IntroductionObstructive jaundice results from increased serum bilirubin levels due to obstruction of bile flow from blockage of the large bile ducts. Obstructive jaundice is commonly due to benign common choledocholithiasis, biliary stricture, cholangitis, pancreaticobiliary malignancies, and metastatic disease . Patients with obstructive jaundice have various pathophysiological changes that affect various organs and physiologic processes. Due to dysfunctional bile excretion, the accumulation of high levels of bilirubin and bile acids (BAs) in the hepatocytes causes acute liver injury as the initial response to oxidative stress , followed by disorder of multiple systems including kidney failure, cardiac dysfunction, hemostatic abnormalities, and altered immunity .Although the exact mechanisms involved in the multiple organ dysfunction caused by obstructive jaundice still remains unclear, the disruption of bilirubin and BAs homeostasis may be, at least in part, an important cause . Bilirubin and BAs homeostasis is maintained by the hepatobiliary transport and metabolism system in the liver . At first, free bilirubin, cholesterol, and BAs are uptaken into hepatocytes via passive diffusion or transporter‐mediated transmembrane transport systems, which include several uptake transporters from the solute carrier (SLC) superfamily (such as the Na+‐taurocholate cotransporting polypeptide [NTCP]) . Then, bilirubin, cholesterol, and BAs are exposed to phase
Journal of Hepato-Biliary-Pancreatic Sciences – Wiley
Published: Jan 1, 2018
Keywords: ; ; ; ; ;
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