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

¹ Unità Complessa di Gastroenterologia ed Epatologia, Dipartimento Biomedico di Medicina Interna e Specialistica (Di.Bi.MI.S.), University of Palermo
² Unità Complessa Ematologia-Emoglobinopatie, Ospedale Pediatrico "G. Di Cristina", ARNAS Civico, Palermo
³ Servizio di Istologia Patologica, University of Palermo
⁴ Servizio di Virologia, University of Palermo, Italy

Correspondence: Vito Di Marco, Cattedra di Gastroenterologia, Dipartimento Biomedico di Medicina Interna e Specialistica, (DiBiMIS), University of Palermo, Piazza delle Cliniche 2, 90127 Palermo, Italy. E-mail:vito.dimarco{at}tin.it

ABSTRACT

Iron overload and HCV 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 HCV-RNA positive and 68 HCV-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 HCV-RNA positivity (OR 11.04) were independent risk factors for advanced liver fibrosis. The majority of HCV-RNA negative patients with low iron load did not develop liver fibrosis, while HCV-RNA positive patients infected with genotype 1 or 4 and iron overload more frequently developed advanced fibrosis. HCV 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 HCV-infection and reduces the risk of developing severe fibrosis in thalassemics with chronic hepatitis C.

Key words: thalassemia, liver iron concentration, ferritin, LIC, hepatitis C virus, serum HCV RNA, liver fibrosis, cirrhosis.

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