Pathogenesis of Fulminant Hepatic Failure

Abstract

Acute liver failure (ALF) is characterized by severe and sudden
liver cell dysfunction leading to coagulopathy and hepatic
encephalopathy in previously healthy persons. A critical
degree of liver cell death not adequately decompensated
by hepatocellular regenerative activity is fundamental to
the development of ALF. Interaction between two dominant
pathological pathways is illustrated as the triggering event:
apoptosis and necrosis. A correlation has been demonstrated
between the etiology of ALF and the dominating pathological
pathway. Liver cell death signaling pathways modulated
by an increasingly recognized number of tyrosine kinases,
adapter molecules, transcription factors, proinflammatory
and vasoactive cytokines and chemokines through both
stimulating and depressant interactions have been demonstrated. What's more Systemic Inflammatory Response Syndrome whether or not precipitated by infection, appears to
be implicated in the progression of encephalopathy, reducing
the chances of transplantation and conferring a poorer
prognosis. Hepatic encephalopathy and brain edema arising
from exposure of the brain to circulating neurotoxins also
signifies a serious prognosis in ALF.
Key words: Fulminant Hepatic Failure, Apoptosis, Necrosis,
Tumour Necrosis Factor, Systemic Inflammatory Response
Syndrome, Caspases, Oxidative Stress, Hepatocellular Regeneration,
Hepatic Encephalopathy, Brain Edema.