Erythropoiesis‐driven regulation of hepcidin in human red cell disorders is better reflected through concentrations of soluble transferrin receptor rather than growth differentiation factor 15

Growth differentiation factor 15 (GDF‐15) is a bone marrow‐derived cytokine whose ability to suppress iron regulator hepcidin in vitro and increased concentrations found in patients with ineffective erythropoiesis (IE) suggest that hepcidin deficiency mediated by GDF‐15 may be the pathophysiological...

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Published in:American journal of hematology 2014-04, Vol.89 (4), p.385-390
Main Authors: Fertrin, Kleber Yotsumoto, Lanaro, Carolina, Franco‐Penteado, Carla Fernanda, Albuquerque, Dulcinéia Martins, Mello, Mariana Rezende Bandeira, Pallis, Flávia Rubia, Bezerra, Marcos André Cavalcanti, Hatzlhofer, Betania Lucena Domingues, Olbina, Gordana, Olalla Saad, Sara Terezinha, Silva Araújo, Aderson, Westerman, Mark, Costa, Fernando Ferreira
Format: Article
Language:English
Subjects:
Anemia, Iron-Deficiency - blood
Case-Control Studies
Erythrocytes - metabolism
Erythropoiesis
Female
Growth Differentiation Factor 15 - blood
Hematologic Diseases - blood
Hematology
Hepcidins - blood
Humans
Iron - blood
Iron - deficiency
Iron - metabolism
Iron Overload - blood
Male
Receptors, Transferrin - blood
Transferrin - metabolism
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Summary:Growth differentiation factor 15 (GDF‐15) is a bone marrow‐derived cytokine whose ability to suppress iron regulator hepcidin in vitro and increased concentrations found in patients with ineffective erythropoiesis (IE) suggest that hepcidin deficiency mediated by GDF‐15 may be the pathophysiological explanation for nontransfusional iron overload. We aimed to compare GDF‐15 production in anemic states with different types of erythropoietic dysfunction. Complete blood counts, biochemical markers of iron status, plasma hepcidin, GDF‐15, and known hepcidin regulators [interleukin‐6 and erythropoietin (EPO)] were measured in 87 patients with red cell disorders comprising IE and hemolytic states: thalassemia, sickle cell anemia, and cobalamin deficiency. Healthy volunteers were also evaluated for comparison. Neither overall increased EPO, nor variable GDF‐15 concentrations correlated with circulating hepcidin concentrations (P = 0.265 and P = 0.872). Relative hepcidin deficiency was found in disorders presenting with concurrent elevation of GDF‐15 and soluble transferrin receptor (sTfR), a biomarker of erythropoiesis, and sTfR had the strongest correlation with hepcidin (rS = −0.584, P 
ISSN:0361-8609
1096-8652
DOI:10.1002/ajh.23649