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. 2013 Apr 21;19(15):2419-24.
doi: 10.3748/wjg.v19.i15.2419.

Exposure to gastric juice may not cause adenocarcinogenesis of the esophagus

Peng Cheng  1 , Jian-Sheng Li, Lian-Feng Zhang, Yong-Zhong Chen, Jun Gong
Affiliations

Exposure to gastric juice may not cause adenocarcinogenesis of the esophagus

Peng Cheng et al. World J Gastroenterol. .

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

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Figures

Figure 1
Figure 1
Gross specimens changes in the esophagus and forestomach mucosa in the sham-operated and model groups. A, B: Gross esophageal specimens of the sham-operated group (A) and animal model group (B); C, D: Gross forestomach specimens of the sham-operated group (C) and animal model group (D).
Figure 2
Figure 2
Changes in the esophagus and forestomach mucosa in the sham-operated and model groups under light microscope (200×). A: Normal esophagus in the sham-operated group; B: Esophagitis and Barrett’s esophagus in the model group; C: Intestinal metaplasia with dysplasia and esophageal adenocarcinoma in the model group; D: Normal forestomach in the sham-operated group; E, F: Inflammation in the forestomach of the model group.
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