A multicenter prospective study on the risk of acquiring liver disease in anti-hepatitis C virus negative patients affected from homozygous β- thalassemia

Daniele Prati, Alberto Zanella, Elena Farma, Claudia De Mattei, Patrizia Bosoni, Manuela Zappa, Alessandra Picone, Fulvio Mozzi, Paolo Rebulla, Maria Domenica Cappellini, Jean Pierre Allain, Girolamo Sirchia

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Abstract

Although the risk of transfusion-transmitted hepatitis has been recently reduced, transfusion-dependent β-thalassemia patients may still develop liver disease due to viral infection or iron overload. We assessed the frequency and causes of liver dysfunction in a cohort of anti-hepatitis C virus (HCV) negative thalassemics. Of 1,481 thalassemics enrolled in 31 centers, 219 (14.8%) tested anti-HCV- by second-generation essays; 181 completed a 3-year follow-up program consisting of alanine-aminotransferase (ALT) measurement at each transfusion and anti-HCV determination by third- generation enzyme-immunoassay (EIA-3) at the end of study. Serum ferritin levels were determined at baseline and at the end of follow-up. Ten patients were anti-HCV+ by EIA-3 at the end of follow-up. Of them, seven were already positive in 1992 to 1993 when the initial sera were retested by EIA-3, one tested indeterminate by confirmatory assay, and two had true seroconversion (incidence, 4.27/1,000 person years; risk of infection, 1/7,100 blood units, 95% confidence interval [CI], 1 in 2,000-1 in 71,000 units). At baseline, 67 of 174 thalassemics had abnormal ALT. Of those with normal ALT, seven subsequently developed at least one episode of moderate ALT increase (incidence, 24.6/1,000 person-years). All of the 20 patients with ferritin values ≥3,000 ng/mL had clinically relevant ALT abnormalities, as compared with 53 of 151 with

Original languageEnglish
Pages (from-to)3460-3464
Number of pages5
JournalBlood
Volume92
Issue number9
Publication statusPublished - Nov 1 1998

ASJC Scopus subject areas

  • Hematology

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