Back to Search
Start Over
Liver disease in chelated transfusion-dependent thalassemics: the role of iron overload and chronic hepatitis C.
- Source :
-
Haematologica [Haematologica] 2008 Aug; Vol. 93 (8), pp. 1243-6. Date of Electronic Publication: 2008 Jun 12. - Publication Year :
- 2008
-
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.
- Subjects :
- Adolescent
Adult
Biopsy
Cohort Studies
Female
Hepacivirus genetics
Hepacivirus metabolism
Hepatitis C, Chronic pathology
Humans
Liver pathology
Liver Cirrhosis etiology
Liver Cirrhosis pathology
Liver Cirrhosis virology
Male
Retrospective Studies
Splenectomy
Thalassemia blood
Viral Load
Hepatitis C, Chronic complications
Iron Overload complications
Thalassemia etiology
Transfusion Reaction
Subjects
Details
- Language :
- English
- ISSN :
- 1592-8721
- Volume :
- 93
- Issue :
- 8
- Database :
- MEDLINE
- Journal :
- Haematologica
- Publication Type :
- Academic Journal
- Accession number :
- 18556410
- Full Text :
- https://doi.org/10.3324/haematol.12554