BACKGROUND AND AIMS:

Helicobacter 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.

METHODS:

From 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.

RESULTS:

A 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).

CONCLUSIONS:

Patients with histologic IM or severe endoscopic atrophy were at increased risk of gastric cancer development after H pylori eradication.

Le risque de cancer gastrique persiste après éradication d’H.pylori et augmente en cas de métaplasie et/ou d’atrophie endoscopique sévère. Les recommandations pour la recherche active de la métaplasie intestinale et de l’atrophie (OLGA/OLGIM) permettant de sélectionner les patients à haut  risque doivent être appliquées.