Relation of topography of inflammation to gastric physiology and clinical outcome. (a) H. pylori–induced antral-predominant inflammation. Antral inflammation results in hypergastrinemia, which stimulates a physiologically intact corpus to secrete acid, increasing risk for duodenal ulceration. (b) H. pylori–induced pan-gastritis. The inflammatory process suppresses corpus acid production, despite the gastrin stimulus from the antrum. Hypochlorhydria enhances risk of gastric ulcer and adenocarcinoma but conversely decreases risk for severe gastro-esophageal reflux disease and its sequelae. ECL, enterochromaffin-like.