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Serum albumin and globulin are usually within normal levels. Decreased
albumin or increased globulin levels should suggest an acute flare of chronic
liver disease. Serum ceruloplasmin levels should be drawn in all patients older
than 5 years who have suspected hepatitis to evaluate for Wilson disease.
Figure 91.3 demonstrates the sequence of clinical, biochemical, and serologic
events in typical HAV and HBV infection. The serodiagnosis of acute hepatitis
is best approached by first testing for anti-HAV IgM, HB surface antigen, HB
e antigen, HB serum DNA (quantitative), anti-HB core Ab, anti-HCV,
hepatitis C serum PCR (quantitative), anti-CMV, and EBV serology. The
finding of serum IgM anti-HAV is diagnostic of acute HAV infection because
the antibody is present at the time of clinical symptoms. A positive HB
surface antigen suggests the diagnosis of HBV in a symptomatic patient. A
positive HB e antigen or anti-HB core Ab is helpful in the rare patient who
rapidly clears HB surface antigen from the serum. It is also important to note
that in long-term HB surface antigen carriers who have HDV superinfection,
the suppression of HBV replication may lead to a transient absence of HBV
markers in the serum; unless HDV markers in the serum are sought, the
diagnosis may be missed. Anti-HCV does not appear in the patient’s
circulation until 1 to 3 months after the onset of acute illness, and in rare
cases, detectable levels may not be demonstrated for up to 1 year. Thus, unless
the acute presentation is actually a flare of chronic HCV, serodiagnosis of an
HCV infection (Hep C PCR) will await long-term follow-up.
FIGURE 91.3 Serologic changes in hepatitis A. HAAg, hepatitis-associated antigen; HAV,
hepatitis A virus.