Liver Failure and Liver Disease

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Acetaminophen-induced acute liver failure: Results of a United States multicenter, prospective study†‡

  1. Anne M. Larson1,§,*,
  2. Julie Polson2,
  3. Robert J. Fontana3,
  4. Timothy J. Davern4,
  5. Ezmina Lalani2,
  6. Linda S. Hynan5,
  7. Joan S. Reisch5,
  8. Frank V. Schiødt2,
  9. George Ostapowicz2,
  10. A. Obaid Shakil6,
  11. William M. Lee2

Article first published online: 29 NOV 2005

DOI: 10.1002/hep.20948

Issue

Hepatology

Hepatology

Volume 42, Issue 6, pages 1364–1372, December 2005

Additional Information

How to Cite

Larson, A. M., Polson, J., Fontana, R. J., Davern, T. J., Lalani, E., Hynan, L. S., Reisch, J. S., Schiødt, F. V., Ostapowicz, G., Shakil, A. O. and Lee, W. M. (2005), Acetaminophen-induced acute liver failure: Results of a United States multicenter, prospective study. Hepatology, 42: 1364–1372. doi: 10.1002/hep.20948

Author Information

  1. 1

    Department of Internal Medicine, Division of Gastroenterology, University of Washington Medical Center, Seattle WA

  2. 2

    Department of Internal Medicine, Division of Digestive and Liver Diseases, University of Texas Southwestern Medical Center, Dallas, TX

  3. 3

    Department of Internal Medicine, Division of Gastroenterology, University of Michigan, Ann Arbor, MI

  4. 4

    Department of Internal Medicine, Division of Gastroenterology, University of California at San Francisco, San Francisco, CA

  5. 5

    Center for Biostatistics and Clinical Science, University of Texas Southwestern Medical Center, Dallas, TX

  6. 6

    Department of Medicine, Division of Gastroenterology, University of Pittsburgh Medical Center, Pittsburgh, PA

  1. §

    fax: 206-598-3884

*University of Washington, Box 356174, Room EE-425, 1959 NE Pacific St., Seattle, WA 98195-6174

  1. †

    See Editorial on Page 1252.

  2. ‡

    Potential conflict of interest: Nothing to report.

  3. §

    fax: 206-598-3884

Publication History

  1. Issue published online: 29 NOV 2005
  2. Article first published online: 29 NOV 2005
  3. Manuscript Accepted: 12 SEP 2005
  4. Manuscript Received: 24 JUN 2005

Funded by

  • NIDDK. Grant Number: R-01-DK58639
  • Stephen B. Tips Fund at Northwestern University
  • FDA. Grant Number: FD-R-001661
  • NIH. Grant Numbers: R-O3 DK52827, R-01 DK58369
  • Stephen B. Tips Fund of Northwestern Medical Foundation
  • Jeanne Roberts Fund of the Southwestern Medical Foundation
  • AASLD/Schering Research Fellowship

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Abstract

Severe acetaminophen hepatotoxicity frequently leads to acute liver failure (ALF). We determined the incidence, risk factors, and outcomes of acetaminophen-induced ALF at 22 tertiary care centers in the United States. Detailed prospective data were gathered on 662 consecutive patients over a 6-year period fulfilling standard criteria for ALF (coagulopathy and encephalopathy), from which 275 (42%) were determined to result from acetaminophen liver injury. The annual percentage of acetaminophen-related ALF rose during the study from 28% in 1998 to 51% in 2003. Median dose ingested was 24 g (equivalent to 48 extra-strength tablets). Unintentional overdoses accounted for 131 (48%) cases, intentional (suicide attempts) 122 (44%), and 22 (8%) were of unknown intent. In the unintentional group, 38% took two or more acetaminophen preparations simultaneously, and 63% used narcotic-containing compounds. Eighty-one percent of unintentional patients reported taking acetaminophen and/or other analgesics for acute or chronic pain syndromes. Overall, 178 subjects (65%) survived, 74 (27%) died without transplantation, and 23 subjects (8%) underwent liver transplantation; 71% were alive at 3 weeks. Transplant-free survival rate and rate of liver transplantation were similar between intentional and unintentional groups. In conclusion, acetaminophen hepatotoxicity far exceeds other causes of acute liver failure in the United States. Susceptible patients have concomitant depression, chronic pain, alcohol or narcotic use, and/or take several preparations simultaneously. Education of patients, physicians, and pharmacies to limit high-risk use settings is recommended. (HEPATOLOGY 2005;42:1364–1372.)

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