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Viral Hepatitis Update

Acute viral hepatitis has been defined as a systemic viral infection in which there is hepatocellular necrosis and inflammation. There are characteristic clinical, biochemical, immuno-serologic, and morphologic features. There are five major viruses: Hepatitis A virus (HAV), hepatitis B virus (HBV), Hepatitis C virus (HCV), hepatitis D virus (delta Virus, HDV), and Hepatitis E virus (enterically transmitted, epidemic non-A, non-B hepatitis, HEV). Chronic viral hepatitis is a necro-inflammatory disorder of the liver initiated by viruses and persisting for longer than six months. It occurs in association with HBV, HCV, and delta virus infection. In contrast, patients with acute hepatitis A and hepatitis E virus infection have no propensity whatsoever to develop a chronic carrier state.

Hepatitis A

The hepatitis A virus (HAV) is a 27 nm RNA virus classified as an enterovirus and belonging to the picornovirus family The nucleic acid of HAV is a single-stranded RNA and. to date, only a Single serotype has been identified.

Susceptibility to HAV infection increases linearly with age and bears an inverse correlation to socioeconomic status. In major metropolitan centers in the United States, 50% of persons 50 years of age or older have detectable antibody to HAV. HAV is spread predominantly by the fecal-oral route via contaminated food viral hepatitis, hepatitis and water. Overcrowding, poor hygiene, and poor sanitation favor the spread of this infection.

The diagnosis is accomplished by testing the serum for antibody to hepatitis A. The IgM antibody appears during the acute phase and is detected by immune adherence hemagglutination.

In the United States, HAV is responsible for 25% of sporadic cases of hepatitis. In most persons, the disorder is mild, self-limited, and anicteric. Constitutional symptoms of fever, and malaise.

The jaundice generally disappears six to eight weeks after onset and most patients have full clinical and biochemical recovery by six months. The disease is more severe in adults.

In the United States, severe cases of clinical hepatitis A are being increasingly recognized. As a consequence of improved sanitation and hygiene practices, many individuals are not exposed to

There are three unusual variants of hepatitis A infection-cholestatic hepatitis, relapsing hepatitis, and fulminant hepatitis. In patients with cholestatic hepatitis, serum bilirubin levels may exceed 25 mg/dL. These patients eventually recover, although it may take several weeks to a few months for full recovery. A short course of corticosteroids can significantly abrogate the illness. Relapsing hepatitis is seen in 10% of patients. During a relapse, the ALT level may exceed 1000

Characteristic laboratory findings include moderate to marked elevations in the serum ALT and AST values.


HAV infection can be effectively curtailed by measures emphasizing good sanitation and personal hygiene. Patients are most contagious in the early phase of the illness before the definitive

Recommendations for Immune Globulin Prophylaxis of Hepatitis A

An inactivated hepatitis A vaccine is available. The immune response occurs in 95.8% of patients after the first dose and in 99.8% of patients after the second dose. The antibody response is 50.

Hepatitis B

There are three antigen-antibody systems related to hepatitis B Hepatitis B surface antigen (HBsAg); hepatitis B core antigen (HBcAg) and e antigen (HBeAg); and their corresponding antibodies.

Hepatitis B surface antigen (HBsAg): A unique feature of HBV infection is that concentrations of viral antigen and viral particles in the blood may reach 500g/mL and 5-10 trillion particles/mL respectively. HBsAg exceeds Dane particles by a factor of 103 to 106 in the circulation. Blood that is positive for HBsAg connotes one of three possibilities: 1) the subject is incubating HBV.

Anti-HBs is a neutralizing body detected in secretions and excretions. Its appearance together with that of core antibody (Anti-HBc) signals recovery from hepatitis B and the development of subsequent immunity. Anti-HBs is the only antibody that appears in persons who have been.

Hepatitis B core antigen (HBcAg): The second antigen-antibody system is hepatitis B core antigen (HBcAg) and core antibody (anti-HBc) HBcAg is present in the nucleus of infected hepatocytes. Testing for core antigen is not a routine aid for diagnosing HBV infection. In contrast in patients with acute hepatitis B, core antibody can be detected in serum before ant-HBs, which generally appears about four months after the acute illness. High titer IgM, anti-HBc is the only serological marker present during the so-called gap or "window" period, which refers to a period of time when the patient has acute infection, but tests for HBsAg and anti-HBs are negative.

Hepatitis B e antigen (HBeAg): There is the e antigen and e antibody (anti-HBe) system. Hepatitis B e antigen appears early, transiently, and universally in the serum of patients with acute HBV infection. Therefore, the mere presence of this antigen does not correlate with severity or with chronicity. However, persistence of this antigen for greater than 12 weeks suggests a high likelihood of the development of a chronic carrier state. In addition, in chronic carriers, e antigen positively correlates.