Hepatitis, viral: B and D
D E FI N I T ION
Hepatitis caused by infection with hepatitis B virus (HBV), which may follow
an acute or chronic (defined as viraemia and hepatic inflammation continuing>6 months)
course.
Hepatitis D virus (HDV), a defective virus, may only co-infect with HBV or superinfect persons
who are already carriers of HBV.
AETIOLOGYHBV
is an enveloped, partially double-stranded DNA virus. Transmission is by
sexual contact, blood and vertical transmission. Various viral proteins are produced,
including core antigen (HBcAg), surface antigen (HBsAg) and e antigen (HBeAg). HBeAg is
a marker of " infectivity.
HDV is a single-stranded RNA virus coated with HBsAg.
Antibody- and cell-mediated immune responses to viral replication lead to liver inflammation
and hepatocyte necrosis. Histology can be variable, from mild to severe inflammation and
changes of cirrhosis.
ASSOCIATIONS/RISKFACTORS
Hepatitis B infection is associated with IV drug abuse,
unscreened blood and blood products, infants of HbeAg-positive mothers and sexual contact
with HBV carriers. Risk of persistant HBV infection varies with age, with younger individuals,
especially babies, more likely to develop chronic carriage. Genetic factors are associated with
" rates of viral clearance.
EPIDEMIOLOGY
Common. 350 million worldwide infected with HBV; 1–2 million deaths
annually. Common in Southeast Asia, Africa and Mediterranean countries. HDV also found
worldwide. HBV is relatively uncommon in the UK.
H ISTORY
Incubation period 3–6 months; 1- to 2-week prodrome of malaise, headache, anorexia,
nausea, vomiting, diarrhoea and RUQ pain.
May experience serum-sickness-type illness (e.g. fever, arthralgia, polyarthritis, urticaria,
maculopapular rash).
Jaundice then develops with dark urine and pale stools.
Recovery is usual within 4–8 weeks. One per cent may develop fulminant liver failure.
Chronic carriage may be diagnosed after routine LFT testing or if cirrhosis or decompensation
develops.
EXAMINATION
Acute:
Jaundice, pyrexia, tender hepatomegaly, splenomegaly and cervical lymphadenopathy
in 10–20%. Occasionally, urticaria/maculopapular rash.
Chronic:
May have no findings; signs of chronic liver disease or decompensation.
INVESTIGATIONS
Viral serology:
Acute HBV: HbsAg positive, IgM anti-HbcAg.
Chronic HBV:
HbsAg positive, IgG anti-HBcAg, HbeAg positive or negative (latter in precore
mutant variant).
HBV cleared or immunity:
Anti-HBsAg positive, IgG anti-HBcAg.
HDV infection:
Detected by IgM or IgG against HDV.
PCR:
For detection of HBV DNA is the most sensitive measure of ongoing viral
replication.
LFT:
"" AST and ALT. " Bilirubin. " AlkPhos.
Clotting: " PT in severe disease.
Liver biopsy:
Percutaneous, or transjugular if clotting is deranged or ascites is present.
MANAGEMENT
Prevention:
Blood screening, instrument sterilization, safe sex practices.
Hepatitis, viral: B and D (continued)
Passive immunization:
Hepatitis B immunoglobulin (HBIG) following acute exposure and to
neonates born to HbeAg-positive mothers (in addition to active immunization).
Active immunization:
Recombinant HbsAg vaccine for individuals at risk and neonates born
to HBV-positive mothers. Immunization against HBV protects against HDV.
Acute HBV hepatitis:
Symptomatic treatment with bed rest, antiemetics, antipyretics and
cholestyramine for pruritus. Notification to the consultant in communicable disease
control.
Chronic HBV:
Indications for treatment with antivirals: HbeAg-positive or HbeAg-negative chronic
hepatitis (depending on ALT and HBV DNA levels), compensated cirrhosis and HBV DNA
>2,000 IU/mL, decompensated cirrhosis and detectable HBV DNA by PCR.
Patients may be treated with interferon alpha (standard or pegylated, which has " half-life), or
nucleos/tide analogues (adefovir, entecavir, telbivudine, tenofovir, lamivudine). The role
of lamivudine as primary therapy has diminished due to high rates of drug resistance.
Interferon alpha is a cytokine which augments natural antiviral mechanisms. Side-effects
include flu-like symptoms, fever, chills, myalgia, headaches, bone marrow suppression
and depression, necessitating discontinuation in 5–10% of patients.
COMPLICATIONS
Fulminant hepatic failure (1%), chronic HBV infection (10% adults,
much higher in neonates), cirrhosis and hepatocellular carcinoma, extrahepatic immune
complex disorders including glomerulonephritis, polyarteritis nodosa. Superinfection with
HDV may lead to acute liver failure or more rapidly progressive disease.
PROGNOSIS
In adults, 10% infections become chronic, and of these, 20–30% will
develop cirrhosis. Factors predictive of a good response to interferon include high serum
transaminases, low HBV DNA, active histological changes and the absence of complicating
diseases.
ليست هناك تعليقات:
إرسال تعليق