ABSTRACT
Objective:To investigate the effect of different drainage methods on pancreatic fistula after pancreaticoduodenectomy (PD).Methods:The data of all patients with PD in Xijing Hospital, the First Affiliated Hospital of the Fourth Military Medical University from January 2007 to December 2018 were retrospectively analyzed. A total of 670 patients were enrolled, including 415 males and 255 females, aged (58.4±7.3) years, ranging from 24 to 82 years. According to the different method of pancreatic duct drainage, the propensity score was matched, and the patients were divided into internal drainage group ( n=529) and external drainage group ( n=141). The pancreatic fistula rate was compared between the two groups. Factors influencing pancreatic fistula after PD were analyzed by univariate and multivariate logistic regression. Results:The incidence of pancreatic fistula in the internal drainage group was 12.5% (66/529), which was significantly higher than that in the external drainage group 6.4% (9/141) (χ 2= 4.16, P=0.041). Multivariate logistic regression analysis showed that age ≥65 years ( OR=2.004, 95% CI: 1.185-3.390), complicated with digestive diseases ( OR=3.087, 95% CI: 1.599-5.959), history of upper abdominal surgery ( OR=2.031, 95% CI: 1.104-3.734) increased the risk of pancreatic fistula after PD (all P<0.05), decreased the risk of pancreatic fistula after PD in patients with external drainage ( OR=0.470, 95% CI: 0.223-0.989, P=0.047), and decreased the risk of pancreatic fistula after PD with the tumor size ( OR=0.725, 95% CI: 0.556-0.944, P=0.017), tumor located in the common bile duct after PD increased the risk of pancreatic fistula ( OR=1.497, 95% CI: 1.192-1.880, P=0.001). Conclusions:Compared with pancreatic duct drainage, external pancreatic duct drainage is better because of preventing postoperative pancreatic fistula.
ABSTRACT
Objective:To study the effect of dystrobrevin binding protein1 (Dysbindin) in pancreatic cancer and the correlations between Dysbindin and the cholinergic agonist Carbachol.Methods:Pancreatic cancer cell lines with Dysbindin overexpressed or knocked down were constructed by lentivirus based lentivirus or small interference RNA respectively, and the function of Dysbindin and Carbachol on invasion and metastasis of pancreatic cancer cells were investigated by Transwell migration and invasion assay, and the effects of Dysbindin and Carbachol on epithelial mesenchymal transition (EMT) related molecules were detected by Western Blot.Results:When Dysbindin was overexpressed, pancreatic cancer migration and invasion were increasedand compared with control group, expression of E-cadherin was decreased [(0.94±0.00) vs (0.74±0.08)], but N-cadherin [(0.60±0.17) vs (1.33±0.10)] and Snail1 was increased [(0.43±0.11) vs (0.81±0.06)], the differences were statistically significant ( P<0.05), and when Dysbindin was blocked, tumor migration and invasion were inhibited. Carbachol can inhibit the expression of Dysbindin, but increase ZO-1 [(0.16±0.06) vs (1.40±0.15)] and N-cadherin level [(1.34±0.13) vs (1.03±0.14)], the differences were statistically significant ( P<0.05) . Conclusions:Dysbindin can promote metastasis and EMT in pancreatic cancer. And Carbachol can decrease Dysbindin expression and inhibit metastasis and EMT of pancreatic cancer.