Background and AimRecently, there has been burgeoning interest in the utilization of fully covered self‐expandable metal stents (FCSEMSs) for managing main pancreatic duct strictures (MPDS) in chronic pancreatitis (CP). The primary aim was to investigate stricture resolution and recurrence rates of FCSEMS placement in patients with symptomatic CP complicated with MPDS.MethodsMEDLINE, EMBASE, and ISI Web of Science and Cochrane Library (up to December 2019) were searched to identify eligible studies. A meta‐analysis of stricture resolution and recurrence rates was carried out using R. The crude rate of adverse events related to stent therapy was also calculated.ResultsTen studies involving 163 patients were included. The weighted pooled rate of MPDS resolution was 93% (95% confidence interval [95%CI] 84–99%) with substantial heterogeneity (I2 = 63%). Duration of stent placement more than 3 months did not result in a significantly higher resolution rate than that of 3 months or less (93% vs 93%, P = 0.91). The weighted pooled rate of stricture recurrence was 5% (95%CI: 0–12%). The stricture recurrence rate for patients with duration of stent placement more than 3 months (3%; 95%CI: 0–10%) was lower than that in patients with 3 months or less of stent placement (7%; 95%CI: 0–23%), but not significantly (P = 0.45). The overall rate of adverse events related to stent therapy was 34.9%, and spontaneous stent migration occurred in 14.1% of patients.ConclusionsThe use of FCSEMSs appears to be effective and safe in the management of MPDS caused by symptomatic CP.

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Background and Aim: The prophylactic effect of nonselective nonsteroidal anti-inflammatory drugs on post-ERCP (endoscopic retrograde cholangiopancreatography) pancreatitis has been observed for a long time. However, whether the selective nonsteroidal anti-inflammatory drugs possess similar abilities and the mechanisms by which nonsteroidal anti-inflammatory drugs work remain unclear. The present study aimed to determine the protective effects of nonsteroidal anti-inflammatory drugs on post-ERCP pancreatitis in a rat model and examine underlying mechanisms. Methods: Thirty-two female rats were equally and randomly divided into four groups: the sham group, post-ERCP pancreatitis model group, indomethacin-pretreated group, and parecoxib-pretreated group. Indomethacin or parecoxib was delivered 30 min prior to surgery; 24 h after post-ERCP pancreatitis establishment, the rats were sacrificed. Serum amylase and lipase activities, inflammatory cytokine release, pancreatic histopathological scores, neutrophil infiltration, and the expression pattern cyclooxygenase at the protein level and pancreatic apoptosis were quantified and analyzed. Results: Both indomethacin and parecoxib inhibited the activities of serum amylase and lipase and reduced the severity of pancreatic histopathology. Mechanistically, both drugs decreased the expression level of cyclooxygenase 2; however, they had no influence on the cyclooxygenase 1 protein level. Moreover, they reduced inflammatory cytokine release, neutrophil infiltration into the pancreas, and NF-κB p65 activation. Notably, we found that apoptotic cells in the pancreas were remarkably diminished after the administration of both nonsteroidal anti-inflammatory drugs. Conclusions: Both selective and nonselective nonsteroidal anti-inflammatory drugs exert protective effects against post-ERCP pancreatitis by restraining inflammation and reducing acinar cell apoptosis through the inhibition of cyclooxygenase 2.

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Background: Cholestasis is a common pathological process in a variety of liver diseases that may lead to liver fibrosis, cirrhosis, and even liver failure. Cholestasis relief has been regarded as a principal target in the management of multiple chronic cholestasis liver diseases like primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC) at present. However, complicated pathogenesis and limited acknowledgments fettered therapeutic development. Therefore, this study aimed to systematically analyze miRNA-mRNA regulatory networks in cholestatic liver injury in order to provide new treatment strategies.Methods: Gene Expression Omnibus (GEO) database (GSE159676) was used to screen differentially expressed hepatic miRNAs and mRNAs in the PSC vs. control comparison and the PBC vs. control comparison, respectively. MiRWalk 2.0 tool was used to predict miRNA-mRNA pairs. Subsequently, functional analysis and immune cell infiltration analysis were performed to explore the pivotal functions of the target genes. RT-PCR was used to verify the result.Results: In total, a miRNA-mRNA network including 6 miRNAs (miR-122, miR-30e, let-7c, miR-107, miR-503, and miR-192) and 8 hub genes (PTPRC, TYROBP, LCP2, RAC2, SYK, TLR2, CD53, and LAPTM5) was constructed in cholestasis. Functional analysis revealed that these genes were mainly involved in the regulation of the immune system. Further analysis revealed that resting memory CD4 T cells and monocytes could potentially participate in cholestatic liver injury. The expressions of DEMis and eight hub genes were verified in ANIT-induced and BDL-induced cholestatic mouse models. Furthermore, SYK was found to have an impact on the response to UDCA, and its mechanism was possibly associated with complement activation and monocyte reduction.Conclusion: In the present study, a miRNA-mRNA regulatory network was constructed in cholestatic liver injury, which mostly mediated immune-related pathways. Moreover, the targeted gene SYK and monocytes were found to be related to UDCA response in PBC.