Brief Article
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World J Gastroenterol. Apr 21, 2013; 19(15): 2419-2424
Published online Apr 21, 2013. doi: 10.3748/wjg.v19.i15.2419
Exposure to gastric juice may not cause adenocarcinogenesis of the esophagus
Peng Cheng, Jian-Sheng Li, Lian-Feng Zhang, Yong-Zhong Chen, Jun Gong
Peng Cheng, Jian-Sheng Li, Lian-Feng Zhang, Yong-Zhong Chen, Department of Gastroenterology, the First Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China
Jun Gong, Department of Gastroenterology, the Second Hospital of Xi’an Jiao Tong University, Xi’an 710004, Shaanxi Province, China
Author contributions: Cheng P designed the study, wrote the manuscript and performed the majority of experiments; Li JS, Zhang LF and Chen YZ provided vital reagents and analytical tools and were also involved in revising the manuscript; Gong J designed the study and provided financial support for this work.
Correspondence to: Peng Cheng, MD, Associate Professor, Department of Gastroenterology, the First Hospital of Zhengzhou University, No. 1, Jianshe Donglu, Zhengzhou 450052, Henan Province, China. cpzxczzc2004@yahoo.com.cn
Telephone: +86-371-66862062 Fax: +86-371-66964992
Received: October 24, 2012
Revised: March 15, 2013
Accepted: March 21, 2013
Published online: April 21, 2013
Processing time: 177 Days and 8.4 Hours
Abstract

AIM: To determine the effects of gastric juice on the development of esophageal adenocarcinoma (EAC).

METHODS: A animal model of duodenogastroesophageal reflux was established in Sprague-Dawley rats undergoing esophagoduodenostomy. The development of EAC and forestomach adenocarcinoma was investigated 40 wk after the treatment. Intraluminal pH and bile of the forestomach were measured.

RESULTS: There were no significant differences in pH (t = 0.117, P = 0.925) or bile (χ2 = 0.036, P = 0.85) in the forestomach before and 40 wk after esophagoduodenostomy. There were also no significant differences between the model and controls during esophagoduodenostomy or 40 wk after esophagoduodenostomy. The incidence of intestinal metaplasia (88%) and intestinal metaplasia with dysplasia and adenocarcinoma (28%) in the esophagus in the model was higher than in the controls 40 wk after surgery (χ2 = 43.06, P < 0.001 and χ2 = 9.33, P = 0.002, respectively) and in the forestomach in the model (χ2 = 32.05, P < 0.001 and χ2 = 8.14, P = 0.004, respectively). The incidence rates of inflammation in the esophagus and forestomach were 100% and 96%, respectively (χ2 = 1.02, P = 0.31) in the model, which was higher than in the esophageal control (6.8%) (χ2 = 42.70, P < 0.001).

CONCLUSION: Gastric juice exposure may not cause intestinal metaplasia with dysplasia or adenocarcinoma of the forestomach and may not be related to EAC.

Keywords: Intestinal metaplasia; Gastric juice; Pathogenesis; Esophageal adenocarcinoma; Gastroesophageal reflux

Core tip: The incidence of esophageal adenocarcinoma (EAC) has rapidly increased, which may be related to the increased incidence of gastroesophageal reflux disease. A better understanding of how refluxate contributes to development of EAC will help decrease the incidence of cancer. We surgically developed a rat model of duodenogastroesophageal reflux and found that although exposure of the forestomach to gastric juice may induce inflammation and mild metaplasia, it does not lead to the development of metaplasia with dysplasia or adenocarcinoma. It is concluded that gastric juice may not be related to the development of EAC.