Background and Aim: Clinical features of patients who develop gastric cancer after successful eradication of Helicobacter pylori are still unclear. We attempted to identify host factors associated with the discovery of gastric cancer, including changes in the background gastric mucosa in patients with atrophic gastritis.

Methods: We enrolled 101 patients (59 men, 42 women; mean age 56.0 years) who underwent successful eradication therapy. All patients had no neoplastic lesion in the stomach and were diagnosed with corpus atrophic gastritis histologically before the eradication therapy. After successful eradication, these patients were followed up by an annual endoscopic examination (mean follow-up time 63.2 months; range 12–157 months). Fasting sera were obtained before and after eradication therapy and the serum levels of gastrin/pepsinogens were evaluated.

Results: Gastric cancer occurred during follow-up in eight of the 101 patients (7.9%). We compared the host features between the cancer-discovered group (n = 8) and the non-discovered group (n = 93). We found no difference in gender, history of previous treatment of gastric cancer, and serum pepsinogen/gastrin levels at entry between them. The trends in alterations of serum markers did not differ between the two groups. However, gastric cancer was more frequently found in older patients (>54 years at eradication) than in others (P < 0.05).

Conclusion: Improvement of gastric inflammation did not correlate with the discovery of gastric cancer after eradication; however, age at the time of eradication seemed to be important. Strict follow-up after eradication is needed in older patients with atrophic gastritis.