Changes in Helicobacter pylori-associated gastritis of the antrum and corpus were investigated in a large number of patients treated with omeprazole, with or without the addition of amoxycillin. To investigate the role of H. pylori-associated gastritis in ulcerogenesis and its interplay with omeprazole, biopsies were taken and evaluated according to the Sydney system. Successful eradication of H. pylori (assessed histologically 4 weeks after the end of therapy) led to prompt and persistent suppression of gastritis activity, slow, partial regression of mononuclear inflammation and an ulcer recurrence rate of only 14% during the 6 months' follow-up. In patients treated with omeprazole and placebo, or where eradication treatment with omeprazole and amoxycillin had failed, transient clearance of H. pylori from the antral (but not oxyntic) mucosa was seen. In both of these groups of patients transient regression in the antrum, and worsening in the corpus, of gastritis activity and mononuclear inflammation were evident, coupled with ulcer recurrence rates of 72 and 46%, respectively. It was concluded that H. pylori colonization and gastritis activity play a crucial role in ulcerogenesis, that acid inhibition treatment improves antral H. pylori gastritis and worsens the oxyntic mucosal gastritis, and that this can be prevented by eradication of the H. pylori infection.