Hepatitis

13/05/2013 by admin | Gastroenterology

Viral Hepatitis

Hep A virus (HAV):

    1. o Common cause of transient hep, no long term carriage, often occurs in epidemics
    2. o Faeco-oral transmission
    3. o After 5/52 infection = IgM peaks and IgG continues to rise
    4. o 50% are subclinical (=have IgG to HAV without jaundice)
    5. o Jaundice: most common presentation in an acute hep. May have a prolonged cholestatic phase, with fatigue, malaise, anorexia, and nausea
  1. Ix:
    1. o LFTs: often shows an acute hepatocellular abnormality = very high AST, with mildly raised bilirubin and alk phos
    2. o HAV IgM serology: in high titre is diagnostic of acute infection
  2. Mx:
    1. o Usually settles with symptomatic mx and rarely requires hospital admission
    2. o Evidence of liver failure (=encephalopathy/coagulopathy): refer to transplant centre
    3. o N.B Hep E gives a similar clinical picture, although Hep E has a high risk of fulminant hepatic failure in pregnancy. Fulminant hepatic failure can also be caused by CMV, EBV, herpes simplex and zoster.

 

Hep B (HBV):

    1. o HBV most common cause of chronic liver disease and hepatoma
    2. o In UK seen amongst IVDUs and homosexuals (and in neonatal-maternal transmission)
    3. o It is a parenterally transmitted (crosses skin barrier) hepatotrophic DNA virus
  1. Clinical features:
    1. o Acute hep: with jaundice seen in 15% of HBV infected
    2. o Fulminant liver failure: rare in HBV – more likely if con-infected with HCV/HIV or the ‘delta’ agent
    3. o Chronic liver disease: 5% of adults exposed to HBV develop chronic infection (especially if immunocompromised, Down’s syndrome and in neonates).
    4. o Hepatocellular carcinoma (HCC): rates increased x10 in HBV carriers
  2. Ix:
    1. o LFTs: non-specific hepatic picture
    2. o HBV serology:
    3. o HBsAg = marker of on-going infection
    4. o HBeAg = marker of active viral replication
    5. o Anti-HBs and HBc = marker of previous infection
    6. o Anti-HBs alone = vaccine induced immunity
    7. o Other tests: liver USS (assess biliary tree or presence of structural abnormality), biopsy (if a prominent cholestatic phase)
  3. Mx:
    1. o Prevention = those at risk should be immunised. Carriers should know the risk to others and use barrier contraception
    2. o General = follow up tests should be completed to ensure virus has been cleared
    3. o Anti-viral therapy = no useful antiviral during acute flare, although Lamivudine is helpful in fulminant liver failure. If immunocompromised and persistent (>6/12) infection with high transaminases = IFN
    4.  
  1. o Screening for HCC: regular liver USS and AFP measurements to rule out cancer
  2. o Liver transplantation = indicated for decompensated cirrhosis and small unifocal hepatoma. Viral recurrence post-transplantation reduced by lamivudine prophylaxis.

 

Hep C (HCV):

    1. o Common cause of chronic liver disease and transplantation in the developed world
    2. o The RNA HCV is transmitted parenterally. It relies on reverse transcriptase for replication (which has an inherently high error rate) = high rates of viral mutation. Result HCV commonly escapes immune response and chronicity of viraemia is the consequence.
  1. Clinical features:
    1. o Acute hep: only occurs in a small number of patients
    2. o Asymptomatic carriage: most are not aware they are carriers. However 90% that are exposed will develop viraemia
    3. o Chronic liver disease: 20% of patients with viraemia develop liver fibrosis and clinical chronic liver disease. clinical course is accelerated by excess alcohol consumption
  2. Ix:
    1. o LFTs: modest elevation in transaminases. The degree of blood test derangement does not reflect degree of underlying fibrosis
    2. o HCV tests: serological antibody tests. Virus is identified by PCR and levels of viraemia can be quantified. Virus genotyping has prognostic value
    3. o Liver biopsy: only way to grade disease in terms of necro-inflammatory changes and degree of fibrosis
  3. Mx:
    1. o Prevention = public health measures and education. No vaccine exists.
    2. o Anti-viral therapy = INF-alpha for 12/12 (=30% will have long-term viral clearance). Greater success if combination therapy (IFN and ribavirin)
    3. o Liver transplantation = only option in end-stage chronic liver disease. Viral recurrence in transplanted organ is common.

 

Autoimmune hepatitis:

    1. o Rare
    2. o Acute autoimmune inflammation centred predominantly on the hepatic lobule causing a range of clinical manifestations (fulminant hepatic failurechronic liver disease with cirrhosis)
  1. p/c: acute, young female, jaundice, fatigue, arthralgia, associated a/i conditions, may have abnormal LFTs (=predominant hepatocellular derangement and high titre of antinuclear antibodies and smooth muscle [antiactin] antibodies). Autoantibodies may be demonstrable (microsomal antibody LKM-1, soluble liver antigen [SLA]). IgG is usually high.
  2. Autoimmune Hep Type 1 = anti-nuclear smooth muscle +ve
  3. Autoimmune Hep Type 2 = anti-liver, kidney, muscle (LKM-1) and Anti-soluble liver antigen (SLA) +ve
  4. Viral serology: must be tested due to acute presentation. HCV must be excluded
  5. Liver biopsy: shows acute lobular inflammation with interface hepatitis
  6. Mx:
    1. o Immunosuppression: high dose steroids, or longer term control with azathioprine
    2. o Liver transplantation: for fulminant liver failure and decompensated chronic liver disease 
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