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Increased serum hepcidin levels during treatment with deferasirox in iron‐overloaded patients with myelodysplastic syndrome
Author(s) -
Ghoti Hussam,
Fibach Eitan,
Westerman Mark,
Gordana Olbina,
Ganz Tomas,
Rachmilewitz Eliezer A.
Publication year - 2011
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2011.08587.x
Subject(s) - deferasirox , hepcidin , medicine , myelodysplastic syndromes , oxidative stress , deferiprone , anemia , endocrinology , gastroenterology , deferoxamine , thalassemia , bone marrow
Summary Hepcidin is a major regulator of iron metabolism. We evaluated changes in serum hepcidin during 3 months of therapy with the iron‐chelator deferasirox in patients with low‐risk myelodysplastic syndrome and iron overload. Serum hepcidin was found to be high in these patients, correlated with their iron and oxidative status, and further increased by treatment with deferasirox. These findings support the concept that the hepcidin level represents a balance between the stimulating effect of iron overload and the inhibitory effects of erythropoietic activity and oxidative stress. These preliminary findings favour the rationale for iron chelation therapy in such patients.