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Viral hepatitis

Common Less common Rare

• Hepatitis A • CMV • HSV

• Hepatitis B ± hepatitis D • EBV • Yellow fever
• Hepatitis C
• Hepatitis E

Clinical features of acute infection

 Non-specific prodromal illness: headache, myalgia, arthralgia, nausea and

anorexia: a few day to 2 weeks before jaundice.
 Vomiting and diarrhoea, abdominal discomfort.
 Dark urine and pale stools may precede jaundice.
 Tender minimally enlarged liver.
 Occasionally, mild splenomegaly and cervical LAP.
 Symptoms rarely last longer than 3–6 weeks.

Complications of acute viral hepatitis

 Acute liver failure

 Cholestatic hepatitis (hepatitis A)
 Aplastic anaemia
 Chronic liver disease and cirrhosis (hepatitis B and C)
 Relapsing hepatitis

Investigations
 A hepatitic pattern of LFTs.
 The plasma bilirubin reflects the degree of liver damage.
 The ALP rarely exceeds twice the upper limit of normal.
 Prolongation of the PT indicates the severity of the hepatitis.
 The WBC is usually normal with a relative lymphocytosis.
 Serological tests confirm the aetiology of the infection.

Management
 Most individuals do not need hospital care.
 Drugs such as sedatives and narcotics, which are metabolised in the liver,
should be avoided.
 No specific dietary modifications are needed.
 Alcohol should be avoided during the acute illness.
 Elective surgery should be avoided in cases of acute viral hepatitis, as there is a
risk of post-operative liver failure.

Incubation (wks)
•HAV 2–4 •HBV 4–20 •HCV 2–26 •HDV 6–9 •HEV 3–8
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Hepatitis A (RNA virus)

 Spread by faecal–oral route.
 Incubation (wks) 2–4.
 Infection is common in children but often asymptomatic.
 Up to 30% of adults: serological evidence of past infection + no history of
jaundice.
 Common in areas of overcrowding and poor sanitation.
 A chronic carrier state does not occur.

Investigations
 Anti-HAV AB is important in diagnosis, as HAV is only present in the blood
transiently during the incubation period.
 Anti-HAV of the IgM type: acute HAV infection.
 Anti-HAV of the IgG type: marker of previous HAV infection.

Prevention and Management

 Improving overcrowding and poor sanitation.

 Active immunisation. (In close contacts of HAV-infected patients, elderly, major
disease and pregnant women.)
 Immune serum globulin.
 Acute liver failure is rare in hepatitis A (0.1%) and chronic infection does not
occur.
 There is no role for antiviral drugs.

Hepatitis B (DNA virus)

 Humans are the only source of infection.
 Hepatitis B is one of the most common causes of CLD and HCC.
 Hepatitis B may cause an acute viral hepatitis and is often asymptomatic.
 Many individuals with chronic hepatitis B are also asymptomatic.
 Horizontal transmission (10%) : Injection drug use , Infected unscreened
blood products Tattoos/acupuncture needles , Sexual.
 Vertical transmission (90%): HBsAg-positive mother and carries the highest
risk of ongoing chronic infection.
Investigations
Serology
Hepatitis B surface antigen (HBsAg):
 Indicator of active infection, and a negative test for HBsAg makes HBV infection
very unlikely.
 The persistence of HBsAg for longer than 6 months indicates chronic infection.
 Anti-HBs : either previous infection( anti-HBc present ) , or previous
vaccination( anti-HBc is not present) .
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Hepatitis B core antigen (HBcAg):

 HBcAg is not found in the blood, but antibody to it (anti-HBc) appears early in
the illness and persists.
Hepatitis B e antigen (HBeAg): HBeAg is an indicator of viral replication.

Viral load and genotype

 HBV-DNA can be measured by PCR in the blood.
 Measurement of viral load is important in monitoring antiviral therapy.
 Specific HBV genotypes (A–H) can also be identified using PCR.

Management of acute hepatitis B

 Full recovery occurs in 90–95% of adults.

 5–10% develop a chronic HB infection.
 Vertical transmission leads to chronic infection in the child in 90% of cases and
recovery is rare.
Management of chronic hepatitis B
 The indication for treatment is a high viral load in the presence of active
hepatitis, as demonstrated by elevated serum transaminases and/or
histological evidence of inflammation and fibrosis.
 Cirrhosis develops in 15–20% of patients with chronic HBV over 5–20 years.
Direct-acting nucleoside/nucleotide antiviral agents
 These act by inhibiting the reverse transcription of pre-genomic RNA to HBV-
DNA by HBV-DNA polymerase
 Lamivudine, Telbivudine, Adefovir.
 Entecavir and tenofovir: is more effective than lamivudine or adefovir in
reducing viral load.

Interferon-alfa
 It acts by augmenting a native immune response.
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 Interferon is contraindicated in the presence of cirrhosis.

 Longer-acting pegylated interferons that can be given once weekly.
 Side-effects are common and include fatigue, depression, irritability, bone
marrow suppression and the triggering of autoimmune thyroid disease.
Liver transplantation
Now it is an acceptable treatment option due to post-liver transplant prophylaxis
with direct-acting antiviral agents and hepatitis B Ig.

Prevention
 A recombinant hepatitis B vaccine containing HBsAg is available (Engerix) and
is capable of producing active immunisation in 95% of normal individuals.
 IM injection of hyperimmune serum globulin.
 Neonates born to hepatitis B-infected mothers should be immunised at birth and
given immunoglobulin.

Hepatitis D (Delta virus) (RNA defective virus)

 It requires HBV for replication and has the same sources and modes of spread.

Investigations
 (anti-HDV)

Management
 Effective management of hepatitis B prevents hepatitis D.

Hepatitis C (RNA virus)

 Acute symptomatic infection with hepatitis C is rare.
 80 % of individuals exposed to the virus become chronically infected.
 Risk factors :
o IV drug misuse (95% of new cases in the UK)
o Unscreened blood products
o Vertical transmission (3% risk)
o Needle stick injury (3% risk)
o Iatrogenic parenteral transmission (i.e. contaminated vaccination
needles)
o Sharing toothbrushes/razors.

Investigations

Serology and virology

 Active infection: serum hepatitis C RNA in anyone who is antibody-positive.

 Anti-HCV antibodies persist in serum even after viral clearance, whether
spontaneous or post-treatment.
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Molecular analysis
 There are six common viral genotypes.
 Genotype affect response to treatment.

Liver function tests

 LFTs may be normal or show fluctuating serum transaminases.

 Jaundice is rare and only usually appears in end-stage cirrhosis.

Liver histology
 Liver biopsy is often required to stage the degree of liver damage.

Management
 Triple therapy :
o Pegylated interferon.
 Side-effects : flu-like symptoms, irritability and depression
o Telaprevir / boceprevir ( protease inhibitors )
o Ribavirin (synthetic nucleotide analogue )
 Side-effects: haemolytic anaemia and teratogenicity.

Liver transplantation
 If complications of cirrhosis occur, such as diuretic resistant ascites.
 Unfortunately, hepatitis C almost always recurs in the transplanted liver and up
to 15% of patients will develop cirrhosis in the liver graft within 5 years of
transplantation.

Prevention and prognosis

 There is no active or passive protection against HCV.
 Progression from chronic hepatitis to cirrhosis occurs over 20–40 years in 20%.
 Risk factors for progression: male, immunosuppression, prothrombotic states
and heavy alcohol misuse.
 Once cirrhosis is present, 2–5% per year will develop primary HCC.

Hepatitis E (RNA virus)

 The clinical presentation and management of hepatitis E are similar to that of
hepatitis A.
 Hepatitis E differs from hepatitis A in that infection during pregnancy is
associated with the development of acute liver failure.
 In acute infection, IgM antibodies to HEV are positive.

Other forms of viral hepatitis

 Non-A, non-B, non-C (NANBNC) or non-A–E hepatitis.
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 CMV, EBV, HSV, chicken pox, measles, rubella and acute HIV infection.