AUTOANTIBODIES AND GASTRIC HELICOBACTER-PYLORI INFECTION - DOES AUTOIMMUNITY AFFECT PROGRESSION TO ATROPHIC GASTRITIS

Aim: To study the mechanism by which Helicobacter pylori-associated ga stritis progresses to atrophic gastritis. Design: The prevalence of ci rculating auto-antibodies reacting with the body of the gastric mucosa was determined by immunohistochemistry in 70 patients undergoing gast roscopy. Results: An immunoglobulin G auto-antibody response was detec ted in 50 of 61 H. pylori-infected patients. The immunostaining was lo calized in the foveolar mucus, in mucous neck cells and in glandular p arietal and chief cells. Two of these patients had atrophic gastritis. Only one of the nine H. pylori-negative patients was auto-antibody-po sitive. He had body atrophic gastritis (type A) and a serum level of a ntibodies against a specific H. pylori antigen with a molecular weight of 64000, indicating a previous infection with this bacterium. Conclu sion: Chronic exposure of gastric epithelial cells to mucosal auto-ant ibodies induced by H. pylori infection may explain the tendency of chr onic gastritis to progress to atrophic gastritis.