After surgery, the patient had significant abdominal pain with an elevated serum amylase and subsequently developed a large fluid collection in the right upper quadrant. The bile-stained fluid collection was drained percutaneously and fluid biochemistry showed both an elevated bilirubin selleck products (19.3 mg/dL) and an elevated amylase (2481 U/L). The suspected bile leak was investigated by endoscopic retrograde

cholangiopancreatography and confirmed the anomalous pancreaticobiliary junction, the relatively narrow lower bile duct, and the choledochal cyst (Figure 2). The bile leak resolved after biliary sphincterotomy and placement of a biliary stent. An anomalous pancreaticobiliary junction is a rare congenital learn more anomaly where the distal bile duct and main pancreatic duct have a long common channel (>15 mm). In most patients, the long common channel extends outside the duodenal wall. Various radiological subtypes have been described but the most common are the apparent insertion of the bile duct into the main pancreatic duct (type I) and the reverse appearance (type II). In some patients, the common channel is dilated and there is a strong association with choledochal cysts. The anomaly is asymptomatic in some patients but others

have relapsing pancreatitis, chronic pancreatitis and complicated gallstones. There is also an association with gallbladder cancer, particularly in Japan. In case reports, several patients with gallbladder cancer have been younger women, often without gallstones. Reasons for the association between an anomalous pancreaticobiliary junction and gallbladder cancer remain unclear but one possibility is promotion

of carcinogenesis by see more the excessive reflux of pancreatic juice into the gallbladder. “
“Herker E, Harris C, Hernandez C, Carpentier A, Kaehlcke K, Rosenberg AR, et al. Efficient hepatitis C virus particle formation requires diacyl-glycerol acyltransferase-1. Nat Med 2010;16:1295-1298. Available at: www.nature.com/nm (Reprinted with permission.) Hepatitis C virus (HCV) infection is closely tied to the lipid metabolism of liver cells. Here we identify the triglyceride-synthesizing enzyme diacylglycerol acyltransferase-1 (DGAT1) as a key host factor for HCV infection. DGAT1 interacts with the viral nucleocapsid core and is required for the trafficking of core to lipid droplets. Inhibition of DGAT1 activity or RNAi-mediated knockdown of DGAT1 severely impairs infectious virion production, implicating DGAT1 as a new target for antiviral therapy. Hepatitis C virus (HCV) infection is a major cause of liver cirrhosis and hepatocellular carcinoma worldwide. An important clinical hallmark of chronic HCV infection is its link with lipid biosynthesis and metabolism. Liver steatosis is frequently observed in HCV infection, and HCV has been implicated in the pathogenesis of steatosis.