see also:

• viruses
• hepatitis C virus
• hepatitis
• cirrhosis
• hepatocellular carcinoma

• Aust. Prescriber 2009 - The management of hepatitis B

• highly transmissible if no vaccination (~10x more infectious than with similar exposure to hepatitis C virus and ~100x more infectious than needlestick exposures to HIV / AIDS)
• can occur via a number of routes - percutaneous (needlestick, IVDU, tatooing, or body piercing), parenteral (transfusions), transdermal if broken skin, mucosal (especially anal intercourse), or vertical transmission during perinatal period.
• it seems vertical transmission from mother to baby can be prevented by giving the mother tenofovir, an antiviral agent, in the 3rd trimester through to 8 weeks post-partum.

• following exposure, acute hepatitis B infection has an incubation period of 6-12 weeks
• adults commonly develop symptoms of jaundice (icterus), anorexia, nausea, RUQ discomfort and fatigue, but fortunately, over 95% will spontaneously clear the virus
• only 30% of children will spontaneously clear the virus
• perinatal acquisition is commonly asymptomatic but only 5% will clear the virus
• 1% may develop acute liver failure and develop hepatic encephalopathy - these patients should be referred to a transplant unit
• Rx is mainly supportive

• affects some 160,000 people in Australia - mainly non-Westerners (presumably due to lack of access to vaccination prior to migration) but including Mediterranean Europe.
• shortens life span of 45% of infected men and 15% of infected women due to development of cirrhosis or hepatocellular carcinoma

• phase 1 - immune tolerance
  • usually lasts for 20-40 years
  • high levels of viral replication, persistently normal ALT
  • HBeAg but no antibodies to this
  • minimal damage, thus no liver biopsy or antiviral Rx required
  • advise periodic LFT monitoring watching for rise in ALT which signals phase 2
• phase 2 - immune clearance
  • more vigorous immune response resulting in liver damage with intermittently raised ALT and elevated viral DNA
  • repeated episodes of inflammation leads to fibrosis, and duration and severity of this phase determines degree of long term liver damage
  • 30-40% of patients emerge with established cirrhosis
  • 5-10% of patients each year will spontaneously lose HBeAg and develop antibodies to HBeAg - “seroconversion” which results in reduced viral replication.
  • median age for seroconversion is 30-32 years
  • if ALT is persistently raised, refer to hepaologist for possible biopsy and Rx.
• phase 3 - immune control
  • immune response suppresses viral replication to low or undetectable levels
  • inflammation reduces and ALT normalises
  • once seroconversion has occurred, patients may remain in this phase indefinitely.
  • most do not require antiviral Rx in this phase, but many will have established cirrhosis and require careful assessment
• phase 4 - immune escape
  • virus mutates and loses it's ability to make the HBeAg allowing it to replicate, resulting in recurrence of active liver disease and progressive fibrosis
  • persistely elevated or fluctuating ALT levels with HBeAg negative status, but elevated viral DNA
  • usually patients are older than 40 years
  • given the high risk of cirrhosis - 8-10% per year, consider long term Rx to suppress viral replication