OBJECTIVE: To determine whether the elimination of bile reflux in the established esophagojejunostomy model of Barrett's esophagus (BE) will reduce or eliminate the risk of developing esophageal adenocarcinoma. SUMMARY BACKGROUND DATA: Reflux of duodenal juice as well as gastric acid plays an important role in the pathogenesis of BE and adenocarcinoma. Duodenoesophageal reflux (DER) per se induces these diseases without carcinogen. However, it is unclear whether antireflux surgery induces regression of BE and prevents adenocarcinoma. METHODS: Two hundred F344 male rats underwent one of following 3 operations: (1) total gastrectomy and esophagojejunostomy to induce DER, followed by killing after 20 (n = 13), 30 (n = 12), and 50 weeks (n = 30); (2) biliary diversion procedure, converted to Roux-en-Y method, to avoid bile regurgitation into the esophagus at 20 (n = 29) and 30 weeks (n = 32) after the operation to induce DER, followed by killing 50 weeks after initial operation; or (3) total gastrectomy and Roux-en-Y esophagojejunostomy followed by killing after 50 weeks served as controls (n = 28). RESULTS: BE developed in more than half of the animals exposed to DER for 20 weeks, in more than 90% of rats with DER for 30 weeks, and in 100% of animals exposed to DER for 50 weeks. In the incidence and the length of BE, there is no difference between the animals that underwent biliary diversion at 20 (62%) and 30 weeks (94%) and those that had DER for 20 (54%) and 30 weeks (92%), respectively. Incidence of adenocarcinoma was significantly lower in the rats that underwent the biliary diversion procedure after 30 (19%) and 20 weeks (3%) than in the rats that had DER for 50 weeks (60%) (P < 0.005). None of the control animals that underwent Roux-en-Y esophagojejunostomy developed BE and carcinoma. CONCLUSIONS: It is likely that the converting procedure from the esophagojejunostomy to induce DER to biliary diversion does not lead to regression of BE but prevents the development of esophageal adenocarcinoma in the rats.
OBJECTIVE: To determine whether the elimination of bile reflux in the established esophagojejunostomy model of Barrett's esophagus (BE) will reduce or eliminate the risk of developing esophageal adenocarcinoma. SUMMARY BACKGROUND DATA: Reflux of duodenal juice as well as gastric acid plays an important role in the pathogenesis of BE and adenocarcinoma. Duodenoesophageal reflux (DER) per se induces these diseases without carcinogen. However, it is unclear whether antireflux surgery induces regression of BE and prevents adenocarcinoma. METHODS: Two hundred F344 male rats underwent one of following 3 operations: (1) total gastrectomy and esophagojejunostomy to induce DER, followed by killing after 20 (n = 13), 30 (n = 12), and 50 weeks (n = 30); (2) biliary diversion procedure, converted to Roux-en-Y method, to avoid bile regurgitation into the esophagus at 20 (n = 29) and 30 weeks (n = 32) after the operation to induce DER, followed by killing 50 weeks after initial operation; or (3) total gastrectomy and Roux-en-Y esophagojejunostomy followed by killing after 50 weeks served as controls (n = 28). RESULTS: BE developed in more than half of the animals exposed to DER for 20 weeks, in more than 90% of rats with DER for 30 weeks, and in 100% of animals exposed to DER for 50 weeks. In the incidence and the length of BE, there is no difference between the animals that underwent biliary diversion at 20 (62%) and 30 weeks (94%) and those that had DER for 20 (54%) and 30 weeks (92%), respectively. Incidence of adenocarcinoma was significantly lower in the rats that underwent the biliary diversion procedure after 30 (19%) and 20 weeks (3%) than in the rats that had DER for 50 weeks (60%) (P < 0.005). None of the control animals that underwent Roux-en-Y esophagojejunostomy developed BE and carcinoma. CONCLUSIONS: It is likely that the converting procedure from the esophagojejunostomy to induce DER to biliary diversion does not lead to regression of BE but prevents the development of esophageal adenocarcinoma in the rats.
Authors: S Oberg; R V Lord; J H Peters; P Chandrasoma; J Theisen; J A Hagen; S R DeMeester; C G Bremner; T R DeMeester Journal: J Surg Res Date: 2000-06-15 Impact factor: 2.192
Authors: W L Hofstetter; J H Peters; T R DeMeester; J A Hagen; S R DeMeester; P F Crookes; P Tsai; F Banki; C G Bremner Journal: Ann Surg Date: 2001-10 Impact factor: 12.969
Authors: Daniel S Oh; Steven R DeMeester; Christy M Dunst; Ryutaro Mori; Bethany J Lehman; Hidekazu Kuramochi; Kathleen Danenberg; Peter Danenberg; Jeffrey A Hagen; Parakrama Chandrasoma; Tom R DeMeester Journal: Surg Endosc Date: 2008-09-24 Impact factor: 4.584