Gastric ulcer and regurgitation gastritis.

Experimental and clinical data have incriminated excess gastric acid secretion as an important factor in the development of duodenal ulcer. On the other hand, gastric ulcer is characteristically associated with normal to low levels of acid secretion, and mucosal resistance factors have been invoked to explain the pathogenesis. The purpose of this report is to summarize the evidence favouring the hypothesis that regurgitation of duodenal contents into the stomach causes gastritis and an attendant decrease in mucosal resistance to ulceration. Recent experimental results from our laboratory support this proposition1' 2 , 4 The concept of regurgitation gastritis is not original with us but has received inadequate attention. Four lines of evidence favour the proposed hypothesis. (1) Gastric ulcer is invariably accompanied by gastritis. (2) Individuals with gastric ulcer have greater than normal regurgitation of duodenal contents into the stomach. (3) Exposure of normal gastric mucosa to intestinal contents leads to gastritis. (4) Gastritis increases the susceptibility of the mucosa to ulcer formation.