Background: Endoscopic retrograde biliary drainage (ERBD) is the most frequently performed procedure for treating benign or malignant biliary obstruction. Although duodenal perforations secondary to the biliary plastic stent are quite rare, they can be life-threatening. The treatment strategies for such perforations are diverse and continue to be debated. Case presentation: We report three cases of duodenal perforation due to the migration of biliary plastic stents that were successfully managed using an endoscope. The three patients were admitted on complaints of abdominal pain after they underwent ERBD. Abdominal computerized tomography (CT) revealed migration of the biliary plastic stents and perforation of the duodenum. Endoscopy was immediately performed, and perforation was confirmed. All migrated stents were successfully extracted endoscopically by using snares. In two of the three cases, the duodenal defects were successfully closed with haemostatic clips after stent retrieval, and subsequently, endoscopic nasobiliary drainage tubes were inserted. After the endoscopy and medical treatment, all three patients recovered completely. Conclusions: Duodenal perforations due to the migration of biliary stents are rare, and the treatment strategies remain controversial. Our cases and cases in the literature demonstrate that abdominal CT is the preferred method of examination for such perforations, and endoscopic management is appropriate as a first-line treatment approach.
Cholestasis is common in multiple clinical circumstances. The NOD-like receptor protein 3 (NLRP3) inflammasome pathway has been demonstrated to play an important role in liver injury and fibrosis induced by cholestasis. We previously proved that MCC950, a selective NLRP3 inhibitor, alleviates liver fibrosis and injury in experimental liver cholestasis induced by bile-duct ligation (BDL) in mice. Herein, we investigate the role of calcipotriol, a potent vitamin D receptor agonist, in experimental liver cholestasis, test its therapeutic efficacy, and explore its potential protective mechanism. C57BL/6 mice were made to undergo BDL or fed the 0.1% 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet to establish two classic cholestatic models. Calcipotriol was administered intraperitoneally to these mice daily. Serum makers of liver damage and integrity, liver histological changes, levels of liver pro-fibrotic markers, bile acid synthetases and transporters were measured in vivo. The underlying mechanism by which calcipotriol alleviates cholestatic liver injury and fibrosis was further investigated. The results of the current study demonstrated that calcipotriol supplement significantly alleviate cholestatic liver injury and fibrosis. Moreover, calcipotriol supplement markedly inhibited NLRP3 inflammasome pathway activation to alleviate liver injury and fibrosis in vivo and inhibit hepatic stellate cell (HSC) activation in vitro. In addition, VDR agonist calcipotriol exert inhibitory effect on NLRP3 inflammasome activation through activating yes-associated protein 1 (YAP1). In conclusion, our findings proved that calcipotriol suppressed the NLRP3 signal by activating YAP1 to alleviate liver injury and retard fibrogenesis in cholestasis.
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