Local cellular and immune response by antral mucosa in patients undergoing treatment for eradication ofHelicobacter pylori

Publisher Website
Google Scholar
Abstract
Thirty-six patients with nonhealing or recurrent duodenal ulcers (DU) were treated with omeprazole; 20 mg/day for one month followed by triple therapies (metronidazole, 400 mg three times a day, tetracyclin, 500 mg four times a day with either colloidal bismuth, 120 mg four times a day or sucralfate 1 g four times a day. At least two gastric mucosal samples were collected from the antral portion of the stomach and from the duodenum before and immediately after omeprazole therapy and four weeks after completion of triple therapies. Samples were fixed in buffered formaldehyde and glutaraldehyde and examined histologically and histochemically for inflammation, density ofH. pylori colonization, and immunohistochemically for the density of gastrin-secreting cells, immunoglobulins (IgA, IgG, IgM), kappa and lambda light chains and T-lymphocyte population.H. pylori colonization of the antral mucosa before treatment was noted in 100% and active gastritis in 86% of patients. The histologically assessed clearance rate after omeprazole treatment was 47.3%, and after triple therapies, 69.5%. The prevalence of gastritis was observed in 63.9% and 33.3% respectively. All therapies were associated with an accumulation of serous fluid, increased population of lymphocytes and plasma cells, and secretion of immunoglobulins, particularly IgG and IgM in the upper part of the lamina propria. These changes, together with increased numbers of T lymphocytes within the crypt epithelium and the lamina propria, were associated with the presence ofH. pylori organisms. Increased cellular response of the lamina propria and accumulation of immunoglobulins in the upper part of mucosa-even with histologically assessed clearance-may indicate a lack of complete eradication ofH. pylori and predict relapse of DU. Omeprazole-treated patients had hyperplasia of gastrin-secreting cells in the antrum, irrespective of the presence or absence ofH. pylori.