The pathophysiology of peptic ulcers, whether gastric or duodenal, is multifac-torial. Ulcers develop depending on the balance of injurious factors and host defense mechanisms. Environmental stressors are numerous. Acid secretion is involved in the final common pathway of ulcer formation. In regards to duodenal ulceration, mucosal exposure of acid is a necessary component of their pathogenesis. In general, patients with duodenal ulcers have an increased capacity for acid secretion. Maximal acid output in normal patients is usually around 20 mEq/hour but patients with duodenal ulcers may exceed 40 mEq/hr. There is, however, variability in this finding to the extent that some patients with duodenal ulcers have maximal acid outputs that are considered in the normal range. Additionally, patients with duodenal ulcer have increased basal acid outputs with normal basal gastrin levels. The role that acid secretion plays with the formation of gastric ulcers is less clear. Hypersecretion of acid is not associated with all subtypes of gastric ulcers. Gastric acid does, however, play a role in the chain of events that leads to ulceration.

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