PEPTIC-ULCER PATHOGENESIS

The role of Helicobacter pylori in peptic ulceration is well established by epidemiological studies and, most importantly, by a large number of clinical trials showing the cure of ulcer disease after the cure of infection. On the other hand, the pathogenesis of ulcer formation is incompletely understood. It is unknown why only some infected individuals develop ulcers and why ulcer disease is a chronic disorder, characterized by recurrent, circumscribed, self-limited, and painful epithelial breaks. The interaction of H. pylori with gastric acid secretion is also unclear. However, several pathophysiological mechanisms possibly contributing to ulceration have been identified. Bacterial virulence factors and their influence on the gastric mucosal barrier, the inflammatory response of the host, and other mucosal alterations such as the development of gastric metaplasia in the duodenum, seem to play an important role. Genetic susceptibility of the host, and environmental co-factors, have been suggested as additional mechanisms.