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目的 探讨胃酸在十二指肠液反流诱发食管腺癌 (EAC)过程中的作用。方法 采用SD大鼠 ,通过手术产生三个实验组 :胃食管反流 (GER)组、十二指肠食管反流 (DER)组以及十二指肠胃食管反流 (DGER)组 ,并设无反流的假手术 (SO)对照组。术后 2 0周观察各组动物食管黏膜病变。结果 SO组未见明显病理学改变。各反流组均引发不同程度的食管炎。DER和DGER组基底细胞增生、鳞状上皮不典型增生和溃疡发生率显著高于GER组 (P <0 .0 1)。GER组没有出现Barrett’s食管 (BE)和食管腺癌 (EAC)。DER和DGER组BE发生率分别为 91.4 %和 84 .4 % ,EAC发生率分别为 2 5 .7%和5 3.1% ,均显著高于GER组 (P <0 .0 1)。DGER组EAC发生率显著高于DER组 (P <0 .0 5 )。结论 胃、十二指肠液反流均造成食管黏膜损伤 ,后者更为严重 ;十二指肠液反流在BE、EAC发展中发挥着尤为关键性的作用 ;胃酸在十二指肠液反流诱发EAC过程中起促进作用 ,显著增加十二指肠液反流诱发EAC的危险性
Objective To investigate the role of gastric acid in esophageal adenocarcinoma (EAC) induced by duodenal reflux. Methods SD rats were used to produce three experimental groups: GER group, DER group, and DGER group. Refluxed sham surgery (SO) control group. Twenty days after operation, esophageal mucosal lesions were observed in all groups. Results SO group showed no obvious pathological changes. Each reflux group induced different degrees of esophagitis. Baseline hyperplasia, dysplasia and ulceration of squamous epithelium in DER and DGER group were significantly higher than those in GER group (P <0.01). Barrett’s esophagus (BE) and esophageal adenocarcinoma (EAC) did not develop in the GER group. The incidence of BE was 91.4% and 84.4% for DER and DGER respectively, and the incidences of EAC were 25.7% and 53.1%, respectively, which were significantly higher than those in GER group (P <0.01). The incidence of EAC in DGER group was significantly higher than that in DER group (P <0.05). Conclusion Gastro-duodenal fluid reflux causes esophageal mucosal injury, the latter is more serious. Duodenal fluid reflux plays a key role in the development of BE and EAC. Gastric acid is induced in duodenal fluid reflux EAC process plays a catalytic role, significantly increased duodenal fluid reflux induced EAC risk