Histologic intestinal metaplasia and endoscopic atrophy are predictors of gastric cancer development after Helicobacter pylori eradication

Background and AimsHelicobacter pylori eradication therapy is effective at reducing the incidence of gastric cancer; however, gastric cancer still develops after eradication. We conducted a cohort study to elucidate the risk factors for gastric cancer development after successful H pylori eradication therapy.MethodsFrom June 1998 to December 2012 we assessed histologic and endoscopic findings of gastritis and performed H pylori eradication therapy in 748 patients without a history of gastric cancer. Patients were classified according to the distribution of intestinal metaplasia (IM) as follows: no IM (IM group A), IM in the antrum only (IM group B), and IM in the corpus (IM group C). We assessed atrophy endoscopically according to the Kimura-Takemoto classification system. Gastric cancer incidence was assessed.ResultsA total of 573 patients underwent follow-up endoscopy; the mean duration of follow-up was 6.2 ± 4.8 years. Gastric cancer developed in 21 (20 intestinal type). The cumulative 5-year incidences of gastric cancer were 3.2% overall; 1.5%, 5.3%, and 9.8% in IM groups A, B, and C; and 0.7%, 1.9%, and 10% in the none/mild, moderate, and severe endoscopic atrophy groups, respectively. Compared with IM group A, the hazard ratio for IM group B was 3.6 (95% confidence interval [CI], 1.2-11), and that for IM group C was 3.7 (95% CI, 1.1-12). Compared with the none/mild endoscopic atrophy group, the hazard ratio for severe atrophy was 9.3 (95% CI, 1.7-174).ConclusionsPatients with histologic IM or severe endoscopic atrophy were at increased risk of gastric cancer development after H pylori eradication.