Objectives: The therapeutic efficacy of metal stents (MSs) for pancreatic fluid collections (PFCs) is invariably controversial. Here, we conducted a meta-analysis to summarize the results of efficacy of MSs and plastic stents (PSs) in PFC drainage. Subjects and Methods: We performed a literature search of PubMed/MEDLINE, EMBASE, and COCHRANE for all of the published studies regarding the use of MSs and PSs for endoscopic transmural drainage of PFCs from January, 1 2015 to June 1, 2020. We extracted data from 9 studies (1359 patients) that met the inclusion criteria. The main outcome measures were the rates of treatment success, including technique success and clinical success (CS), adverse events, recurrence, procedure time, and length of hospital stay (LOS). Results: There was no difference in overall technique success between patients treated with MSs and PSs for PFCs. However, MSs showed a higher CS rate 92% versus 82% (P<0.01) and a lower overall adverse event rate 20% versus 31% (P<0.01) than PSs. The recurrence rate of PFCs using MSs also had significant advantages over PSs 3% versus 10% (P<0.01) and MSs needed a shorter procedure time than PSs (26.73 vs. 45.40 min, P<0.01). In comparing direct endoscopic necrosectomy use and LOS, there was no difference between MSs and PSs. Conclusions: Bringing together the results of the current study, endoscopic ultrasound-guided drainage of PFCs using MSs may be superior to PSs in terms of CS, adverse events rates and recurrence rate, with similar LOS and direct endoscopic necrosectomy use.
Objectives: Acute pancreatitis (AP) has a high incidence of hospitalizations, morbidity, and mortality worldwide. A growing number of studies on AP pathogenesis are based on cerulein-induced experimental model, which simulates human AP in vivo. It has been demonstrated that both pancreatic acinar cells and peritoneal macrophages are involved in pancreatic inflammation and damage. However, their connection has not been well understood. Methods: A cerulein-induced AP model was established on the pancreatic acinar cell line AR42J. Rat macrophages were isolated from the peritoneal cavity. The effects of cerulein-induced pancreatic exosomes on the peritoneal macrophage and pancreas in vivo and in vitro were examined. The underlying molecular mechanism was investigated by exploring the regulatory role of downstream molecules. Results: We found that exosomes derived from cerulein-treated AR42J cells induced rat peritoneal macrophage M1 polarization and pyroptosis. miR-24-3p was upregulated in cerulein-stimulated exosomes, whereas the miR-24-3p inhibitor counteracted the effect of pancreatic exosomes on peritoneal macrophage M1 polarization and pyroptosis. Furthermore, miR-24-3p inhibited March3 expression, whereas MARCH3 mediated NLRP3 ubiquitination in rat peritoneal macrophages, which, in turn, contributed to the apoptosis, reactive oxygen species production, and inflammation in AR42J cells. Conclusions: Exosomes derived from cerulein-stimulated pancreatic acinar cells mediate peritoneal macrophage M1 polarization and pyroptosis via an miR-24-3p/MARCH3/NLRP3 axis in AP.
4 May 2020 in Journal of Gastroenterology and Hepatology
The role of microRNA-132 in human pancreatic ductal adenocarcinomas is still ambiguous. We explored the association between microRNA-132 and pancreatic ductal adenocarcinoma prognosis. The expression of microRNA-132 in 50 pancreatic ductal adenocarcinoma tissue samples and pancreatic ductal adenocarcinoma cell lines was examined, and the association between its expression and pancreatic ductal adenocarcinoma prognosis was assessed. Functional analysis and factors downstream of microRNA-132 were investigated. Kaplan-Meier survival curves showed that high expression of microRNA-132 was a significant prognostic factor for 1-year survival of patients with pancreatic ductal adenocarcinoma (P = .028). Multivariate analysis for overall survival indicated that high expression of microRNA-132 was an independent prognostic factor for patients with pancreatic ductal adenocarcinoma (P = .044). Low expression of microRNA-132 was associated with poor prognosis in pancreatic ductal adenocarcinoma. Ectopic expression of microRNA-132 significantly inhibited proliferation and promoted apoptosis of 2 pancreatic ductal adenocarcinoma cell lines. Bioinformatic analysis revealed that microRNA-132 may exert its effects on pancreatic ductal adenocarcinoma through downregulating mitogen-activated protein kinase 3 and nuclear transcription factor Y subunit α. The results of this study further our understanding of the relationship between microRNA-132 and pancreatic ductal adenocarcinoma by showing that microRNA-132 might inhibit the progression of pancreatic ductal adenocarcinoma by regulating mitogen-activated protein kinase and nuclear transcription factor Y subunit alpha.
Endoscopic ultrasonography (EUS)-guided drainage has become the first-line therapy for late peri-pancreatic fluid collection (PFC). Double pigtail plastic stents (DPPS) and lumen-apposing metal stents (LAMS) are commonly used for PFC drainage. Recently, a multi-institutional consensus on PFC drainage has recommended that LAMS should be the standard care for patients with walled-off necrosis (WON). However, given the poor quality of evidence, we aim to perform a large-scale randomized controlled trial to determine whether LAMS is superior to DPPS for WON drainage. The study is an open-label, prospective, parallel-group, superiority, multicenter randomized controlled trial. Two hundred and fifty-six patients with WON who will attend 18 tertiary hospitals in China will be randomly allocated to the LAMS or DPPS group before the procedure. The primary endpoint is the clinical success at one month after drainage (reduction in the size of WON to < 2 cm). Secondary endpoints include technical success, operation time, recurrence, adverse events, and secondary interventions. The LVPWON trial is designed to determine whether LAMS is effective, safe, and superior to DPPS for WON drainage. ClinicalTrials.gov, NCT03027895 . Registered on 14 January 2017.