title: The molecular pathogenesis of cholestasis in sepsis.
abstract: Sepsis-induced cholestasis is a complication of infection. Infections cause systemic and intrahepatic increase in proinflammatory cytokines which result in impaired bile flow ie. cholestasis. Several other mediators of impairment in bile flow have been identified under conditions of sepsis such as increased nitric oxide production and decreased aquaporin channels. The development of cholestasis may also further worsen inflammation. The molecular basis of normal bile flow and mechanisms of impairment in sepsis are discussed.
authors.affiliation: Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University School of Medicine, Richmond, VA 23298-0341, USA.
authors.forename: Harjit K
authors.initials: HK
authors.lastname: Bhogal
authors.forename: Arun J
authors.initials: AJ
authors.lastname: Sanyal
mesh_terms: D001647:Bile Acids and Salts / Q000096:biosynthesis / Q000378:metabolism; D002779:Cholestasis / Q000209:etiology* / Q000503:physiopathology*; D003937:Diagnosis, Differential; D006801:Humans; D007565:Jaundice / Q000175:diagnosis* / Q000209:etiology; D008099:Liver / Q000378:metabolism / Q000502:physiology*; D008954:Models, Biological; D009569:Nitric Oxide / Q000378:metabolism; D018805:Sepsis / Q000150:complications* / Q000503:physiopathology*
chemical_list: D001647:Bile Acids and Salts; D009569:Nitric Oxide