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Previous Volume 331:268-269 July 28, 1994 Number 4 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Fulminant hepatic failure is characterized by the rapid appearance of jaundice, coagulopathy, and encephalopathy and reflects severe hepatocellular injury or necrosis. Acute viral hepatitis and drug-induced liver injury account for the vast majority of cases in developed nations; other causes include toxins, venous-outflow obstruction, and ischemia. Despite advances in our understanding of the pathophysiologic features of the disease and the establishment of specialized liver-failure units, mortality from fulminant hepatic failure ranges from 50 to 80 percent, depending on the cause.

The liver destruction in fulminant hepatic failure is potentially reversible; the liver usually returns to normal in people who recover. . . . [Full Text of this Article]

References

This article has been cited by other articles:

• Ning, Q., Liu, M., Kongkham, P., Lai, M. M. C., Marsden, P. A., Tseng, J., Pereira, B., Belyavskyi, M., Leibowitz, J., Phillips, M. J., Levy, G. (1999). The Nucleocapsid Protein of Murine Hepatitis Virus Type 3 Induces Transcription of the Novel fgl2 Prothrombinase Gene. J. Biol. Chem. 274: 9930-9936 [Abstract] [Full Text]