Mild gastric acid hypersecretion resulting from (1) increased release of gastrin, presumably due to (a) stimulation of antral G cells by cytokines released by inflammatory cells and (b) diminished production of somatostatin by D cells, both resulting from H. pylori infection; and (2) an exaggerated acid response to gastrin due to an increased parietal cell mass resulting from gastrin stimulation. These abnormalities reverse rapidly with eradication of H. pylori. However, a mildly elevated maximum gastric acid output in response to exogenous gastrin persists in some pts long after eradication of H. pylori, suggesting that gastric acid hypersecretion may be, in part, genetically determined. H. pylori may also result in elevated serum pepsinogen levels. Mucosal defense in duodenum is compromised by toxic effects of H. pylori infection on patches of gastric metaplasia that result from gastric acid hypersecretion or rapid gastric emptying. Other risk factors include glucocorticoids, NSAIDs, chronic renal failure, renal transplantation, cirrhosis, and chronic lung disease.