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- W1558106820 abstract "Acute liver failure (ALF) is characterized by severe and suddenliver cell dysfunction leading to coagulopathy and hepaticencephalopathy in previously healthy persons. A criticaldegree of liver cell death not adequately decompensatedby hepatocellular regenerative activity is fundamental tothe development of ALF. Interaction between two dominantpathological pathways is illustrated as the triggering event:apoptosis and necrosis. A correlation has been demonstratedbetween the etiology of ALF and the dominating pathologicalpathway. Liver cell death signaling pathways modulatedby an increasingly recognized number of tyrosine kinases,adapter molecules, transcription factors, proinflammatoryand vasoactive cytokines and chemokines through bothstimulating and depressant interactions have been demonstrated. What’s more Systemic Inflammatory Response Syndrome whether or not precipitated by infection, appears tobe implicated in the progression of encephalopathy, reducingthe chances of transplantation and conferring a poorerprognosis. Hepatic encephalopathy and brain edema arisingfrom exposure of the brain to circulating neurotoxins alsosignifies a serious prognosis in ALF. Key words: Fulminant Hepatic Failure, Apoptosis, Necrosis,Tumour Necrosis Factor, Systemic Inflammatory ResponseSyndrome, Caspases, Oxidative Stress, Hepatocellular Regeneration,Hepatic Encephalopathy, Brain Edema." @default.
- W1558106820 created "2016-06-24" @default.
- W1558106820 creator A5075762990 @default.
- W1558106820 creator A5089127171 @default.
- W1558106820 date "2007-04-17" @default.
- W1558106820 modified "2023-09-24" @default.
- W1558106820 title "Pathogenesis of Fulminant Hepatic Failure" @default.
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