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

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

Risultato della ricerca: Article

39 Citazioni (Scopus)

Abstract

AbstractIron 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

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

In: Haematologica, Vol. 93, 2008, pag. 1243-1246.

Risultato della ricerca: Article

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title = "Liver disease in chelated transfusion-dependent thalassemics: the role of iron overload and chronic hepatitis C.",
abstract = "AbstractIron 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.",
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author = "Daniela Cabibi and Donatella Ferraro and Almasio, {Pier Luigi} and {Di Stefano}, Rosa and Antonio Craxi and {Di Marco}, Vito and Fabrizio Bronte and Francesco Gagliardotto and Ruffo, {Giovanni Battista} and Zelia Borsellino and Liana Cuccia and Marcello Capra",
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TY - JOUR

T1 - Liver disease in chelated transfusion-dependent thalassemics: the role of iron overload and chronic hepatitis C.

AU - Cabibi, Daniela

AU - Ferraro, Donatella

AU - Almasio, Pier Luigi

AU - Di Stefano, Rosa

AU - Craxi, Antonio

AU - Di Marco, Vito

AU - Bronte, Fabrizio

AU - Gagliardotto, Francesco

AU - Ruffo, Giovanni Battista

AU - Borsellino, Zelia

AU - Cuccia, Liana

AU - Capra, Marcello

PY - 2008

Y1 - 2008

N2 - AbstractIron 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 - AbstractIron 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 - HCV

KW - Iron

KW - thalassemics

UR - http://hdl.handle.net/10447/33713

M3 - Article

VL - 93

SP - 1243

EP - 1246

JO - Haematologica

JF - Haematologica

SN - 0390-6078

ER -