Tierexperimentelle Untersuchungen zur Karzinogenese durch duodenogastralen Reflux

摘要: Background: The fact that the incidence of Barrett carcinoma is rapidly increasing has renewed interest on mechanisms carcinogenesis induced by duodenogastric reflux (DGR). aim was to investigate whether DGR carcinogenic in rodent esophagus and caused nitroso bile acids. Methods: Experiment I: 77 Sprague-Dawley rats (8 weeks old) were operated three groups: (A) Esophagojejunostomy induce mixed acid DGR; (B) gastrectomy esophagojejunostomy alone; (C) Roux-en-Y reconstruction divert reflux. columnar lining compared after 16 weeks. 2: Preop, 2 6 operation analyzed for bacterial contamination with standard methods, acids compounds high performance liquid chromatography coupled mass spectroscopy (HPLC-MS), genotoxicity micronucleus test (n = 15). Results 1. 85% adenocarcinoma 48% animals (A + B). There no difference between group A B. control C had significantly less adenocarcinoma. 2. Elimination food passage through stomach resulted overgrowth fecal bacteria (E. coli, proteus, enterococcus). In each sample, primary secondary identified HPLC-MS. Despite using highly specific techniques nitro so not detected (selective reaction monitoring, detection limit < 1 ‰ concentration). cytotoxic, but genotoxic. Conclusion: esophagus. nitrosation could be excluded as relevant mechanism carcinogenesis. observed cytotoxicity suggests chronic inflammation esophageal mucosa main DGR. Chronic injury pancreatic enzymes which act synergistically