Pathophysiology of Helicobacter pylori infection

Helicobacter pylori (H.p.) causes active chronic gastritis in nearly all in fected patients. Cytotoxic factors elaborated by H.p. as well as autoimmune cell damage from the abundant inflammatory response contribute to gastric epithelial cell injury. Antrum gastritis increases gastrin release. The imp act of II. p.-infection on gastric acid physiology is complex and usually r esults in increased gastric acid secretion in duodenal ulcer patients and d iminished acid output in patients with gastric cancer. Multiple clinical outcomes including asymptomatic gastritis, duodenal ulcer , gastric ulcer, gastric carcinoma and gastric MALT lymphoma are associated with li,p.-infection. Differences in disease manifestation seem to result from a complex interaction of bacterial virulence, host factors as well as environmental factors. The acid-secretory ability of the infected individua l seems to be the main variable determining outcome: Patients with high aci d production typically develop antrum-predominant gastritis and are at an i ncreased risk for duodenal ulcer, In contrast patients with low gastric aci d secretion frequently develop pangastritis, which may progress to chronic atrophic gastritis and carcinoma.