Bile acid promotes intestinal metaplasia and gastric carcinogenesis
Menée sur 767 patients (452 hommes, 325 femmes, âge moyen : 51,1 ans), cette étude japonaise montre qu'une concentration élevée d'acide biliaire dans le jus gastrique favorise la survenue d'une métaplasie intestinale et la carcinogenèse de l'estomac
Background: Bile acid and Helicobacter pylori are important toxic factors for gastric mucosal injury. We examined the role of bile acid in promoting histological gastritis and gastric carcinoma in Japanese patients. Methods: A total of 767 patients (452 men, mean age 51.1 y.o.) were studied. Gastric juice was collected by gastro-endoscopic examination, and the bile acid concentration was examined by enzymatic method. The grade of histological gastritis was evaluated by gastric biopsies, and the relationship between the bile acid concentration and the gastritis score was examined. The occurrence of gastric cancer was examined by a retrospective cohort study. CDX2/CINC1 expression in RGM-1 cells was evaluated by real-time PCR. Results: In H. pylori-positive patients, we found significant positive correlation between the bile acid concentration and the grades of atrophy/intestinal metaplasia (P<0.01). However, we found significant negative associations between the bile acid concentrations and the histological scores of mononuclear cell/neutrophil infiltrations (P<0.01). Patients with a high concentration of bile acid developed gastric cancer more frequently than those with a low concentration (P<0.05). Cholic acid treatment significantly increased CDX2 expression in RGM-1 cells. CINC1 expression in RGM-1 cell was significantly induced by co-culture with H. pylori and the induction was reduced by glycochenodeoxycholic acid treatment. Conclusion: The bile acid in gastric juice contributes to the progression of histological atrophy and intestinal metaplasia without inflammatory cell infiltration, followed by carcinogenesis in H. pylori-positive patients. Impact: Bile acid promotes intestinal metaplasia and gastric carcinogenesis without inflammatory cell infiltration.