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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 , ALF continues to be an incredible concentration of scientific and examine realization. With the arrival 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 exceptional staff of members to explain the etiology, pathology and therapy of this crucial syndrome. additionally coated are consensus concepts in liver transplantation for ALF sufferers, in addition to descriptions of synthetic and bioartificial liver support units. a piece on destiny remedies contains hepatocyte transplantation, auxiliary grafts and different transitority liver help. remarkable for the excessive point of the authors' services, this complete quantity may still turn out valuable.

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J VirolMeth 35: 343-52. , Sheen, I-S. and Liaw, Y-F. 1994. The role of hepatitis C virus in fulminant viral hepatitis in an area with endemic hepatitis A and B. Gastroenterology 107: 189-95. D. G. 1992. Postinfantile giant-cell transformation in hepatitis. Hepatology 16: 327-33. , Dehara, K. and Iwatsuki, S. 1994. Liver transplantation for fulminant hepatic failure. ASAIOJ 40:86-8. M. et al. 1992. Toga viruslike particles in acute liver failure attributed to sporadic non-A, non-B hepatitis and recurrence after liver transplantation.

1976. Enhanced HBsAb production in pathogenesis of fulminant viral hepatitis type B. BMJ2: 669-71. , Donegan, E. et al. 1991. Hepatitis C virus not found in fulminant non-A, non-B hepatitis. Ann Intern Med 115: 111-12. , Coombs, C. et al. 1992. Hepatitis B virus and apparent fulminant non-A, non-B hepatitis. Lancet 339: 952-5. , Hou, M-C et al. 1994. Multiple viral infection as the most common cause of fulminant and subfulminant viral hepatitis in an area endemic for hepatitis B: application and limitations of the polymerase chain reaction.

Intrinsic toxins and anoxia usually kill cells via a lytic process which ultimately involves loss of mitochondrial integrity with opening of a megachannel, that is the mitochondrial membrane permeability transition, with loss of mitochondria membrane potential and matrix constituents and with subsequent cytoskeletal changes, swelling and rupture of cell membrane (lysis) (Zahrebelski et al. 1995). This can be induced by oxidative stress, peroxides, calcium, GSH depletion and can be blocked by cyclosporin A.

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