Liver disease in chelated transfusion-dependent thalassemics: the role of iron overload and chronic hepatitis C.
- Authors: DI MARCO, V; CAPRA, M; GAGLIARDOTTO, F; BORSELLINO, Z; CABIBI, D; BARBARIA, F; FERRARO, D; CUCCIA, L; RUFFO, GB; BRONTE, F; DI STEFANO, R; ALMASIO, PL; CRAXI', A
- Publication year: 2008
- Type: Articolo in rivista (Articolo in rivista)
- Key words: Iron, HCV, thalassemics
- OA Link: http://hdl.handle.net/10447/33713
Abstract
Abstract Iron 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.