Liver disease in chelated transfusion-dependent thalassemics: the role of iron overload and chronic hepatitis C.

Antonio Craxi, Vito Di Marco, Fabrizio Bronte, Donatella Ferraro, Rosa Di Stefano, Pier Luigi Almasio, Daniela Cabibi, Francesco Gagliardotto, Giovanni Battista Ruffo, Giovanni Battista Ruffo, Zelia Borsellino, Liana Cuccia, Marcello Capra

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41 Citations (Scopus)

Abstract

AbstractIron overload and hepatitis virus C infection cause liver fibrosis in thalassemics. In a monocentric retrospective analysis of liver disease in a cohort of 191 transfusion-dependent thalassemics, in 126 patients who had undergone liver biopsy (mean age 17.2 years; 58 hepatitis virus C-RNA positive and 68 hepatitis virus C-RNA negative) the liver iron concentration (median 2.4 mg/gr dry liver weight) was closely related to serum ferritin levels (R = 0.58; p<0.0001). Male gender (OR 4.12) and serum hepatitis virus C-RNA positivity (OR 11.04) were independent risk factors for advanced liver fibrosis. The majority of hepatitis virus C-RNA negative patients with low iron load did not develop liver fibrosis, while hepatitis virus C-RNA positive patients infected with genotype 1 or 4 and iron overload more frequently developed advanced fibrosis. Hepatitis virus C infection is the main risk factor for liver fibrosis in transfusion-dependent thalassemics. Adequate chelation therapy usually prevents the development of liver fibrosis in thalassemics free of hepatitis virus C-infection and reduces the risk of developing severe fibrosis in thalassemics with chronic hepatitis C.
Original languageEnglish
Pages (from-to)1243-1246
Number of pages4
JournalHaematologica
Volume93
Publication statusPublished - 2008

All Science Journal Classification (ASJC) codes

  • Hematology

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