27. Drug-Induced Liver Disease

  1. Eugene R. Schiff MD, MACP, FRCP2,
  2. Willis C. Maddrey MD, MACP, FRCP3 and
  3. Michael F. Sorrell MD, FACP4
  1. Shivakumar Chitturi MD and
  2. Geoffrey C. Farrell MD, FRACP

Published Online: 31 OCT 2011

DOI: 10.1002/9781119950509.ch27

Schiff's Diseases of the Liver, Eleventh Edition

Schiff's Diseases of the Liver, Eleventh Edition

How to Cite

Chitturi, S. and Farrell, G. C. (2011) Drug-Induced Liver Disease, in Schiff's Diseases of the Liver, Eleventh Edition (eds E. R. Schiff, W. C. Maddrey and M. F. Sorrell), Wiley-Blackwell, Oxford, UK. doi: 10.1002/9781119950509.ch27

Editor Information

  1. 2

    Center for Liver Diseases and Schiff Liver Institute, University of Miami Miller School of Medicine, Miami, FL, USA

  2. 3

    Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA

  3. 4

    University of Nebraska College of Medicine, Omaha, NE, USA

Author Information

  1. Department of Hepatic Medicine, Australian National University Medical School, Gastroenterology and Hepatology Unit, Canberra Hospital, Garran, Australia

Publication History

  1. Published Online: 31 OCT 2011
  2. Published Print: 9 DEC 2011

ISBN Information

Print ISBN: 9780470654682

Online ISBN: 9781119950509



  • Drug-induced liver injury;
  • pharmacogenetics;
  • acute liver failure;
  • complementary and alternative medicine;
  • herbal medicine;
  • idiosyncratic drug reactions;
  • reactive metabolite syndrome


Drug-induced liver injury (DILI) encompasses a spectrum of liver diseases from acute and chronic hepatitis, cholestatic syndromes, and vascular lesions through to benign and malignant liver neoplasms. Idiosyncratic drug reactions constitute the majority of cases. Newer agents associated with DILI include tyrosine kinase and tumor necrosis factor α inhibitors, while telithromycin, troglitazone, and ximelagatran have been withdrawn due to hepatotoxicity. A variety of drug- and host-related characteristics are associated with DILI. Of the latter, pharmacogenetic factors are becoming increasingly relevant (e.g., flucloxacillin- and amoxicillin-clavulanate-associated liver injury with specific HLA alleles; valproic acid and mitochondrial DNA repair-related gene POLG1 polymorphisms). Interactions between drugs and other liver diseases (e.g., antituberculous drugs and viral hepatitis B and C; tamoxifen and nonalcoholic fatty liver disease) are also now better characterized. Acetaminophen is the leading cause of acute liver failure in the United States. N-acetylcysteine remains the only antidote available for such cases and is also of value in the setting of acute liver failure from drugs other than acetaminophen. Immediate cessation of the offending drug and supportive care, along with corticosteroids, ursodeoxycholic acid, and liver transplantation in selected cases, is critical to improving outcomes of patients with DILI.