Signs and symptoms
The average incubation period is 60 to 90 days (range is 40 to 160 days).
In the initial stages of HBV infection the symptoms are vague and ill-defined.
The onset of hepatitis B is typically insidious, with nonspecific symptoms of malaise, poor appetite and nausea, with pain in the right upper quadrant.
Fever, when present, is usually mild.
Roughly 30 to 50% of adult patients will develop jaundice. As jaundice sets in, the urine becomes darker and the stools paler.
The disease generally lasts from one to six weeks but may be prolonged and can be fulminant. Acute hepatitis B resembles other forms of acute hepatitis clinically and cannot easily be distinguished by history, physical examination or routine serum biochemical tests.
Unusually, fulminant hepatitis B can occur during acute infection. This occurs in approximately 2 to 3% of cases. Fulminant hepatitis can lead to the rapid onset and development of acute hepatic failure with encephalopathy, coma and death.
Interpreting laboratory results
Various classifications of antibody indicate the stages of the immune response.
The diagnosis of acute hepatitis B generally rests upon the finding of hepatitis B surface antigen (HBsAg) and IgM antibody to hepatitis B core (anti-HBc) in the serum of a patient with clinical and biochemical evidence of acute hepatitis.
• The first serological marker to be detectable in the serum is HBsAg which appears during the incubation period and rapidly rises in titre. In about 10% of patients HBsAg is cleared early and may not be detectable when the patient is first seen by the physician.
• Concurrent with or shortly after the appearance of HBsAg in serum, HBeAg and HBV DNA are detectable. Disappearance of HBeAg, seroconversion to anti-HBe and a decline in HBV DNA indicates resolution of viral replication and predicts resolution of acute hepatitis B.
• In patients who develop chronic hepatitis B, by contrast, HBeAg and HBV DNA remain high. HBcAg is not found in the serum.
• The first antibody to arise during the course of typical acute hepatitis B is anti-HBc. IgM anti-HBc is positive in acute hepatitis B and is used to document the acute disease, rather than an exacerbation of disease.
It generally persists for only a few months, making it a useful marker for the diagnosis of acute hepatitis B. IgG anti-HBc, indicative of chronic infection, generally persists for life. A proportion of patients with active chronic hepatitis B may also develop IgM anti-HBc, detected by sensitive tests.
• Antibodies to HBsAg (anti-HBs) usually appear during convalescence following the surface antigen’s disappearance. Anti-HBs alone is also a marker of immunisation.
|
The three main HBV antigens are:
- HBcAg Hepatitis B core antigen (HBcAg is not found in serum)
- HBsAg Hepatitis B surface antigen
- HBeAg Hepatitis B e-antigen (denotes active viral replication)
|
HBcAg can stimulate IgM and IgG antibodies:
- immunoglobulin ‘M’ (IgM) indicating that HBV infection has occurred within the last six months
- immunoglobulin ‘G’ (IgG) indicating that HBV infection occurred more than six months earlier
|
The diagnosis of acute hepatitis B generally rests upon the finding of hepatitis B surface antigen (HBsAg) and IgM antibody to hepatitis B core (anti-HBc) in the serum of a patient with clinical and biochemical evidence of acute hepatitis.
• The first serological marker to be detectable in the serum is HBsAg which appears during the incubation period and rapidly rises in titre. In about 10% of patients HBsAg is cleared early and may not be detectable when the patient is first seen by the physician.
• Concurrent with or shortly after the appearance of HBsAg in serum, HBeAg and HBV DNA are detectable. Disappearance of HBeAg, seroconversion to anti-HBe and a decline in HBV DNA indicates resolution of viral replication and predicts resolution of acute hepatitis B.
• In patients who develop chronic hepatitis B, by contrast, HBeAg and HBV DNA remain high. HBcAg is not found in the serum.
• The first antibody to arise during the course of typical acute hepatitis B is anti-HBc. IgM anti-HBc is positive in acute hepatitis B and is used to document the acute disease, rather than an exacerbation of disease.
It generally persists for only a few months, making it a useful marker for the diagnosis of acute hepatitis B. IgG anti-HBc, indicative of chronic infection, generally persists for life. A proportion of patients with active chronic hepatitis B may also develop IgM anti-HBc, detected by sensitive tests.
• Antibodies to HBsAg (anti-HBs) usually appear during convalescence following the surface antigen’s disappearance. Anti-HBs alone is also a marker of immunisation.