APOPTOSIS IN CHRONIC GASTRITIS AND ITS CORRELATION WITH ANTIGASTRIC AUTOANTIBODIES

In the course of time, chronic gastritis may result in gastric atrophy , as in type A gastritis, where autoimmune reactions against parietal cells result in a loss of corpus glands. Two antigastric autoantibodie s have been detected in Helicobacter pylori gastritis and are describe d as anti-luminal and anti-canalicular autoantibodies. The aim of this study was to determine whether increased apoptosis may be responsible for the loss of gastric epithelium and whether this apoptosis is corr elated with antigastric autoimmunity. Gastric biopsies from normal muc osa and Helicobacter pylori gastritis were analysed for the presence o f apoptosis using the TUNEL method. Helicobacter pylori gastritis was divided into cases (1) without autoantibodies, (2) with anti-luminal, and (3) with anti-canalicular autoantibodies. Apoptotic cells of the f oveolar and of the glandular epithelium in the antrum and corpus were counted. The number of apoptotic cells in the gastric mucosa was signi ficantly increased in all cases of gastritis. The highest number of ap optotic cells was observed in the gastric glands of the corpus mucosa in Helicobacter pylori gastritis with anticanalicular autoantibodies. Apoptosis contributes to the development of gastric atrophy and there are various types of Helicobacter pylori gastritis. The positive corre lation between apoptotic cell loss in the glandular zone of the corpus mucosa and the presence of anti-canalicular autoantibodies indicates a possible link between antigastric autoimmunity and atrophy in this t ype of Helicobacter pylori gastritis - similar to that in classic type A gastritis.