Abstract
The increased duodeno-gastric reflux often associated with gastric or duodenal ulcer disease causes hypersecretion of acid in response to pentagastrin and hypergastrinaemia in response to a meal. It is proposed that these functional changes are mediated by an alteration in somatostatin activity that is produced by the alkaline nature or pancreatic component of the reflux. When duodenal reflux is confined to the antrum, an increased acid output from normal secretory mucosa is delivered to the duodenum where ulceration may occur. When alkaline reflux affects the body of the stomach, gastritis is produced, with local fundic hypersecretion, which may lead to ulceration of the damaged gastric mucosa. Duodenal reflux may therefore be a common factor in the pathogenesis of gastric and duodenal ulcers, and it probably acts by producing a hormonal defect.
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