By William M. Lee, Roger Williams, Jean-Pierre Benhamou, Jacques Bernuau
Acute liver failure (ALF), or fulminant hepatic failure, is a special medical syndrome that crosses scientific disciplines. a comparatively infrequent situation, ALF is still a massive concentration of medical and study consciousness. With the arrival of transplantation, the significance of figuring out administration of ALF has taken on a brand new urgency. during this first quantity devoted to ALF, the editors compile a exotic staff of individuals to explain the etiology, pathology and remedy of this crucial syndrome. additionally lined are consensus strategies in liver transplantation for ALF sufferers, in addition to descriptions of synthetic and bioartificial liver help units. a piece on destiny remedies contains hepatocyte transplantation, auxiliary grafts and different transitority liver help. outstanding for the excessive point of the authors' services, this accomplished quantity should still end up important.
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Additional info for Acute Liver Failure
Hepatotoxicity is usually avoided through the electrophilic metabolite preferentially conjugating to nucleophilic glutathione. However, when a large dose is ingested (>10g), the increased level of toxic metabolites exhausts the available glutathione stores, resulting in intracellular accumulation of the toxic metabolite and hepatotoxicity. Chronic alcohol ingestion can lead to acetaminophen toxicity with doses of much less than 10 g. One theory is that alcoholic livers are depleted in glutathione, especially in the mitochondria, and have a much reduced capacity to detoxify the reactive metabolite.
Phenytoin is metabolized by P450 to several products including parahydroxylated, dihydrodiol metabolites, and arene oxides, all of which are reactive, electrophilic compounds. The arene oxides, when generated in vivo, are capable of binding to cellular macromolecules. These drug-macromolecular complexes could lead directly to cytotoxicity, or act as immunogens 25 and initiate allergic responses (Stanley and Fallon-Pellicci 1978; Mullick and Ishak 1979; Spielberg et al. 1981). In patients with the hypersensitivity syndrome to phenytoin, antibodies have been identified that primarily recognized CYP3A1 (Leeder et al.
Et al. 1992. Syncytial giant-cell hepatitis-a specific disease entity? JHepatol 15: 216-19. K. etal. 1993. Fulminant or subfulminant non-A, non-B viral hepatitis. The role of hepatitis C and E viruses. Gastroenterology 104: 55662. , Chu, CM. and Huang. J. 1986. Appearance and persistence of hepatitis A IgM antibody in acute clinical hepatitis A observed in an outbreak. Infection 14: 156-8. P. et al. 1980. Hepatitis type A, B, and non-A, non-B in fulminant hepatitis. Gut 21:72-7. J. et al. 1984.