Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (185 page)

   
Acute HBV infection
: HBsAg and anti-HBc antibodies (total and IgM) are positive, and anti-HBs is negative. HBV DNA is detectable.

   Acute HBV infection usually lasts for 1–6 months with mild or no symptoms. Aminotransferases are increased >10-fold. HBsAg gradually arises to high titers during the active phase; HBeAg also appears. Serum bilirubin is usually normal or only slightly increased in acute disease. Immune complex– mediated diseases may be seen in 10–20% of patients (e.g., serum sickness, arthritis, dermatitis, glomerulonephritis, vasculitis). Immune complex– mediated glomerulonephritis or nephrotic syndrome may progress to chronic renal failure. Acute HBV usually resolves in 3–6 months in uncomplicated infection. In patients who recover from acute HBV infection, titers of HBsAg fall to undetectable levels, followed by the emergence of anti-HBs after 4 to 8 weeks. During this “window,” anti-HBc total and IgM antibodies are detectable; HBV DNA is also usually detectable.

   
Acute HBV infection with recovery
: After complete resolution of HBV infection, patient testing shows HBsAg negative, anti-HBs positive, HBeAg negative, anti-HBe positive, anti-HBc-IgG positive, and HBV DNA falls to undetectable levels. Full recovery is more common after clinically apparent acute HBV infection. Acute liver failure is uncommon, occurring in 0.1–1% of patients.

   
Chronic HBV infection
: Chronic infection is uncommon, occurring in 1–10% of patients overall, but approximately 90% perinatal infections. The typical pattern of HBV markers shows that HBsAg and total anti-HBc are positive, while anti-HBc-IgM and anti-HBs are negative.

   
Laboratory Evaluations for Patients with Chronic HBV Infection
:

   Tests for HBV active replication (e.g., HBeAg/anti-HBe, HBV viral load) are used for initial assessment and ongoing monitoring of patients.

   Laboratory tests to assess impact of infection (e.g., CBC, PT, hepatic function panel) are used for initial assessment and ongoing monitoring of patients.

   Laboratory tests to rule out coinfection with other viruses (e.g., HCV, HDV, HIV).

   Consider liver biopsy to stage liver disease histologically.

   Consider screening for hepatocellular carcinoma (e.g., AFP, ultrasound).

Continued transaminase elevation for >6 months is seen in chronic hepatitis. Chronic HBV infection may last for only 1 year or for several decades with mild or severe symptoms. Most patients resolve spontaneously, but some develop progressive liver failure and cirrhosis. AST and ALT fall to 2–10 times normal range. Detection of HBeAg indicates continuing active viral replication, but patients with active HBV replication, as demonstrated by HBV DNA, may be HBeAg negative. A chronic carrier state with nonreplicating virus may also develop. Patients are usually asymptomatic. AST and ALT fall to normal or <2 times normal levels. Anti-HBe is detectable; HBeAg is negative. HBsAg is present but at decreasing titers. HBV viral load may be negative or low positive. Total anti-HBc is usually present in high titer (>1:512). HBV carrier patients may experience flares of active, symptomatic hepatitis accompanied by a change in their serologic markers: HBsAg positive, anti-HBc-IgM positive, anti-HBs negative, anti-HBe negative, and HBeAg may be detected. The development of anti-HBs marks the end of the carrier stage. Chronic replicative infection may be caused by hepatitis B viruses with mutations that affect normal HBeAg expression, resulting in an atypical pattern of HBV markers. Patients infected with precore or core promoter mutants tend to have more severe disease, more flares, and more rapid progression to cirrhosis. Patients are HBsAg positive, anti-HBs negative, anti-HBc-IgG positive, anti-HBc-IgM negative, HBeAg negative, and anti-HBe positive. Effective treatment of chronic HBV hepatitis causes ALT, HBeAg, and HBV DNA to become normal.