Anastomotic leak is still a severe complication in esophageal surgery due to high mortality. This article reviews the updates on the treatment of anastomotic leak after esophagectomy in order to provide reference for clinical treatment and research. The relevant studies published in the Chinese Zhiwang, Wanfang, and MEDLINE databases to December 21, 2021 were retrieved, and esophageal carcinoma, esophagectomy, anastomotic leakage, and fistula selected as the keywords. A total of 78 studies were finally included. The treatments include traditional surgical drainage, new reverse drainage trans-fistula, stent plugging, endoscopic clamping, biological protein glue injection plugging, endoluminal vacuum therapy (EVT), and reoperation, etc. Early diagnosis, accurate classification and optimal treatment can promote the rapid healing of anastomotic leaks. EVT may be the most valuable approach, simultaneously with good commercial prospects. Reoperation should be considered in patients with complex fistula in which conservative treatment is insufficient or has failed.
Background: Barrett’s esophagus (BE) is the premalignant condition for the development of esophageal adenocarcinoma, and occurs when the stratified epithelium is replaced by an intestinal-type epithelium with goblet cells. Bile acids (BAs) may play a dominant role in esophageal metaplasia, which is characterized by the expression of intestine-specific nuclear transcription factor caudal type homeobox transcription factor 2 (CDX-2). Notch-1 is frequently downregulated in BE, and protects squamous epithelia from becoming malignant and inducing intestinal metaplasia. However, the molecular mechanisms of this pathway are unclear. Methods: We first investigated Notch-1 and CDX-2 in human BE epithelium. Then Wister rats were used to develope animal models to test the role of BAs in the pathogenesis of BE. Effects of deoxycholic acid (DCA) on Notch-1 and CDX-2, as well as Notch signaling pathway blockage with DATP or with si-Hes-1 in vitro were observed through RT–PCR and western blotting techniques in human EAC cells (OE-19) and esophageal epithelial cells (Het-1a). Results: We found that the Notch -1 gene was inhibited in human and rodent BE specimens and BAs induced Barrett’s-like metaplasia. DCA decreases Notch-1 in a time and concentration dependent manner in both EAC cells (OE-19) and esophageal epithelial cells (Het-1a). Notch signaling inhibition increased CDX-2 expression but also blocked the influence of DCA. Conclusions: These data imply that BAs induce BE by inhibiting Notch-1 in esophageal cells. Notch signal pathway inhibition presents a therapeutic strategy for premalignant conditions of the esophagus.
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