Hepatitis B (HBV) is a hepadnavirus that is a common cause of chronic liver disease and hepatocellular carcinoma. Hepatitis D virus may be co-infected with HBV or superinfect chronic carriers of HBV.
One third of the world’s population has past or current HBV infection. There are 400 million chronic HBV carriers worldwide.
Mechanism of spread
HBV is spread through blood and body fluids. Therefore, it can be spread through sexual intercourse, intravenous drug use, infected blood products and tattoos.
It may also be spread vertically during pregnancy.
HBV infection can produce acute or hepatitis. However, most infections (>65%) are subclinical and resolve without symptoms.
Mimics infection with hepatitis A virus but can be more severe to include polyarthritis and fever. Viraemia initially causes patients to feel unwell with non-specific symptoms, such as nausea, anorexia and myalgia. After 1-2 weeks, patients can become jaundiced. As jaundice deepens, urine becomes darker and stools turn pale due to intrahepatic cholestasis. Abdominal discomfort and pruritus are common features at this point. The liver may be tender and the spleen enlarged.
1-10% of patients develop chronic HBC infection after an acute episode. This may be:
- Non-progressive (60-80% of cases): do not develop progressive liver disease, although some have reactive hepatitis episodes. Usually asymptomatic or with mild hepatitis.
- Active/progressive (20-40%): raised ALT with evidence of HBV multiplication. It can lead to cirrhosis and hepatocellular carcinoma.
Blood tests are all that are required to confirm the diagnosis. These primarily look at:
- LFTs: raised bilirubin and ALT
- FBC: leucopaenia, raised ESR
- Viral serology: viral antigens to request include HBsAg (surface antigen), HBeAg (e antigen)and HBV DNA.
- HBsAg: indicates acute or chronic infection. Rises 1-6 months following exposure to virus
- HBeAg: indicates patient is highly infectious
- HBV DNA: implies viral replication
- Anti-viral antibodies: antibodies to request include anti-HBs (surface antibody), IgM anti-HBc (core antibody), IgG anti-HBc (core antibody). Active immunisation relies on the production of anti-HbsAb.
- Anti-HBsAb: Immunised or cured
- IgM Anti-HBcAb: New infection (as IgM is the first antibody produced)
- IgG Anti-HBcAb: New/old infection
Examples of viral serology and antibody results include:
- Anti-HBs AB positive only = Vaccinated
- HBsAg and anti-HBcAb positive = Chronic infection
- Anti-HBsAb and anti-HBcAb positive = Resolved infection
General advice includes avoiding alcohol.
Mainly symptomatic management as retroviral drugs have no proven efficacy.
Active chronic hepatitis
Treatments are still limited as no drug can completely eradicate HBV. Indications for drug therapy include liver inflammation (raised ALT), high viral load (HBV DNA >20,000 U/mL) and cirrhosis. The aim is to prevent cirrhosis and hepatocellular carcinoma.
Drug therapies include pegylated interferon alpha (PEG) and direct-acting nucleotide antiviral agents (e.g. tenofovir, lamivudine). Effective therapy should:
- Reduce HBV DNA
- Seroconvert HBe (HbeAg cleared and HbeAb have developed)
- Normalise LFT
Decompensated cirrhosis is an indication for liver transplantation.
Chronic infection can lead to cirrhosis and hepatocellular carcinoma.
Active immunisation: Vaccination
Passive immunisation: Anti-HBV immunoglobulins
Neonates born to HBV positive mothers should be immunised at birth and given anti-HBV immunoglobulin; viral serology should be check at the age of 12 months.