Greene Christina L, Worrell Stephanie G, DeMeester Tom R
Keck School of Medicine of the University of Southern California, Los Angeles, CA.
Ann Surg. 2015 Dec;262(6):910-24. doi: 10.1097/SLA.0000000000001207.
The epidemiologic shift in esophageal cancer from squamous cell carcinoma to esophageal adenocarcinoma coincided with popularization of proton pump inhibitors and has focused attention on gastroesophageal reflux disease as a causative factor in this shift. The aim of this study is to review the literature on the rat reflux model in an effort to elucidate this phenomenon.
An extensive online literature review (PubMed) was carried out to identify all seminal contributions to the study of esophageal adenocarcinoma using the rat reflux model.
The rat reflux model is a validated reproducible model for the development of Barrett's esophagus and esophageal adenocarcinoma. Esophageal reflux of an admixture of gastric acid and duodenal juice induces Barrett's esophagus followed by adenocarcinoma. A high-pH environment created by surgical gastrectomy or proton pump inhibitor therapy in combination with a high-fat diet seems to potentiate the development of Barrett's esophagus and adenocarcinoma. Early surgical intervention to prevent reflux reduces the progression toward esophageal adenocarcinoma. Anti-inflammatory, antioxidant, and nitrate-trapping agents reduce the incidence of tumorigenesis.
As in the rat so also in humans, reflux of an admixture of gastric acid and duodenal juice in a high-pH environment induces the development of Barrett's esophagus followed by esophageal adenocarcinoma. This has led to the hypothesis that to prevent Barrett's esophagus and subsequent esophageal adenocarcinoma in humans, the reflux of an admixture of acid and bile must be controlled before the development of Barrett's esophagus by methods other than acid-suppression therapy.
食管癌从鳞状细胞癌向食管腺癌的流行病学转变与质子泵抑制剂的普及同时发生，这使得胃食管反流病作为这种转变的一个致病因素受到关注。本研究的目的是回顾有关大鼠反流模型的文献，以阐明这一现象。
进行了广泛的在线文献综述（PubMed），以确定使用大鼠反流模型对食管腺癌研究的所有重要贡献。
大鼠反流模型是用于巴雷特食管和食管腺癌发展的经过验证的可重复模型。胃酸和十二指肠液混合物的食管反流会诱发巴雷特食管，随后发展为腺癌。手术胃切除术或质子泵抑制剂治疗联合高脂肪饮食所创造的高pH环境似乎会促进巴雷特食管和腺癌的发展。早期进行预防反流的手术干预可减少向食管腺癌的进展。抗炎、抗氧化和硝酸盐捕获剂可降低肿瘤发生的发生率。
与大鼠一样，在人类中，在高pH环境下胃酸和十二指肠液混合物的反流会诱发巴雷特食管，随后发展为食管腺癌。这导致了一种假设，即要在人类中预防巴雷特食管及随后的食管腺癌，必须在巴雷特食管发展之前，通过除抑酸治疗之外的方法控制酸和胆汁混合物的反流。
