New therapeutic aspects in fulminant hepatic failure.

Mortality rates for fulminant hepatic failure range between 50% and 90%. Several independent factors influence survival: age, etiology, depth and duration of the encephalopathy, and prevention of complications. The main causes of fulminant hepatic failure are hepatotropic viruses, adverse drug effects, and toxins (Table 1). All major hepatotropic viruses can induce fulminant hepatic failure. We distinguish hepatitis A virus (HAY), hepatitis B virus (HBV), hepatitis D (delta) virus (HDV), hepatitis C virus (HCV), non-A, non-B viruses, and hepatitis E virus (HEV); However, the risk for the development of fulminant hepatic failure varies with the different viruses (Table 2). The prevalence of fulminant hepatic failure after acute HAy infection is relatively low, about 0.2%, whereas as many as 20% of patients coinfected with HBV and HDV reportedly develop fulminant hepatic failure. The prevalence of fulminant hepatic failure is also high in pregnant women infected by the recently discovered HEY.2 This virus has recently been identified in tropical countries, first in India and Kashmir, and later in the Soviet Union. The clinical and epidemiologic characteristics of HEV infection are similar to those of HAV infection; HEY infection is therefore sometimes known as waterborne hepatitis. Clinical and experimental evidence indicates that HBV itself is not cytopathogenic, and that the host’s immunologic response to virus-infected liver cells is responsible for the organ damage. An overwhelming immune system response is regarded as the main pathogenetic mechanism leading to fulminant hepatic failure in acute HBY infection. Therefore, hepatitis B surfaceantigen (HBsAG) and the complete virus may already have been cleared from serum by the time the signs of fulminant hepatic failure appear. Immunoglobulin (Ig) M antibody to hepatitis B core antigen (anti-HBc) may be the only serologic marker for acute HBV infection in these cases. The mechanisms by which HAY and non-A, non-B viruses induce fulminant hepatic failure are unclear. However, the presence of 1gM antibody to HAY (anti-HAY) is diagnostic of fulminant hepatic failure due to HAY. The presence of 1gM anti-delta antibodies is diagnostic of HDY-induced fulminant hepatic failure, and the simultaneous detection of 1gM anti-HBc is diagnostic of a coinfection with HBY and HDV, a condition associated with a poor prognosis. For a long time, the search for the etiologic agents of sporadic and