Fulminant Hepatic Failure. Viral hepatitis is responsible for about 12% of cases of fulminant hepatic failure; of these, two-thirds are caused by HBV infection and the rest by HAV. Survival for more than 1 week may permit recovery to occur via replication of residual hepatocytes. Activation of the stem/progenitor cells in the canals of Hering gives rise to very prominent ductular reactions but is usually insufficient to accomplish full restitution. Fulminant hepatic failure that follows acute viral hepatitis is treated supportively. Liver transplantation is the only option for patients whose disease does not resolve, as death from secondary infections and failure of other organs is otherwise inevitable.
6 months. The clinical features are extremely variable and are not predictive of outcome. In some patients, the only signs of chronic disease are elevations of serum transaminases. Laboratory studies also may reveal prolongation of the prothrombin time and, in some instances, hyperglobulinemia, hyperbilirubinemia, and mild elevations in alkaline phosphatase levels. In symptomatic individuals, the most common finding is fatigue; less commonly, there is malaise, loss of appetite, and bouts of mild jaundice. In precirrhotic chronic hepatitis, physical findings are few, the most common being spider angiomas, palmar erythema, mild hepatomegaly, hepatic tenderness, and mild splenomegaly. Occasionally, in cases of HBV and HCV, immune complex disease develops that results in vasculitis (subcutaneous or visceral, Chapter 10) and glomerulonephritis (Chapter 14). Cryoglobulinemia is found in about 35% of individuals with chronic hepatitis C.
The Carrier State. A carrier is an individual who is chronically infected with a hepatropic virus and has no or sub-clinical evidence of liver disease. In both cases, particularly the latter, these individuals constitute reservoirs for infection. In the case of HBV, “healthy carriers” typically have serum studies that show an absence of HBeAg, the presence of anti-HBe, normal aminotransferases, and low or undetectable serum HBV DNA and liver biopsies showing a lack of significant inflammation or parenchymal injury. HBV infection acquired early in life in endemic areas (such as Southeast Asia, China, and sub-Saharan Africa) gives rise to a carrier state in more than 90% of cases, whereas in non-endemic regions the carrier state is rare. By contrast, it has been estimated that HCV infection in the United States produces a carrier state in 10% to 40% of cases.
HIV and Chronic Viral Hepatitis. Because of their similar transmission modes and overlapping risk factors, coinfection of HIV and hepatitis viruses is a common clinical problem. In the United States, 10% of HIV-infected individuals are coinfected with HBV and 25% with HCV, and, when untreated, chronic HBV and HCV infection are important causes of morbidity and mortality in HIV-infected individuals, even in those who receive effective anti-HIV therapy. Similarly, in individuals who progress to acquired immunodeficiency syndrome (AIDS), liver disease is the second most common cause of death. However, in adequately treated immunocompetent HIV patients, the severity and progression of HBV and HCV infection and response to anti–hepatitis virus therapy resembles that seen in non-HIV–infected individuals.