At a Glance

Hepatitis A is a viral hepatitis caused by hepatitis A virus (HAV), primarily transmitted by the fecal-oral route. The incidence has been declining in the United States during the past decade, mostly because of immunization. Major pathways of transmission include close contact with an infected person; male homosexual practice; contact with contaminated food or water; eating raw or undercooked shellfish; transmission in institutions, including day cares, residential facilities, and the military; and blood-borne transmission. There are also sporadic cases with no identifiable risk factors.

Patients with hepatitis A present 2-7 weeks after exposure with fever, fatigue, malaise, and gastrointestinal (GI) symptoms. Within a week, symptoms of hepatitis (e.g., jaundice, alcoholic stools, dark urine, and pruritus) appear. Jaundice and hepatomegaly are the most common physical findings.

The disease may be asymptomatic or present as a mild febrile syndrome without jaundice; this is more common in infants and children than in adults. Chronic HAV is rare. Fulminant hepatitis A is seen primarily in patients with significant underlying liver disease, especially pre-existing hepatitis C.

Some patients have one or more relapses after the initial episode.


Markers of liver damage are typical; elevated serum aminotransferases are usually greater than 1000 IU/dL; serum total, direct bilirubin, and alkaline phosphatase are markedly elevated. Aminotransferase elevations precede the rise in bilirubin, and bilirubin peaks, often above 10 mg/dL, after aminotransferase levels begin to fall. None of these results are specific for hepatitis A.

For diagnosis of hepatitis A, the test of choice is HAV IgM antibody. HAV IgM is usually present at the onset of symptoms and persists 4-6 months after resolution.

For assessment of HAV immune status due either to past infection or immunization, HAV total antibody is commonly used in lieu of a test for HAV IgG alone (Table 1).

Table 1
Elevated liver indicators HAV IgM Ab HAV total Ab
Aspartate aminotransferase (ALT) alanine aminotransferase (AST), bilirubins, alkaline phosphatase; markers of hepatic injury; not specific to HAV but indicate hepatitis is present Marker of acute HAV infection Marker of immunity to HAV from prior infection or vaccine; also positive in acute HAV


Other causes of hepatic injury or dysfunction, other viral hepatitides, chemical or autoimmune hepatitis, can cause abnormalities of the nonspecific liver tests.

HAV antibody testing is relatively specific; however, false positives are occasionally seen, especially of HAV IgM. Avoid testing asymptomatic patients for HAV IgM. Anti-HAV IgM can be below cut-off very early and very late in the course of illness. False positives are seen in patients with heterophilic antibodies due to animal exposure or animal serum administration and are more common in cord-blood and neonatal samples.

What Lab Results Are Absolutely Confirmatory?

Confirmatory testing is rarely indicated. Polymerase chain reaction (PCR) of stool for HAV is primarily a research and epidemiological tool.


A positive IgM in a patient with a likely other etiology for hepatic disease or an asymptomatic patient can be followed with HAV IgM and HAV total antibody. HAV total antibody should become positive, and HAV IgM should vanish within 6 months, except in relapsing infections in which IgM can persist.

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