Viral A Hepatitis
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.
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.
Relapsing hepatitis A occurs in about 10% of patients with hepatitis A infection. If you see patient who you make the diagnosis of hepatitis A and then 3 weeks later they call you as they seem to be recovering, but they call you and say I’m feeling sick again. You check the ALT and it is 1200 IU,
they may complain of arthralgia, arthritis, and immune complex mediated phenomenon may be present. That is relapsing hepatitis A, and it is worth knowing that because you can save them unnecessary testing like ERCP, ultrasounds, and CAT scans. In these 2 variants of cholestatic and relapsing hepatitis A infection, it is worth using corticosteroids if the patient is very symptomatic. They all recover and it never leads to chronic hepatitis. If it does lead to chronic hepatitis a year later the patient has abnormal LFTs and they are they complaining of symptoms that are probably autoimmune
chronic hepatitis. Hepatitis A has triggered that. On rare occasions you can
see chronic liver disease develop. With classic autoimmune they respond
beautifully to steroids. They usually have a positive ANA. They have
hypergammaglobulinemia.
Vaccine is now available and it has wonderful vigorous antibody response up
to 1000 fold compared to immune serum globulin. It will confer protection
for 10 to 20 years as opposed to Gamma globulin which can confers
protection for 4 to 6 months. Vaccine should be given to people who travel
frequently to parts of the world where hepatitis A is endemic, to people who
work with non-human primates like a zoo or a laboratory, to gay men with
multiple sex partners, and also to military personnel who might be called upon
to go to a part of the world where hepatitis A is endemic. It is also
recommended for patients with severe chronic liver disease like
hemochromatosis with cirrhosis, Wilson’s, or hepatitis B or C. If they were to
get hepatitis A they have a much higher mortality. We should look for
hepatitis A antibody in our patients with severe chronic liver disease because
if it is negative, they should get the vaccine. That is a recent recommendation.
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.
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 IU/L,
and fecal excretion of HAV may recur. Although patients can have a protracted
course, complete recovery is the rule, and there is no propensity for the chronic
carrier state. Fulminant HAV infection is rare and the estimated case mortality rate
is about 0.1% among patients hospitalized with this illness.
Characteristic laboratory findings include moderate to marked elevations in the
serum ALT and AST values. The peak transaminase values range from 400 to
several thousand international units, and the rise in the levels of these enzymes
often precedes the elevation in serum bilirubin concentration. Leukopenia is a
routine finding, and atypical lymphocytosis is common. The presence of
leukocytosis is suggestive of fulminant disease or coexisting infection.
Prevention
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 diagnosis is established. Passive immunization with
regular immune serum globulin is 80-98% effective in preventing HAV infection.
Recommendations for Immune Globulin Prophylaxis of Hepatitis A
Related Posts :
Leave a Reply
You must be logged in to post a comment.