cancer develops in persons infected with H. pylori but
not in uninfected persons. Those with histologic findings of severe gastri
c atrophy, corpus-predominant gastritis, or intestinal metaplasia are at in
creased risk. Persons with H. pylori infection and nonulcer dyspepsia, gast
ric ulcers, or gastric hyperplastic polyps are also at risk, but those with
duodenal ulcers are not. (N Engl J Med 2001;345:784-9.) Copyright (C) 2001
Massachusetts Medical Society.