Viral Hepatitis Update

Spencer Wilson, MD
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 or chronic liver disease.

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 single-stranded RNA and. to date, only a Single serotype has been identified. The virus is stable for several months at 40cbut can be inactivated by exposure to heat to 100BC for five minutes. The virus can be transmitted to chimpanzees and marmosets and has been recently grown in tissue culture.
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 and water. Overcrowding, poor hygiene, and poor sanitation favor the spread of this infection. A chronic viremic or fecal carrier state does not occur. Hence, patients are only transiently infectious. Viremia and fecal shedding occur over a short and finite period of time lasting several days to a few weeks. Transmission occurs via serial spread from one infected individual to another susceptible individual. Parenteral transmission of hepatitis A infection is extremely rare. Intravenous drug users, dialysis patients, transfusion recipients, and health care workers are not at increased risk of infection. Acquisition of HAV secondary to frequent oral-anal sexual contact has been documented in homosexual men.
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, as well as by radioimmunoassay and usually disappears within 4 to 12 weeks. Persistent anti-HAV IgG antibody, is then detectable and confers homologous immunity. Fecal shedding of the hepatitis A virus occurs in the early phase of the illness. HAV is detected in stool during the first week of infection in 50% of patients, during the second week in 25% of patients, and in the third and fourth weeks only rarely.
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, malaise, and anorexia are common and an abrupt onset is characteristic. If the patient develops jaundice, the urine may darken and the stool may lighten a few days before the onset of jaundice. When jaundice begins, the other symptoms usually subside. Tender hepatomegaly is common. Splenomegaly and lymphadenopathy are present in less than a third of patients.
Hepatitis A has an incubation period is 15 to 50 days. The virus is present in the blood stream for a short final period of time. The viremic phase is very short lived. It is shed in the stool for a short period of time. The majority of individuals do not develop jaundice. The ratio of anicteric hepatitis to jaundice is 20 to 1. Patients recover by in large. There are 2 antibodies, which are the IgM and the IgG. The way to make the diagnosis of acute hepatitis A is to look at a single sample of serum and if it is positive for IgM Anti-HV your patient with acute hepatitis has acute hepatitis A infection. IgG antibody appears during the convalescence phase, and confers life long immunity. There are 3 variants of hepatitis A virus infection which are cholestatic hepatitis, relapsing, and fulminant. Fulminant occurs rarely but can lead to fatalities and the only treatment in that setting is to do a liver transplant. Cholestatic hepatitis occurs more often in middle-aged or elderly individuals. They can have bilirubins in excess of 20 or 30 mg/dL. They develop marked pruritus. We can do an IgM antibody and make the diagnosis of acute hepatitis A. The patient has a bilirubin of 30, so we can get an ultrasound and make sure the bile ducts are not dilated and make the diagnosis of hepatitis A infection. This is the one time to consider a short course of corticosteroids. Prednisone, 30 or 40 mg, for week and then taper it, will significantly truncate or abrogate the illness.
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