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

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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.
Lingua originaleEnglish
pagine (da-a)1243-1246
Numero di pagine4
RivistaHaematologica
Volume93
Stato di pubblicazionePublished - 2008

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Iron Overload
Chronic Hepatitis C
Hepacivirus
Liver Cirrhosis
Liver Diseases
Hepatitis Viruses
RNA
Virus Diseases
Liver
Fibrosis
Iron
Chelation Therapy
Ferritins
Serum
Genotype
Biopsy
Weights and Measures

All Science Journal Classification (ASJC) codes

  • Hematology

Cita questo

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title = "Liver disease in chelated transfusion-dependent thalassemics: the role of iron overload and chronic hepatitis C.",
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.",
keywords = "Iron, HCV, thalassemics",
author = "{Di Stefano}, Rosa and Antonio Craxi and Almasio, {Pier Luigi} and Donatella Ferraro and {Di Marco}, Vito and Daniela Cabibi and Fabrizio Bronte",
year = "2008",
language = "English",
volume = "93",
pages = "1243--1246",
journal = "Haematologica",
issn = "0390-6078",
publisher = "Ferrata Storti Foundation",

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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 -