Haematologica
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Haematologica, Vol 93, Issue 1, 111-115 doi:10.3324/haematol.11656
Copyright © 2008 by Ferrata Storti Foundation
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Red Cell Disorders

Anemia in β-thalassemia patients targets hepatic hepcidin transcript levels independently of iron metabolism genes controlling hepcidin expression

Emilie Camberlein1, Giuliana Zanninelli2, Lénaïck Détivaud1, Anna Rita Lizzi2, Francesco Sorrentino2, Stefania Vacquer4, Marie-Bérengère Troadec1, Emanuele Angelucci3, Emmanuelle Abgueguen1, Olivier Loréal1, Paolo Cianciulli2, Maria Eliana Lai4, Pierre Brissot1,

1 Inserm U-522, IFR 140, University Hospital Pontchaillou, Rennes, France
2 Ospedale San Eugenio, Day Hospital Talassemie, Rome, Italy
3 Ospedale Oncologico, Divisione di Ematologia, Cagliari, Italy
4 Ospedale Regionale per le Microcitemie, Centro Talassemici Adulti, Dipartimento Scienze Mediche, Università degli Studi di Cagliari, Italy

Correspondence: Pierre Brissot, Service des Maladies du Foie, Hôpital Pontchaillou 35033 Rennes Cedex, France. E-mail: pierre.brissot{at}univ-rennes1.fr

Thalassemia associates anemia and iron overload, two opposite stimuli regulating hepcidin gene expression. We characterized hepatic hepcidin expression in 10 thalassemia major and 13 thalassemia intermedia patients. Hepcidin mRNA levels were decreased in the thalassemia intermedia group which presented both lower hemoglobin and higher plasma soluble transferrin receptor levels. There was no relationship between hepcidin mRNA levels and those of genes controlling iron metabolism, including HFE, hemojuvelin, transferrin receptor-2 and ferroportin. These results underline the role of erythropoietic activity on hepcidin decrease in thalassemic patients and suggest that mRNA modulations of other studied genes do not have a significant impact.

Key words: anemia, β-thalassemia, hepcidin, gene expression, iron overload.






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