High Viral Load and Mild Liver Injury in Children with Hemophilia Compared with Other Children with Chronic Hepatitis C Virus Infection

Author:

Zellos Aglaia1,Thomas David L.2,Mocilnikar Cathleen1,Perlman Elizabeth J.3,Boitnott John K.3,Casella James F.1,Schwarz Kathleen B.1

Affiliation:

1. Department of Pediatrics Baltimore Maryland U.S.A.

2. Department of Medicine Baltimore Maryland U.S.A.

3. Department of Pathology Johns Hopkins University School of Medicine Baltimore Maryland U.S.A.

Abstract

ABSTRACTBackground: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 liver injury and viral load in children with chronic HCV infection, independent 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, HCV viral load, HCV genotype, and liver histology were assessed.Results:Serum HCV viral load was higher in group 2 (4.27 ± 1.0 × 106 copies/ml; p = 0.006) than in group 1 (0.73 ± 0.3 × 106 copies/ml) and in group 3 (0.83 ± 0.2 × 106 copies/ml). Conversely, group 2 had less severe liver injury compared with children of similar age in group 1 (p = 0.022). Despite a shorter duration of infection, group 3 had liver injury similar to that in group 1. Hepatitis C virus genotype did not influence the level of viremia or liver injury.Conclusions:Although children with hemophilia exhibited a high HCV viral load, liver histopathology was less severe than in children who had acquired HCV by blood transfusion or maternal‐fetal transmission. These observations support the need to investigate the role of host immune response rather than the virus per se in the pathogenesis of HCV infection in children.

Funder

National Institutes of Health

Publisher

Wiley

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