By William M. Lee, Roger Williams, Jean-Pierre Benhamou, Jacques Bernuau
Acute liver failure (ALF), or fulminant hepatic failure, is a special scientific syndrome that crosses clinical disciplines. a comparatively infrequent , ALF is still a big concentration of scientific and examine recognition. With the appearance of transplantation, the significance of realizing administration of ALF has taken on a brand new urgency. during this first quantity devoted to ALF, the editors compile a special group of members to explain the etiology, pathology and remedy of this significant syndrome. additionally lined are consensus concepts in liver transplantation for ALF sufferers, in addition to descriptions of man-made and bioartificial liver support units. a bit on destiny remedies comprises hepatocyte transplantation, auxiliary grafts and different transitority liver help. striking for the excessive point of the authors' services, this finished quantity may still end up beneficial.
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Extra resources for Acute Liver Failure
Therefore, susceptibility factors for halothane may include individual variability in the level of expression of the cytochrome P450 isoenzyme responsible for bioactivation of halothane (probably CYP2E1), the level of expression of the protein targets, the presentation of antigens to the immune system, and/ DRUG HEPATOTOXICITY AS A CAUSE OF ACUTE LIVER FAILURE or the immune response itself. Of note, obesity has been recognized as a risk factor and is associated with increased expression of CYP2E1.
1991. Fungal infection: a common, unrecognised complication of acute liver failure. Hepatology 12:1-9. , Bradley, D. and Williams, R. 1994. Hepatitis C and E in fulminant hepatic failure: a polymerase chain reaction and serological study. JHepatol 20: 580-8. , Yones, A. and Vokota, K. 1990. Cerebrovascular reactivity to CO2 in patients with hepatic or septic encephalopathy. Resuscitation 19: 125—34. , Otto, G. and Goeser, T. 1992. Role of hepatitis C FAILURE virus infection in German patients with fulminant and subacute hepatic failure.
In at least some geographical areas cases of fulminant hepatitis B are frequently associated with HBV strains possessing mutations encoding precore stop codons that interfere with translation of HBeAg, or mutations in the core promoter that interfere with transcription of the HBeAg coding region (Sato et al. 1995). HBeAg and HBeAg possess CLINICAL SYNDROME AND ETIOLOGY significant amino acid sequence identity and HBeAg has been shown to induce T cell tolerance to both HBeAg and HBeAg in mice exposed to this antigen in utero (Milich et al.