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Acute Liver Failure - download pdf or read online

By William M. Lee, Roger Williams, Jean-Pierre Benhamou, Jacques Bernuau

Acute liver failure (ALF), or fulminant hepatic failure, is a different scientific syndrome that crosses scientific disciplines. a comparatively infrequent situation, ALF is still an incredible concentration of scientific and examine consciousness. With the arrival of transplantation, the significance of knowing administration of ALF has taken on a brand new urgency. during this first quantity devoted to ALF, the editors assemble a individual staff of members to explain the etiology, pathology and therapy of this significant syndrome. additionally lined are consensus recommendations in liver transplantation for ALF sufferers, in addition to descriptions of synthetic and bioartificial liver help units. a bit on destiny remedies contains hepatocyte transplantation, auxiliary grafts and different transitority liver aid. impressive for the excessive point of the authors' services, this complete quantity may still turn out worthy.

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1992. Role of hepatitis C virus infection in German patients with fulminant and subacute hepatic failure. EurJClin Invest 22:569-71. F. et al. 1988. Aplastic anemia complicating orthotopic liver transplantation for non-A, non-B hepatitis. N EnglJ Med3l9: 393-6. Williams, R. and Wendon, J. 1994. Indications for orthotopic liver transplantation in fulminant liver failure. Hepatology 20: 5S-9S. , Cullens, H. et al. 1976. Enhanced HBsAb production in pathogenesis of fulminant viral hepatitis type B.

Recurrent and de novo giant cell hepatitis after orthotopic liver transplantation. Am J Surg Pathol 18: 804-13. , Poucell, S. et al. 1991. Syncytial giant-cell hepatitis. Sporadic hepatitis with distinctive pathological features, a severe clinical course, and paramyxoviral features. N EnglJ Med 324: 455-60. , Naoumov, N. et al. 1993. Occult HBV in NANB fulminant hepatitis. Lancet 341: 123. , Purdy, M. et al. 1994. Hepatitis C and E in non-A non-B fulminant hepatic failure: a polymerase chain reaction and serological study.

The explanation for enhanced endotoxin activation of Kupffer cells in hepatotoxicity is unknown. Since the ultimate and full extent of liver injury involves these extra-hepatocyte events, targeting therapy or prevention of hepatotoxicity toward blocking tumor necrosis factor (TNF) or leukocyte adhesion appears to be a fruitful area for future clinical investigation. PREDICTABLE VERSUS UNPREDICTABLE HEPATOTOXICITY Hepatotoxicity from drugs can be viewed as predictable or unpredictable. Predictable injury is dose-related, usually reproducible in animal models and the liver injury is due to the intrinsic toxicity of a drug or its metabolites.

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