I read with interest the recent study on this subject(1). In this connection I seek the following clarifications:

1. In this study, Hepatitis A virus (HAV) alone or in combination was implicated in 50% cases. Generally it has been mentioned that children almost always recover from HAV infection(2) and mortality is exceedingly rare in HAV infection(3). Another interesting observation in the study(1) was isolation of Hepatitis B virus (HBV) markers in only 5 out of 36 cases and none of these 5 cases were associated with Hepatitis delta virus (HDV) marker. Standard text book teaching is that HBV has the greatest potential to cause FHF and death than with other Hepatitis viruses, parti-cularly when co-infected by HDV.

Can the discrepancy between study and text book statements be explained solely on changing epidemiology in a particular area? Can Hepatitis B vaccination (being promoted actively) account for this radical change in viral etiology of fulminant hepatic failure?

2. In the study(1), viral hepatitis caused 50% deaths but contribution of individual viruses was not defined. Further, amongst HAV infected children it is not clear now many of them were belonging to upper socio-economic status. Likewise age related positivity of HAV markers in FHF needs elaboration because results depicted the age range of 1.5 years to 9 years. However, it is stated that 85% HAV infections in children up to 5 years are mostly asymptomatic(4).

Exploration of these facts is essential in view of the current recommendation that HAV vaccine shouldn’t be actively promoted in any community(5) and the most efficient approach is to offer HAV vaccine to children above 5 years after screening for antibodies against HAV(5) in families who can afford the vaccine.

1. Bendre SV, Bavdekar AR, Bhave SA, Pandit AN, Chitamber SD, Arankalle VA. Fulminant hepatic failure: Etiology, viral markers and outcome. Indian Pediatr 1999; 36: 1107-1112.

2. Synder JD, Pickering LK. Hepatitis A through E. In: Nelson Text Book of Pediatrics, Vol. 1, 15th edn. Eds. Behrman RE, Kleigmen, Arvin. Banglore, Prism Books Pvt. Ltd, 1996; pp 910-912.

3. John TJ. Hepatitis A vaccine. Indian Pediatr 1995; 32: 1249-1251.

4. Mathur P, Arora NK. Considerations for HAV vaccine in India. Indian J Pediatr 1999; 66: 111-120.

5. IAP Guidelines on optional vaccines and related matters. Indian Pediatr 1999; 36: 677-679.

 

1. An important finding of our study is documentation of association of HAV infection with Fulminant Hepatic Failure (FHF) in a significant proportion of children from Pune thereby imprssing upon the need for testing such patients for evidence of acute HAV infection. Though as compared to the total number of HAV infections, the proportion of FHF cases may be small, the data does indicate the importance of HAV in causing fatal disease in children. HBV and HDV have been associated with FHF. However, proportions of these infections can vary depending upon the extent of circulation of these viruses in a given population and the operating transmission mechanisms. As far as Pune is concerned, even in adults HDV does not play a significant role in causing FHF(1). HEV represents the major cause of sporadic acute viral hepatitis (AVH) as well as FHF in adults(2).

The text book information is generally based on the studies conducted in the developed countries. It is a well known fact that the epidemiology of different hepatitis viruses varies in different geographic areas of the world as well as in different parts of a country. This is especially true for a vast country like India with divergent geographic and socio-economic factors. The discrepancy between the text book and the present study cannot be explained on the basis of changing epidemiology of HAV alone. The change is expected to reflect clinical hepatitis A leading to severe course of the disease among adults belonging to higher socio-economic status (already being observed) and not FHF in children as noted in the present study.

History of Hepatitis B vaccination was not elicited in these children.It is not likely that most children were immunized with HB vaccine and therefore lower HBV etiology may not be related to the use of vaccine. With greater coverage of hepatitis B vaccine, it is expected that the incidence of HBV infection will be reduced with concomitant reduction in the number of AVH and FHF cases as well as the carrier pool. However, unless data from the same community is available before and after the introduction of mass vaccination, such conclusions cannot be drawn.

2. In our study, 7 of the FHF deaths (50%) were due to AVH. Of these 7, four had HAV, one each had HBV, HAV+HBV and HAV+HEV infection. Most of our study children belonged to middle socio-economic status as our hospital mainly caters to this society. It is a fact that almost 90% of HAV infections among children remain asympto-matic(3). However, approximately 10% do present with clinical disease. In fact, 70-80% of sporadic AVH in Indian children has been shown to be due to HAV(2).

As far as hepatitis A vaccine is concerned, it is absolutely correct not to recommend the same for all children. Our data (manuscript under preparation) reviewing HAV serology in Pune children over almost two decades has clearly shown that whereas the situation has remained unchanged in children belonging to lower socio-economic status (very high exposure rate), a significantly higher proportion of children belonging to higher socio-economic status do not get exposed to HAV. It is therefore likely that such individuals when exposed to HAV at a later age can develop severe course of the disease. Vaccine can and should be recommended for higher socio-economic children who fortunately can afford the same. Theoretically, pre-vaccination screening for anti-HAV antibodies is desirable. However, the test is expensive and not easily available. Currently, most Indian mothers are likely to be anti-HAV positive, and hence the vaccine should not be given at birth as recommended in other countries, but may be offered at the age of nine months(4).

Sheila Bhave,
Department of Pediatrics,
K.E.M. Hospital, Pune 411 011, Indiaand *Hepatitis Department,
National Institute of Virology, Pune, India.

1. Arankalle VA, Tsarev SA, Chadha MS, Alling DW, Emerson SU, Banerjee K, et al. Age-specified prevalence of antibodies to hepatitis A and E viruses in Pune, India, 1982 and 1992. J Infect Dis 1995; 171: 447-450.

2. Chadha MS, Chitambar SD, Shaikh NJ, Arankalle VA. Exposure of Indian children to hepatitis A virus and vaccination age. Indian J Med Res 1999; 109: 11-15.

3. Arankalle VA, Jha J, Favorov MO, Chaudhari A, Fields HA, Banerjee K. Contribution of HEV and HCV in causing fulminant non-A, non-B hepatitis in western India. J Viral Hepat 1995; 2: 189-193.

4. Arankalle VA, Chobe LP, Jha J, Chadha MS, Banerjee K, Favorov MO, et al. Etiology of acute sporadic non-A, non-B viral hepatitis in India. J Med Virol 1993; 40: 121-125.