Reflux gastritis syndrome: mechanism of symptoms.

Despite numerous observations indicating the deleterious effect of refluxed intestinal contents upon the stomach, the mechanism of injury and symptoms in the reflux gastritis syndrome is unclear. Much speculation has centered around the role of bile acids in the production of symptoms and histologic damage. Accordingly, the aims of our study were (a) to determine whether administration of autologous intestinal contents into the stomach can produce the symptoms of the reflux gastritis syndrome, (b) to measure and conpare the concentrations of bile acids in upper intestinal contents of postsurgical patients with and without the syndrome, and (c) to determine whether artificial bile acid solutions can reproduce the symptoms reported by the patients. Eleven patients with reflux gastritis syndrome and 10 asymptomatic postgastric surgery patients were evaluated. Autologous intestinal contents obtained after cholecystokinin injection and normal saline were infused in a random, double-blind fashion into the stomach of the patients. Determinations for total and individual bile acids, as well as the bile acid conjugated/unconjugated and glycine/taurine ratios were made on aliquots of upper intestinal contents of symptomatic and asymptomatic patients. Finally, saline and two artificial bile acid solutions with bile acid compositions similar to those of upper intestinal contents from symptomatic and asymptomatic patients were infused in random, double-blind fashion into the stomach of 8 patients from each group. Positive symptom responses to autologous intestinal contents were found in 10 of 11 symptomatic patients and only 2 of 10 asymptomatic patients (P < 0.01), both of whom showed positive responses to both autologous intestinal contents and saline. No symptomatic patients had a positive response to saline. Symptomatic patients had bile acid concentrations significantly greater (P < 0.001) than asymptomatic patients. A positive response to artificial bile acid solution infusion was found in only 1 symptomatic patient. It is concluded that (a) symptoms of the reflux gastritis syndrome are reproduced by gastric infusion of upper intestinal contents and (b) bile acids alone are not responsible for the production of symptoms.