Evaluation of Antibodies to Hepatitis C Virus in a Long‐Term Prospective Study of Posttransfusion Hepatitis Among Thalassemic Children

Abstract

SummaryDuring an 8‐year prospective study of post‐transfusion hepatitis conducted at the Thalassemic Center of Cagliari (Italy), including 135 newly diagnosed thalassemic children on long‐term transfusion maintenance, 83 children (61%) developed non‐A, non‐B hepatitis (NANBH). Resolution of NANBH was observed in 17 (20%) cases, and chronicity in 57 (69%), whereas the remaining 9 (11%) experienced one or two additional bouts of acute NANBH. Of the 83 children with NANBH, 75 (90%) showed anti‐hepatitis C virus (HCV) seroconversion when tested by second‐generation enzyme‐linked immunosorbent assay (ELISA), whereas first‐generation ELISA showed anti‐HCV in only 59 (71%) cases (p = 0.003). Moreover, the newly developed assay allowed an earlier detection of anti‐HCV response in most of the patients who seroconverted by both assays, reducing significantly the mean onset‐seroconversion interval (5 ± 9.4 weeks vs. 14.5 ± 20.8 weeks, p < 0.05). It was significantly more sensitive for the identification of HCV infection, not only in resolving NANBH, but also in NANBH progressing to chronicity (79 vs. 35%, respectively, p = 0.008; and 93 vs. 79%, p = 0.028). The pattern of antibody response with first‐generation assay was characterized by clearance of anti‐HCV with time, in most of the patients who recovered, and by persistence of anti‐HCV in the majority of those who progressed to chronicity, whereas second‐generation ELISA usually showed persistence of anti‐HCV over time, regardless to the outcome of the disease. The pattern of anti‐HCV observed by first‐generation assay in children who experienced multiple episodes of acute NANBH was generally characterized by clearance of anti‐HCV after recovery, followed by reappearance and rise of the antibody titer concomitant with the new episode of acute hepatitis, whereas second‐generation assay revealed again the persistence of the antibody in most cases. This study shows that HCV is the major cause of NANBH among polytransfused thalassemics. Whether some posttransfusion NANBH without detectable anti‐HCV (10%) may be caused by viruses other than HCV remains to be clarified.