High viral load and mild liver injury in children with hemophilia comparedwith other children with chronic hepatitis C virus infection

Citation
A. Zellos et al., High viral load and mild liver injury in children with hemophilia comparedwith other children with chronic hepatitis C virus infection, J PED GASTR, 29(4), 1999, pp. 418-423
Citations number
37
Categorie Soggetti
Pediatrics,"Medical Research General Topics
Journal title
JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION
ISSN journal
02772116 → ACNP
Volume
29
Issue
4
Year of publication
1999
Pages
418 - 423
Database
ISI
SICI code
0277-2116(199910)29:4<418:HVLAML>2.0.ZU;2-3
Abstract
Background: In adults with hepatitis C virus (HCV) infection, the severity of liver disease may be influenced by the mode of transmission. The purpose of this study was to evaluate whether the mode of transmission affects liv er injury and viral load in children with chronic HCV infection, independen t of duration of infection and/or HCV genotype. Methods: Thirty-nine anti-HCV (EIA-2) positive patients, were divided into three groups: group 1, children with a history of blood transfusion (n = 9; age, 13.3 +/- 1.3 years), group 2, children with hemophilia (n = 19; age, 11.6 +/- 0.8 years); and group 3, children with maternal-fetal transmitted disease (n = 10; age, 4.7 +/- 1.1 years). Serum alanine aminotransferase, H CV viral load, HCV genotype, and liver histology were assessed. Results: Serum HCV viral load was higher in group 2 (4.27 +/- 1.0 x 10(6) c opies/ml; p = 0.006) than in group 1 (0.73 +/- 0.3 x 10(6) copies/ml) and i n group 3 (0.83 +/- 0.2 x 10(6) copies/ml). Conversely, group 2 had less se vere liver injury compared with children of similar age in group 1 (p = 0.0 22). Despite a shorter duration of infection, group 3 had liver injury simi lar to that in group 1. Hepatitis C virus genotype did not influence the le vel of viremia or liver injury. Conclusions: Although children with hemophilia exhibited a high HCV viral l oad, liver histopathology was less severe than in children who had acquired HCV by blood transfusion or maternal-fetal transmission. These observation s support the need to investigate the role of host immune response rather t han the virus per se in the pathogenesis of HCV infection in children.