Animal models of fulminant hepatic failure: A critical evaluation

PN Newsome*, JN Plevris, LJ Nelson, PC Hayes

*Corresponding author for this work

Research output: Contribution to journalLiterature reviewpeer-review

Abstract

Few conditions in medicine are more dramatic or more devastating than acute liver failure. Our understanding and treatment of this condition have been limited by the lack of satisfactory animal models. The most widely used models consist of surgical anhepatic and devascularization procedures and hepatotoxins, such as galactosamine and acetaminophen. Potential disadvantages with surgical models are their inability to recreate the inflammatory milieu that exists in acute liver failure and their reliance on surgical expertise. Models using hepatotoxins are free of such constraints. Galactosamine-induced hepatotoxicity is more predictable than acetaminophen, but its cost and lack of a human equivalent clinical syndrome has restricted its use. Acetaminophen-based models offer the greatest potential but have proven the most difficult to develop because of difficulties with reproducibility and refractory anemia. Although progress has been made, research must continue in this area to establish an animal model with minimal disadvantages that would accurately reflect the clinical syndrome seen in humans. Copyright (C) 2000 by the American Association for the Study of liver Diseases.

Original languageEnglish
Pages (from-to)21-31
Number of pages11
JournalLiver Transplantation
Volume6
Issue number1
Publication statusPublished - Jan 2000

Keywords

  • ACUTE LIVER-FAILURE
  • BIOARTIFICIAL LIVER
  • COVALENT BINDING
  • DRUG-METABOLISM
  • GEL-ENTRAPMENT
  • DOG-MODEL
  • ACETAMINOPHEN
  • NECROSIS
  • GLUTATHIONE
  • MICE

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