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Mucosal loss as a critical factor in esophageal stricture formation after mucosal resection: a pilot experiment in a porcine model.
Surgical Endoscopy ( IF 2.4 ) Pub Date : 2019-04-12 , DOI: 10.1007/s00464-019-06793-z
Bing-Rong Liu 1 , Dan Liu 1 , Wenyi Yang 2 , Saif Ullah 1 , Zhen Cao 2 , Dezhi He 1 , Xuehui Zhang 2 , Yang Shi 1 , Yangyang Zhou 1 , Yong Chen 2 , Donghai He 2 , Lixia Zhao 1 , Yulian Yuan 1 , Deliang Li 1
Affiliation  

BACKGROUND AND AIM Esophageal stricture is a major complication of large areas endoscopic submucosal dissection (ESD). Until now, the critical mechanism of esophageal stricture remains unclear. We examined the role of mucosal loss versus submucosal damage in esophageal stricture formation after mucosal resection using a porcine model. MATERIALS AND METHODS Twelve swine were randomly divided into two groups, each of 6. In each group, two 5-cm-long submucosal tunnels were made to involve 1/3rd of the widths of the anterior and posterior esophageal circumference. The entire mucosal roofs of both tunnels were resected in group A. In group B, the tunnel roof mucosa was incised longitudinally along the length of the tunnel, but without excision of any mucosa. Stricture formation was evaluated by endoscopy after 1, 2, and 4 weeks, respectively. Anatomical and histological examinations were performed after euthanasia. RESULTS Healing observed on endoscopy in both groups after 1 week. Group A (mucosa resected) developed mild-to-severe esophageal stricture, dysphagia, and weight loss. In contrast, no esophageal stricture was evident in group B (mucosa incisions without resection) after 2 and 4 weeks, respectively. Macroscopic examination showed severe esophageal stricture and shortening of esophagus in only group A. Inflammation and fibrous hyperplasia of the submucosal layer was observed on histological examination in both groups. CONCLUSION The extent of loss of esophageal mucosa appears to be a critical factor for esophageal stricture. Inflammation followed by fibrosis may contribute to alteration in compliance of the esophagus but is not the main mechanism of postresection stricture.

中文翻译:

粘膜切除术是粘膜切除术后食管狭窄形成的关键因素:在猪模型中的先导实验。

背景与目的食管狭窄是大面积内镜下黏膜下剥离术(ESD)的主要并发症。直到现在,食管狭窄的关键机制仍不清楚。我们使用猪模型检查了粘膜切除术后食管狭窄形成中粘膜损失与粘膜下破坏的关系。材料与方法将十二头猪随机分为两组,每组6只。每组中,制作2条5厘米长的粘膜下隧道,覆盖食管前后壁宽度的1/3。在A组中切除了两个隧道的整个粘膜顶。在B组中,沿隧道的长度纵向切开了隧道顶粘膜,但未切除任何粘膜。分别在1、2和4周后通过内窥镜评估狭窄的形成。安乐死后进行解剖和组织学检查。结果1周后两组内镜均观察到He愈。A组(切除粘膜)出现轻度至重度食管狭窄,吞咽困难和体重减轻。相比之下,B组(未切除的粘膜切口)分别在2周和4周后没有发现食管狭窄。肉眼检查仅在A组中显示出严重的食道狭窄和食道缩短。在组织学检查中,两组均观察到了粘膜下层的炎症和纤维增生。结论食管粘膜丢失的程度似乎是食管狭窄的关键因素。炎症继之以纤维化可能会导致食管顺应性改变,但不是切除后狭窄的主要机制。
更新日期:2020-01-14
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