[Apoptosis in chronic gastritis: correlation of glandular apoptosis with antigastric autoantibodies].

In the course of time, chronic gastritis results in gastric atrophy. A typical example is type A-gastritis. Parietal cell antibodies lead to a loss of glands in the corpus mucosa. Atrophy is preceded by a preatrophic state (active type A-gastritis). Recently, gastric autoantibodies could also be detected in Helicobacter pylori induced type B-gastritis and could be specified as canalicular and luminal antibodies. The question of this study was whether apoptosis is responsible for the loss of gastric epithelium. Gastric biopsies from normal mucosa, type B-gastritis and active type A-gastritis were analysed for the presence of apoptosis using the TUNEL-method. Type B-gastritis was subdivided in cases without autoantibodies, with canalicular and luminal autoantibodies and with both types. In each case antrum- and corpus-mucosa was available and 200 cells of the foveolar as well as of the glands were counted. Normal mucosa showed only few apoptotic cells. The number of apoptosis was significantly elevated in all cases of type B-gastritis in the whole antrum and in the foveolar epithelium of the corpus. Active type A-gastritis revealed the highest number of apoptosis in the gastric glands of corpus mucosa. Subdividing type B-gastritis the most interesting result was the cases with canalicular antibodies had a similar high number of apoptosis in the corpus glands as active type A-gastritis. These cases were in this regard significantly different from cases of type B-gastritis without autoantibodies. The findings suggest that gastric atrophy might be the result of apoptosis in the gastric epithelium and that, possibly, different types of type B-gastritis lead to atrophy in different regions of the stomach.