Objective To evaluate retrospectively the clinical efficacy of percutaneous transhepatic gallbladder drainage (PTGBD) in the patients with acute biliary pancreatitis (ABP). Methods A total of 244 patients with ABP recei-ving treatment in our department from January 2014 to November 2021 were included in this study. There were 76 cases in study group using PTGBD treatment, among them, 41 cases with performed endoscopic retrograde cholangiopancreatography (ERCP) after symptoms remission, and 168 cases without PTGBD in control group with 49 cases using ERCP and 119 cases with conservative treatment. The rate of post-ERCP pancreatitis (PEP) and postoperative adverse events were compared between two groups. Results The rate of PEP was significantly lower in study group (11/41) than in control group (23/49), 26.8% vs.46.9%, P=0.008. The patients in both groups were performed cholecystectomy or cholecystectomy with bile duct drainage in late stage (73 cases in study group and 152 cases in control group). The shorter operative time [(76.3±28.3) min vs.(121.6±34.9) min, P=0.011], less intraoperative blood loss [(65.7±27.6) mL vs. (99.2±60.3) mL, P=0.028], shorter abdominal drainage duration [(3.6±2.5) d vs. (8.9±4.9) d, P=0.016] in study group than in control group. The rate of postoperative sepsis [2.7% (2 cases) vs. 5.3% (8 cases), P=0.003], rate of reoperation [1.4%(1 case) vs. 3.9%(6 cases), P<0.001], rate of admission to intensive care unit [4.1%(3 cases) vs. 7.2%(11 cases), P=0.028], and mortality [0 vs. 1.3% (2 cases), P<0.001] in study group were lower than those in control group. Conclusions PTGBD could be simple and effective in the treatment of ABP and consistent with treatment of damage control surgery which should be worthy clinical application.

Objective:To evaluate the safety and reliability of percutaneous management of benign extrahepatic biliary strictures with biliary duct dilatation and large-bore catheter placement .Methods:The clinical data of 17 patients at Shengjing Hospital from Mar 2017 to Mar 2020 was retrospectively analyzed.Results:There were 7 cases of bilioenteric anastomotic strictures and 10 cases of iatrogenic biliary tract injury strictures (6 cases of Bismuth type Ⅰ and 4 cases of Bismuth type Ⅱ). Fourteen of the 17 patients completed the treatment with a success rate of 82.3%.The catheter was gradually upsized to 22-24Fr.Catheters were left in place for 6-9 months (median time 7.6 months). Patients were followed up for 6-28 months (median follow-up time was 19 months), no recurrent stricture occurred.Conculsion:Percutaneous management of benign extrahepatic biliary strictures with bile duct dilatation and placement of large-bore catheter is a safe and effective minimally invasive treatment method.

Objective To study the mechanisms involved in the regulation of endogenous β-glucuronidase expression and to explore the more effective methods to prevent recurrence of hepatolithiasis formation.Methods The expression levels of c-myc and endogenous β-glucuronidase in the liver specimens of hepatolithiasis were examined by immunohistochemical staining.The expressions of c-myc and endogenous β-glucuronidase in the human intrahepatic biliary epithelial cell line (HiBEpiC),and normal liver cell line (L02) treated with different concentrations of lipopolysaccharide (LPS) were studied using western blot.The c-myc siRNA transfection was utilized to detect the role of c-myc in the regulation of the expression of endogenous β-glucuronidase.Results Compared with normal liver samples,the expressions of endogenous β-glucuronidase and c-myc in the liver specimens of hepatolithiasis were significantly increased,and they were positively correlated with each other.LPS induced increased expressions of endogenous β-glucuronidase and c-myc in a dose-dependent manner.C-myc siRNA transfection effectively inhibited the increased expression of endogenous β-glucuronidase as induced by LPS.Conclusion LPS played a crucial role in the formation of hepatolithiasis by stimulating the endogenous expression of β-glucuronidase in liver and biliary epithelial cells via c-myc.