Etiology and management of fulminant hepatic failure

Department of Medicine, Northwestern Feinberg Medical School, Searle 10-573, 303 East Chicago Avenue, Chicago, IL 60611, USA.
Current Gastroenterology Reports 03/2003; 5(1):39-47. DOI: 10.1007/s11894-003-0008-8
Source: PubMed


Fulminant hepatic failure (FHF) remains a rare but devastating disease. Viruses and drug-induced hepatotoxicity are the most common causes of the syndrome, but the relevance of each differs depending on the geographic area. In a large proportion of patients no cause for FHF can be identified. Good intensive care is critical for patient survival. Orthotopic liver transplantation (OLT) remains a definitive therapeutic option. Prognostic indices have helped to optimize patient selection and timing for performance of OLT. However, the accuracy of these prognostic indices decreases when they are applied to different populations, probably because of regional differences in etiology and peculiar native host factors. More accurate prognostic criteria and new therapeutic alternatives to OLT are required.

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    • "It showed in patients with hepatic failure that incidence of brain edema reached 51.4% with autopsy, whereas it was 30.1% with clinical examination. When encephalopathy and brain edema occur, the disease takes a rapidly progressive and lethal course [2, 3]. "
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    ABSTRACT: Brain edema in acute liver failure (ALF) remains lethal. Cytotoxic mechanisms associated with brain edema have been well recognized, but the role of vasogenic mechanisms of brain edema has not been explored. Intact tight junctions (TJs) between brain capillary endothelial cells are critical for normal BBB function. Recent reports found significant alterations in the tight junction elements including occludin and claudin-5, suggesting a vasogenic injury in the blood-brain barrier (BBB) integrity. However, the role of TJ in ALF has not been completely understood. This paper reviews the role of the paracellular tight junction in the increased selective BBB permeability that leads to brain edema in ALF and furthermore explores the effect of systemic inflammatory cytokines on the tight junction dysfunction.
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    • "Fulminant hepatitis is a devastating liver disease caused by autoimmune hepatitis, alcohol consumption, chronic or acute viral hepatitis infection, which remains a significant cause of morbidity and mortality internationally [1], [2]. Fulminant hepatitis is associated with severe hyperbilirubinemia, hepatic encephalopathy and death. "
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    • "Patients in early stages of FHF may recover spontaneously. However, during stages III and IV (comatose stages), when encephalopathy and brain edema occur, the disease takes a rapidly progressive and lethal course [1] [2] [3]. Brain edema in FHF results from compromised blood-brain barrier (BBB) permeability, leading to increased extravasation of water and other small molecules into the brain [2] [3]. "
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