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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 situation, ALF is still a big concentration of scientific and study realization. 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 unique crew of participants to explain the etiology, pathology and remedy of this significant syndrome. additionally coated are consensus suggestions in liver transplantation for ALF sufferers, in addition to descriptions of man-made and bioartificial liver help units. a bit on destiny remedies comprises hepatocyte transplantation, auxiliary grafts and different transitority liver help. extraordinary for the excessive point of the authors' services, this finished quantity may still turn out useful.

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1992. Role of hepatitis C FAILURE virus infection in German patients with fulminant and subacute hepatic failure. EurJClin Invest 22: 569-71. Trewby, P. and Williams, R. 1977. Pathophysiology of hypotension in patients with fulminant hepatic failure. GH/18: 1021-6. Trey, C. I 970. The management of fulminant hepatic failure. In Progress in Liver Failure, eds. H. Popper, F. Schaffner, 282-98. New York: Grune and Stratton. , Roberts, J. and Lake, J. 1991. Hepatitis C virus not found in fulminant non-A non-B hepatitis.

1994). 2. Fatality rates in patients hospitalized for acute viral hepatitis City Type Total cases («) Athens, Greece3 HAV HBV 1190 Melbourne, Australia5 non-A non-B HAV HBV non-A non-B a b Papaevangelou et al. 1984. McNeil etal. 1984. 3. Hepatitis C and E as causes of fulminant or subfulminant hepatic failure in the US and Europe Author/country Wright et al. 1991, 1992 - USA Feray et al. 1993 - France Liang etal. 1993-USA Sallieetal. 1993, 1994-UK Theilmann et al. 1992 - Germany Laskus etal. 1994 Kuwadaetal.

G. azathioprine and monocrotaline; Yan andHuxtable 1995). 1) as well as other types of liver diseases (Laskin 1990). Neutrophils are recruited to areas of injury by cytokines, leukotrienes, and products of oxidative stress by increased expression of adhesion molecules on locally damaged endothelium. Activated neutrophils injure cells by releasing proteases, such as elastase, and oxidants such as H2O2 and hypochlorous acid. A recent hypothesis suggests that oxidant generation functions as a permissive factor for protease induced injury (Laskin 1990).

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