Page 206 - Medicine and Surgery

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202 Chapter 5: Hepatic, biliary and pancreatic systems

Neonatal infections are normally asymptomatic
Surface coat
(HBsAg) (98%), but often become chronic with a 40% risk of
developing cirrhosis.
Inner core Infections in adulthood generally cause an acute
(HBcAg)
symptomatic hepatitis (70%) which may rarely result
DNA in fulminant hepatic failure (0.1–0.5% of infections).
Polymerase Only 1–2% of infections during adulthood result in
Circular DNA
(with one incomplete cirrhosis.
strand)
Complications
42nm Increased risk of cirrhosis and hepatocellular carci-
noma. Carriers may develop extra-hepatic disease, such
Figure 5.7 The Dane particle. as glomerulonephritis in children and polyarteritis no-
dosa following chronic hepatitis. These may be due to
immune complex formation.
cell death include bystander damage from T cell derived
cytokines and antibody-dependent cell-mediated cyto- Investigations
Hepatitis B is diagnosed and followed using serological
toxicity. The complete virion or Dane particle is spheri-
markers (see Fig. 5.8).
cal, 42 nm in diameter (see Fig. 5.7).
In carrier states the HBsAg remains high with an ab-
The Dane particle is found in the serum of HBV-
infected patients, its presence denoted by HBsAg. This senceofanti-HBsindicatingcontinuedpresenceofvirus.
denotes when there is first a viraemia. If the e-antigen (HBeAg) remains present and there is
The viral particle is seen in body fluids, saliva, semen, no anti-HBe, there is active viral replication indicating a
vaginal secretions, faeces, breast milk as well as serum. super-carrier or high-infectivity state. Presence of anti-
HBcAg is found in the nuclei of liver cells, where HBV
HBs alone (without other antibodies) indicates a previ-
replicates. ous successful vaccination.
The e-antigen or HBeAg is related to the core pro-

Management
teins.Thepresenceofthee-antigendenotesactiveviral
Acute hepatitis is managed supportively.
replication. It is detectable in acute hepatitis, chronic
In patients with chronic high infectivity (HBeAg pos-
active hepatitis or in high infectivity carriers (super-
itive) and the evidence of active hepatitis (elevated ALT)
carriers). Conversely, anti-HBe antibodies indicate a
interferonα canbeused.Ifthereisnoresponseorrelapse
better prognosis.
following treatment, nucleoside analogues and other an-
Carrier status is defined as presence of HbsAg for

tiviral drugs can be tried.
more than 6 months. Carrier status is associated with
Vaccines are available which are effective:
chronic hepatitis in people with lowered immunity Active immunisation by recombinant protein (HB-
and with neonatal or childhood infection. It has also
sAg made in yeast cells) is given to at risk individuals
been noted that patients who present with jaundice
including health-care workers and in areas of high
during the acute infection rarely convert to a carrier
prevalence. The WHO recommends that hepatitis B
status, compared to those who have an anicteric acute
vaccine should be included in routine childhood im-
hepatitis.
munisation schedules for all children in all countries.
Active immunisation should be given to all infants

born to HBsAg-positive mothers, passive immuni-
Clinical features sation with hepatitis B immunoglobulin is given, in
Hepatitis B can cause a range of clinical disease, from addition, to infants born to HBeAg positive moth-
asymptomatic to fulminating hepatic failure or chronic ers. Combined active and passive immunisation is
hepatitis. The likelihood of these conditions depends on also used as post-exposure prophylaxis for needlestick
the age of the patient: injuries.