Abstract
| Lingua originale | English |
|---|---|
| pagine (da-a) | 1243-1246 |
| Numero di pagine | 4 |
| Rivista | Haematologica |
| Volume | 93 |
| Stato di pubblicazione | Published - 2008 |
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All Science Journal Classification (ASJC) codes
- Hematology
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TY - JOUR
T1 - Liver disease in chelated transfusion-dependent thalassemics: the role of iron overload and chronic hepatitis C.
AU - Di Stefano, Rosa
AU - Craxi, Antonio
AU - Almasio, Pier Luigi
AU - Ferraro, Donatella
AU - Di Marco, Vito
AU - Cabibi, Daniela
AU - Bronte, Fabrizio
PY - 2008
Y1 - 2008
N2 - 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.
AB - 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.
KW - Iron, HCV, thalassemics
UR - http://hdl.handle.net/10447/33713
M3 - Article
VL - 93
SP - 1243
EP - 1246
JO - Haematologica
JF - Haematologica
SN - 0390-6078
ER -