Nk. Arora et al., ACUTE VIRAL-HEPATITIS TYPE-E, TYPE-A, AND TYPE-B SINGLY AND IN COMBINATION IN ACUTE LIVER-FAILURE IN CHILDREN IN NORTH-INDIA, Journal of medical virology, 48(3), 1996, pp. 215-221
The aetiological agents responsible for, and the outcome of, acute liv
er failure were investigated prospectively in 44 children (29 males, 1
5 females) attending a tertiary health care facility in India. The chi
ldren were between the ages of 2 months and 13 years. Studies for vira
l infections and other etiologies could be carried out in 40 patients.
Specific aetiological labels were possible in 35 (87.5%) patients. Th
irty (75%) had evidence of acute viral hepatitis. Acute hepatitis E vi
rus (HEV) infection was found in a total of 18 children, with hepatiti
s A (HAV) in 16, hepatitis B in 5, and C in 1. Seven had isolated infe
ction with hepatitis E, five with A, and four with B. Nine had both E
and A infection. Superinfection of HEV was observed in a child with In
dian childhood cirrhosis (ICC). Acute HEV infection was confirmed by i
mmunoblot assay in all the patients and in eight of these, HEV-RNA was
also detected in the serum. HAV was involved in 37.5% of cases with i
solated infection in 10% (4 of 40). The aetiological factors associate
d with acute liver failure, apart from HAV and HEV, were other hepatot
ropic viruses (22.5%), Wilson's disease (5%), ICC (5%), and hepatotoxi
c drugs (7.5%). In five patients, no serological evidence of acute vir
al hepatitis could be found, neither did the metabolic screen yield an
y result. It was observed that enterically transmitted hepatitis virus
es (HAV and HEV) were associated with 60% of acute hepatic failure in
children. Mixed infection of HAV and HEV formed the single largest aet
iological subgroup. In developing countries, where hepatitis A and E i
nfections are endemic, severe complications can arise in the case of m
ixed infection. This may contribute to most of the mortality from acut
e liver failure during childhood. (C) 1996 Wiley-Liss, Inc.