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.
acute infection
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
chronic hepatitis B
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
in patients with HBV, each daily consumption of 12 g of alcohol increased the risk of cirrhosis by 6.2% and the risk of HCC by 11.5% 1)
phases of chronic hepatitis B
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