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Chronic Hepatitis C Virus Infection After Treatment for Pediatric Malignancy
Simone Cesaro,
Maria Grazia Petris,
Flavio Rossetti,
Riccardo Cusinato,
Corrado Pipan,
Maria Guido,
Lucia Masiero,
Giuseppe A. Botta,
Giovanni A. Meloni, and
Luigi Zanesco
From the Division of Hemato/Oncology, the Department of Pediatrics, Università di Padova; the Servizio di Microbiologia, Azienda Ospedale di Padova; the Istituto di Microbiologia, Università di Udine; the Cattedra di Istochimica e Immunoistochimica Patologica, Università di Padova-ULSS 15, Ospedale di Cittadella, Italy.
Sera of 658 patients who had completed treatment for pediatric malignancy were analyzed by a second-generation enzyme-linked immunosorbent assay and recombinant immunoblot assay test to assess the prevalence of hepatitis C virus (HCV)-seropositivity. All HCV-seropositive patients underwent detailed clinical, laboratory, virologic, and histologic study to analyze the course of HCV infection. One hundred seventeen of the 658 patients (17.8%) were positive for HCV infection markers. Among the 117 anti-HCV+ patients, 41 (35%) were also positive for markers of hepatitis B virus infection with or without delta virus infection markers, 91 (77.8%) had previously received blood product transfusions, and 25 (21.4%) showed a normal alanine aminotransferase (ALT) level during the last 5-year follow-up (11 of them never had abnormal ALT levels). The remaining 92 patients showed ALT levels higher than the upper limit of normal range. Eighty-one of 117 (70%) anti-HCV+ patients were HCV-RNA+, with genotype 1b being present in most patients (54%). In univariate analysis, no risk factor for chronic liver disease was statistically significant. In this study, the prevalence of HCV infection was high in patients who were treated for a childhood malignancy. In about 20% of anti-HCV+ patients, routes other than blood transfusions are to be considered in the epidemiology of HCV infection. After a 14-year median follow-up, chronic liver disease of anti-HCV+ positive patients did not show progression to liver failure.
Blood, Vol. 90 No. 3 (August 1), 1997:
pp. 1315-1320
© 1997 by The American Society of Hematology.
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