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Drug-induced bile duct injury
Authors:Michele Visentin  Daniela Lenggenhager  Zhibo Gai  Gerd A. Kullak-Ublick
Affiliation:1. Department of Clinical Pharmacology and Toxicology, University Hospital Zurich, University of Zurich, Switzerland;2. Department of Pathology and Molecular Pathology, University Hospital Zurich, University of Zurich, Switzerland;3. Patient Safety, Novartis Pharma, Basel, Switzerland
Abstract:
Drug-induced liver injury includes a spectrum of pathologies, some related to the mode of injury, some to the cell type primarily damaged. Among these, drug-induced bile duct injury is characterized by the destruction of the biliary epithelium following exposure to a drug. Most of the drugs associated with bile duct injury cause immune-mediated lesions to the epithelium of interlobular ducts. These share common histopathological features with primary biliary cholangitis, such as inflammation and necrosis at the expense of cholangiocytes and, if the insult persists, bile duct loss and biliary cirrhosis. Some drugs selectively target larger ducts. Such injury is often dose-dependent and thought to be the result of intrinsic drug toxicity. The histological changes resemble those seen in primary sclerosing cholangitis. This overview focuses on the clinical and pathological features of bile duct injury associated with drug treatment and on the immunological and biochemical effects that drugs exert on the biliary epithelium. This article is part of a Special Issue entitled: Cholangiocytes in Health and Disease edited by Jesus Banales, Marco Marzioni, Nicholas LaRusso and Peter Jansen.
Keywords:DILI  drug-induced liver injury  DILIN  Drug-Induced Liver Injury Network  HLA  human leukocyte antigen  PBC  primary biliary cholangitis  PSC  primary sclerosing cholangitis  RUCAM  Roussel Uclaf Causality Assessment Method  TCR  T cell receptor  UDCA  ursodeoxycholic acid  VBDS  vanishing bile duct syndrome  Bile duct  Cholangiocyte  Cholangiopathy  Drug-induced liver injury  Idiosyncrasy  Vanishing bile duct syndrome
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