Hepatitis B

Highly infectious blood borne virus. A single contaminated needle stick injury carries a significant risk of transmission. In endemic areas, significant rates of postnatal infection in children, presumably from minor trauma.

Acute infection develops over 1-6 weeks and can be fulminant. Symptoms are non-specific fever, lethargy, abdo pain.  15% have serum sickness type  symptoms in pre-icteric phase viz fever, arthralgia, urticaria. Jaundice then develops.   Various antigens, which may or may not clear as antibodies produced, used to diagnose, judge stage of infection, and infectivity.

  • HBsAg – shows Acute or chronic hepatitis B infection. Can be negative in acute fulminant disease.
  • Anti HBs (or Anti HBs) – Immunity to hepatitis B, postinfective (only 6% of patients) or with active or passive immunization
  • Anti HBc IgM – first antibody to appear, even before HBsAg.  High titer: acute hepatitis; Low titer: chronic infection
  • Anti HBc IgG – Past exposure to hepatitis B, or maternal antibody crossing placenta in young infants
  • HBeAg – highly infectious.  Without treatment, 85% of children clear HBe.
  • anti HBe – not immune, but low infectivity. Do not develop chronic hepatitis; but low risk of hepatocellular carcinoma persists.

NB there may be an interval following the disappearance of a hep B antigen before its antibody becomes detectable.

For acute hepatitis, no specific treatment is required, just supportive. If fulminant, some people use antivirals, but basically the issue is whether you need to transplant – see below.

Carrier rate (ie chronic infection, = HBsAg pos for 6/12, and hence potential for serious sequelae) is higher in males and greatest in those infected in first 3 years of life.  Also higher in those with mild symptoms viz anicteric with minimal elevation of transaminases.

Some carriers will be inactive with anti-HBe, low levels of DNA (<100 000 copies on PCR) and normal transaminases. Liver disease progresses very slowly if at all, although hepatocellular carcinoma risk is still higher than normal (but much less than in HbeAg positive). Monitor LFTs every 6-12 months.

In active chronic infection, DNA levels are high indicating active replication, transaminases are 2x the upper limit of normal or higher, and biopsy will show stage 4 histological activity or more. HBeAg is usually positive although some mutants will be negative. Adults with chronic hep B have 20% cirrhosis rate after 10 years and 37% after 15 years. Alcohol intake is an independent factor. Hepatocellular Ca rate is about half that.

When to biopsy is tricky, partly because the clinical course is unpredictable but also because treatment is ineffective. Transaminases can be raised transiently, so repeat after 1-3 months. Histological cirrhosis has a poor prognosis. With treatment, 32% of patients with chronic disease clear HBeAg cf 11% of untreated (metanalysis). There is no benefit in patients with normal LFTs.

Do USS and alpha fetoprotein every 2 years as screening for hepatocellular Ca for both inactive carriers and chronically infected.

Other management points –

  • immunisation of household contacts
  • vaccination against hepatitis A (in low prevalence areas)
  • avoiding alcohol
  • safe sexual practices
  • weight reduction
  • Careers advice
  • Immunosuppressive drugs may activate hepatitis B infection. Equally, immunosuppressed children may have hepatitis B infection without serological evidence – so do PCR.


For acute, no specific treatment, just supportive. If fulminant, look for co-infections that may have precipitated episode. Main issue is whether transplant required, although American Association for study of liver diseases recommends using antivirals in adults: no great evidence but seem reasonably safe, and reduces risk of re-infection of grafted liver after transplant (pretty inevitable – HBIg post transplant also delays infection but resistant mutants come through). Lamivudine or telbivudine suggested when the anticipated duration of treatment is short; otherwise, entecavir is preferred. Treat until HBsAg cleared or indefinitely in transplants. Interferon is contraindiated.

For chronic infection:

  • Pegylated IFN alpha (5 million units a day or 10 MU thrice SC for 48 weeks) both antiviral and immunomodulatory activity.

Other issues:

  • Co-infection with HCV has a poorer prognosis even though DNA levels may be less; treatment should be considered at 1000+ copies.
  • In decompensated cirrhosis, transplantation is the only definitely effective option. Lamivudine may help (historical controls). IFN increases complications.