Background: Gastric cancer commonly follows a long-standing inflammation, mainly due to Helicobacter pylori (HP) infection. After resection, the stump develops precancerous alterations.
Design: Prospective study of patients undergoing endoscopy from April 1, 2000, through March 31, 2006.
Setting: University departments of Surgery and Experimental Medicine and Pathology.
Patients: One hundred eighty-seven patients receiving upper gastrointestinal tract endoscopy many years after surgery for duodenal ulcer or gastric cancer. Ten to 12 postoperative endoscopic biopsy samples were taken from the remnant stomach.
Main outcome measure: The risk of gastric cancer precursor lesions associated with HP infection.
Results: The gastric cancer precursor lesions were more common in the entire HP-positive population (odds ratio [OR], 2.37; 95% confidence interval [CI], 1.25-4.49; P = .007). However, HP-positive patients undergoing resection for cancer had a higher risk of the precursor lesions compared with HP-negative patients in the same diagnostic group (OR, 4.20; 95% CI, 1.10-15.96) and all patients undergoing resection for duodenal ulcer (OR, 1.59; 95% CI, 0.44-5.73).
Conclusion: The results of this investigation support the role of HP in gastric carcinogenesis and suggest that the HP eradication therapy might prevent the development of metachronous gastric cancer after gastric resection.