Pathology and autoimmunity

One of the present tasks of pathology is to define distinct topographical patterns and phenotypes of Helicobacter pylori gastritis with clinical and prognostic implications. There are indications that a diffuse antral-predominant gastritis is associated with duodenal and prepyloric ulcers, that pangastritis with progressive intestinal metaplasia and atrophy predispose to gastric ulcers or cancer, and that a non-ulcer pangastritis without intestinalization follows an uncomplicated course in the majority of patients. Gastritis risk indices reflecting these patterns can be useful for the evaluation of such phenotypes in routine diagnosis, even though the exact histological criteria for the diagnosis and grading of atrophy still need to be improved. A decisive pathogenic cofactor for the development of atrophy and intestinal metaplasia in H. pylori gastritis seems to be an antigastric autoimmunity. Autoantibodies with major specificities for the canalicular folds of parietal cells and the gastric H+,K+-ATPase are significantly associated with H. pylori infection and indicate a link between bacterial and classical autoimmune gastritis, Molecular mimicry involving Lewis antigens is probably relevant in the pathogenesis of the anti-gastric autoreactivity in animal experimental models, but not in human H. pylori infection, Apparently, the H. pylori-induced immune and cytokine response itself initiates changes of the gastric microenvironment in infected patients, which predispose to the local autoimmune attacks. Curr Opin Gastroenterol 14 (suppl 1):S35-S39 (C) 1998 Lippincott Williams & Wilkins.