[Pathophysiology of Helicobacter pylori infection]

The (re)discovery of the gastric pathogen Helicobacter pylori almost one and a half decade ago completely changed our conception on gastroduodenal ulcer disease and gastric cancer. The most important issue is that Helicobacter pylori induces a mild, antrum dominant chronic pangastritis without increased risk of severe diseases in most of the cases. A smaller part of the infected develops antrum dominant gastritis with increased risk of duodenal ulcer. In a few cases the corpus is also affected, pangastritis occurs with increased risk to develop gastric ulcer and gastric cancer. Until now it is not quite obvious why some of the infected patients get ill while others not, and why different diseases develop in different patients. 1. From the bacterial point of view it is ascertained that toxin-producing strains (VacA, CagA positive) are more likely to induce ulcer formation and gastric carcinoma. 2. Genetic phenotype of the infected patients (blood-group and HLA antigens) may also be of importance. 3. Environmental factors may affect (promote or inhibit) disease development. All of these factors determine the complex immunological, functional and morphological changes characteristic for the developing disease.