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

Fabrizio Bronte, Pier Luigi Almasio, Donatella Ferraro, Antonio Craxi, Vito Di Marco, Daniela Cabibi, Francesco Gagliardotto, Giovanni Battista Ruffo, Zelia Borsellino, Liana Cuccia, Marcello Capra, Francesco Barbaria, Massimo Capra

Risultato della ricerca: Article

36 Citazioni (Scopus)

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. ©2008 Ferrata Storti Foundation.
Lingua originaleEnglish
pagine (da-a)125-128
Numero di pagine4
RivistaDefault journal
Volume93
Stato di pubblicazionePublished - 2008

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

All Science Journal Classification (ASJC) codes

  • Hematology

Cita questo

Liver disease in chelated transfusion-dependent thalassemics: the role of iron and chronic hepatitis C. / Bronte, Fabrizio; Almasio, Pier Luigi; Ferraro, Donatella; Craxi, Antonio; Di Marco, Vito; Cabibi, Daniela; Gagliardotto, Francesco; Ruffo, Giovanni Battista; Borsellino, Zelia; Cuccia, Liana; Capra, Marcello; Barbaria, Francesco; Capra, Massimo.

In: Default journal, Vol. 93, 2008, pag. 125-128.

Risultato della ricerca: Article

Bronte, F, Almasio, PL, Ferraro, D, Craxi, A, Di Marco, V, Cabibi, D, Gagliardotto, F, Ruffo, GB, Borsellino, Z, Cuccia, L, Capra, M, Barbaria, F & Capra, M 2008, 'Liver disease in chelated transfusion-dependent thalassemics: the role of iron and chronic hepatitis C', Default journal, vol. 93, pagg. 125-128.
Bronte, Fabrizio ; Almasio, Pier Luigi ; Ferraro, Donatella ; Craxi, Antonio ; Di Marco, Vito ; Cabibi, Daniela ; Gagliardotto, Francesco ; Ruffo, Giovanni Battista ; Borsellino, Zelia ; Cuccia, Liana ; Capra, Marcello ; Barbaria, Francesco ; Capra, Massimo. / Liver disease in chelated transfusion-dependent thalassemics: the role of iron and chronic hepatitis C. In: Default journal. 2008 ; Vol. 93. pagg. 125-128.
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title = "Liver disease in chelated transfusion-dependent thalassemics: the role of iron and chronic hepatitis C",
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. {\circledC}2008 Ferrata Storti Foundation.",
author = "Fabrizio Bronte and Almasio, {Pier Luigi} and Donatella Ferraro and Antonio Craxi and {Di Marco}, Vito and Daniela Cabibi and Francesco Gagliardotto and Ruffo, {Giovanni Battista} and Zelia Borsellino and Liana Cuccia and Marcello Capra and Francesco Barbaria and Massimo Capra",
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T1 - Liver disease in chelated transfusion-dependent thalassemics: the role of iron and chronic hepatitis C

AU - Bronte, Fabrizio

AU - Almasio, Pier Luigi

AU - Ferraro, Donatella

AU - Craxi, Antonio

AU - Di Marco, Vito

AU - Cabibi, Daniela

AU - Gagliardotto, Francesco

AU - Ruffo, Giovanni Battista

AU - Borsellino, Zelia

AU - Cuccia, Liana

AU - Capra, Marcello

AU - Barbaria, Francesco

AU - Capra, Massimo

PY - 2008

Y1 - 2008

N2 - 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. ©2008 Ferrata Storti Foundation.

AB - 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. ©2008 Ferrata Storti Foundation.

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