Q: How common is viral hepatitis?
A. It is estimated that Hepatitis A virus infection prevalence approaches 100 % by age of 5 years in developing countries. Hepatitis B accounts for 20 -25 % of all acute viral hepatitis in children . Hepatitis D coexists along with hepatitis B. Hepatitis C virus is usually seen in children with thalassemia, sickle cell disease, hemophilia and children undergoing hemodialysis. Hepatitis E is an important agent in sporadic and epidemic hepatitis in our country . Recently Hepatitis F and G viruses have also been identified.

Q: How does it spread ?
A. It spreads by person to person contact and feco-oral route. Parenteral transmission is rare.

Q: What are the clinical manifestations?
A. They may go unrecognised. Non-specific symptoms like nausea, vomiting, abdominal pain , leg pain , loss of appetite followed by clinical jaundice and tender hepatomegaly are seen in majority of patients.

Q: What is the clinical course?
A. The disease is self-limiting. Jaundice resolves in 2-3 weeks. Some children may have a cholestatic phase. Hepatitis A does not cause a carrier state or chronic liver disease.

Q: What are the danger signs?
A. Fever persisting in spite of jaundice, persistent vomiting, drowsiness and no recovery in appetite after 15 days.

Q: Are any laboratory tests necessary?
A. They may be necessary if there are any danger signs. Otherwise the diagnosis remains clinical and the treatment is not altered based on liver function tests. Elevated anti HAV IgM remains the gold standard serological test.

Q: What is the differential diagnosis?
A. Many other infectious diseases like typhoid, malaria especially falciparum, dengue, leptospirosis may present as jaundice but these don't have marked elevation in liver enzymes.

Q: Is there any specific treatment?
A. It is a self-limiting disease. No specific treatment is available. Bed rest and restricted protein and fat intake helps in early recovery.

Q: What about alternative medicines?
A. These are all anecdotal and based on hearsay evidence and not proven in medical literature.

Q: Is prevention possible?
A. Immune serum globulin 0.02 ml /kg intramuscular may be given to contacts and to travellers to endemic region. HAV vaccine is available but currently is an optional vaccine as per IAP recommendations as India is an endemic area. A practical approach would be to do anti HAV IgG titres by the time the child is 6 -7 years old and if found negative to give the vaccine. Vaccine is available as 2 doses to be given 6 months apart.

Q: What is the prevalence and natural history of Hepatitis B?
A. India falls into intermediate category of HBsAg prevalence with a carrier rate of 4.2 %. In < 10 years old, the infection is mostly silent however, the chances of becoming a chronic carrier is higher. If a newborn is infected, he rarely suffers but has 90 % chance of becoming a carrier. HbeAg positivity in the mother predisposes to neonatal HBV infection . 25 % of all HBsAg positive new-borns develop chronic liver disease by third to fourth decade of life.

Q: What is the mode of transmission?
A. Vertical transmission from mother to child, horizontal transmission from close contact in the family and parenteral and sexual transmission.

Q: What are the atypical features of Hepatitis B?
A. Skin and joint involvement leading to urticaria, purpura, maculo- papular rashes, arthralgia, polyarteritis, glomerulonephritis and aplastic anaemia.

Q: What are the laboratory diagnostic features?
A. HBsAg positive is seen with onset of symptoms and clears off from the serum after 6 - 12 months. If it persists then it is marker of chronic liver disease. IgM antiHBc is the most valuable serological marker of acute HBV infection and appears in serum several weeks after HBsAg and persist before anti HBsAg is detectable.

Q: What are the problems of chronic HBV infection?
A. Chronic HBV carriers have hundred fold increased risk of developing hepatocellular carcinoma .They also may develop chronic liver disease with cirrhosis and liver cell failure. Chronic liver disease in these patients can't be predicted.

Q: Is there any treatment for chronic HBV infection?
A. Alpha interferon and Lamivudine are two agents used currently but experience in children is limited.

Q: Can Hepatitis B be prevented?
A. Yes, IAP and WHO recommend universal immunisation with Hepatitis B vaccine which gives 95-98% protection. Currently the recombinant DNA vaccine is used universally in the dosage schedule of 0 , 1 and 6 months starting as early in life as possible . A booster is given after 10 years.

Hepatitis C behaves like hepatitis B and Hepatitis D is a defective virus requiring HBV infection for its propagation. Coinfection causes more severe acute disease and carries a higher risk of fulminant hepatitis .Hepatitis C vaccine is not currently available and Hepatitis D infection can be prevented by universal immunisation with Hepatitis B vaccine.

It is a major agent for enterically transmitted non A non B hepatitis. It is an acute self limiting disease resembling HAV infection but has greater morbidity and mortality in pregnant women. Anti HEV IgM is the serological marker.

It is a parenterally transmitted virus, which is closely associated with HCV infection but is unclear whether HGV can cause clinically significant disease.

Also See Pattern of infective hepatitis(viral)
Also See Pattern of anicteric hepatitis
Also See Biochemical profile in Hepatitis B vaccine

Last created on 23-02-2001
Last updated on 01-05-2007