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Acute viral hepatitis may be caused by hepatitis A, B, C, D and E, and less commonly by CMV and EBV. These can cause severe liver disease (esp. hepatitis B and C) from end-stage liver failure to hepatocellular carcinoma. A and D are spread by the faecal–oral route, B and C from blood and possible other body fluids. See also 326–8.
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Diagnostic markers for acute hepatitis
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Hepatitis A: IgM anti-HAV (Ab)
Hepatitis B: surface antigen (HBsAg)
Hepatitis C: anti-HCV (Ab)
IgM antibodies = recent infection
IgG antibodies = previous exposure
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Fever, malaise, anorexia, nausea, arthralgia → jaundice
Recovery usu. in 3–6 wks—self-limiting
Sometimes a subclinical illness
No carrier state
Does not cause chronic liver disease
Fulminant hepatitis with coma and death is rare
LFTs and viral markers confirm diagnosis
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Similar clinical presentation to hepatitis A but arthralgia and uriticaria more common
Transmission by blood spread, sex, perinatal spread, percutaneous
5% become chronic carriers but
95% with infant-acquired HBV → carriers
15–40% of carriers → cirrhosis
LFTs and viral markers confirm diagnosis
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HBV antigens of virus particle
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HBsAg = surface antigens—a marker of viral replication and infection
HBcAg = inner core antigens—a marker of exposure rather than vaccination
HBeAg = a soluble protein from pre-core and core → high-level infection and infectivity
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Antibodies develop to each of these (see Fig. H10).
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HBsAg = acute/persistent infection (the main investigation for HBV)
Anti-HBs = past infection and immunity
HBeAg = highly infective
HBV DNA = circulating and replicating virus
Anti-HBc IgM = recent infection and earliest indicator
Anti-HBc IgG = past infection
Anti-HBe = seroconversion
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Serological patterns
HBsAg+ve + anti-HBc IgM+ve + anti-HBs−ve = acute hepatitis B
HBsAg+ve + anti-HBc IgG+ve + anti-HBs−ve = chronic hepatitis B
HBsAg−ve + anti-HBc IgG+ve + anti-HBs+ve = resolved hepatitis B
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Progress is monitored 6–12 mthly with HBeAg, HBV DNA and LFTs:
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