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INTRODUCTION

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 image 326–8.

Diagnostic markers for acute hepatitis

  • Hepatitis A: IgM anti-HAV (Ab)

  • Hepatitis B: surface antigen (HBsAg)

  • Hepatitis C: anti-HCV (Ab)

  • IgM antibodies = recent infection

  • IgG antibodies = previous exposure

HEPATITIS A

Features

  • 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

Serology

  • IgM anti-HAV = active infection

  • IgG antibodies = immunity

Treatment

  • Rest as appropriate

  • Avoid sedatives, NSAIDs

  • Cease alcohol until LFTs normal

  • Cease OCP

  • Fat-free diet

  • Advise on infection control

Prevention

  • Sanitary health measures

  • 2 dose primary vaccine 0 → 6–12 mth

HEPATITIS B (HBV)

Features

  • 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

HBV antigens of virus particle

  • 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

Antibodies develop to each of these (see Fig. H10).

Figure H10

Time course of acute hepatitis B infection

Serology guidelines

  • 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

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

Interpretation

  • HBsAg = diagnosis and/or carrier

    • – if +ve do full viral profile

Progress is monitored 6–12 mthly with HBeAg, HBV DNA and LFTs:

  • HBsAg –ve + HBV DNA + anti-HBe = resolving

  • as above + anti-HBs = ...

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