Gastrin represents a direct pathogenic factor only in rare subgroups of ulcer patients, such as in the Zollinger-Ellison syndrome, the antral G-cell hyperplasia syndrome, and in patients in whom the gastric antrum was erroneously retained following partial gastrectomy. Gastrin may play a contributory role in the pathogenesis of uncomplicated peptic ulcer disease, as an exaggerated, but reversible gastrin release appears to be associated with Helicobacter pylori colonization. The known trophic effects of gastrin could account for the overall increase in the parietal cell mass of patients suffering from duodenal ulcer disease. Circumstantial evidence suggests that the abnormal gastrin release could also explain the upregulation of the parietal cell to the acid stimulatory effect and the consequent increase in gastrin sensitivity in patients suffering from duodenal ulcer disease. Conversely, the trophic effects of gastrin have also been linked to ulcer healing, especially since potent acid inhibitors induce a substantial hypergastrinemia. The evidence for such an association, however, is only circumstantial and potent and selective gastrin receptor antagonists are necessary to fully clarify the role gastrin exerts in ulcer healing.