[Helicobacter pylori gastritis: a new infectious disease. Reflections from personal experience].

To determine the relationship of microscopic chronic antral gastritis to Helicobacter pylori, 69 consecutive patients were studied. In a prospective longitudinal study, at least 2 successive gastroscopies with antral biopsies were performed (177 investigations on the whole). Sixty six of the 69 patients were treated with various therapeutic regimens i.e. antiulcer drugs and/or antibiotics. The type and intensity of inflammation (as based on whole inflammatory infiltrate density, polymorphonuclear cells presence or absence and IgA and IgM plasma cells counts) were correlated with H. pylori status (Giemsa staining and/or biopsy culture). The presence of the organism (Hp) and the gastritis were significantly correlated (high grade of whole inflammatory infiltrate Hp + ve: 98/109 90 p. cent, Hp-ve: 9/61 15 p. cent, p less than 0.001--presence of neutrophil PMNC Hp + ve: 80/109 73 p. cent, Hp-ve: 1/61 2 p. cent; p less than 0.001--IgA and IgM plasma cells respectively Hp + ve: 7.6 +/- 6.6, 10.6 +/- 7.1, Hp-ve 1.9 +/- 2.9, 4.2 +/- 4.5; p less than 0.005). Clearance and/or eradication of H. pylori after antibiotic treatment were associated with the disappearance of chronic gastritis activity and a statistically significant decrease of whole inflammatory infiltrate density (p less than 0.001) and IgA (p less than 0.005) and IgM (p less than 0.01) plasma cells counts. Mucosal inflammation was unchanged in case of H. pylori persistence and inflammation worsening occurred in case of infection relapse. H. pylori gastric mucosa colonization seemed to be responsible for the antral chronic inflammation associated with its presence. This study documents that antral chronic gastritis is a microbial disease associated with infection by H. pylori, against which there is an inflammatory response characterized by a significant mucosal infiltration with granulocytes and IgA and IgM secreting plasma cells.