THE GASTRIN LINK OF HELICOBACTER-PYLORI

Aim: To form a hypothesis on how Helicobacter pylori causes peptic ulcers. Method: Survey of available studies. Hypothesis: The effects of H. pylori on gastric physiology fit the following hypothesis, although several elements remain to be tested. Cytokines released in H. pylori-associated gastritis affect mucosal endocrine cells, decreasing the expression of somatostatin and increasing gastrin release. Acid secretion is excessive when the luminal pH is low and during fasting, due to a lack of somatostatin to inhibit acid secretion at these times. H. pylori can also decrease acid secretion in primary infection, and probably also by initiating atrophic gastritis.