Long-term histologic consequences of suppression/eradication of Helicobacter pylori in antral mucosa

Purpose To assess histological and local immunological consequences of Helicobacter pylori suppression/eradication. Design Thirty-four patients with non-healing or recurrent duodenal ulcer were treated with omeprazole followed by triple therapy. At least two gastric mucosal samples from the antral portion of the stomach and from the duodenum were collected prior to, and immediately after omeprazole therapy, 4 weeks after completion of triple therapy, and subsequently at monthly intervals up to 2 years. Twenty antral biopsies collected from 10 patients uninfected with H. pylori served as controls. Methods Samples were fixed in buffered formaldehyde and examined histologically and histochemically for inflammation, mucin secretion, atrophy, intestinal metaplasia, density of H. pylori colonization, and immunohistochemically for the density of gastrin-secreting cells, immunoglobulins (IgA, IgG, IgM), T lymphocytes and complement C3c. Results At the initial examination, all 34 patients had endoscopically and histologically confirmed active duodenal ulcer. All had histologically diagnosed H. pylori infection and antral gastritis of varying degrees of severity. Eradication was noted in 68% of patients when tested 1 month following triple therapy. Gastric mucosa after eradication of H. pylori showed improvement in epithelial cells, disappearance of inflammatory infiltrate and normal secretion of previously reduced mucin content. One patient showed recurrence of infection within 2 years of follow-up. G-cell hyperplasia observed after cessation of omeprazole and triple therapy was not present in the sequential biopsies. Glandular atrophy and intestinal metaplasia present before therapy in nine out of the 34 patients failed to resolve during the follow-up period. Atrophy and intestinal metaplasia developed during the 2-year follow-up period in four out of 23 patients in whom H. pylori was eradicated, and in two out of 11 with persistent H. pylori infection. Conclusion Atrophic/metaplastic mucosal lesions are resistant for eradication of H. pylori, when present initially or when they occur after therapy. Local cellular and immune response by antral mucosa is not responsible for the pathogenesis of these lesions.