Title |
Mechanisms of plasma non‐transferrin bound iron generation: insights from comparing transfused diamond blackfan anaemia with sickle cell and thalassaemia patients
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Published in |
British Journal of Haematology, September 2014
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DOI | 10.1111/bjh.13081 |
Pubmed ID | |
Authors |
John B. Porter, Patrick B. Walter, Lynne D. Neumayr, Patricia Evans, Sukhvinder Bansal, Maciej Garbowski, Marcela G. Weyhmiller, Paul R. Harmatz, John C. Wood, Jeffery L. Miller, Colleen Byrnes, Guenter Weiss, Markus Seifert, Regine Grosse, Dagmar Grabowski, Angelica Schmidt, Roland Fischer, Peter Nielsen, Charlotte Niemeyer, Elliott Vichinsky |
Abstract |
In transfusional iron overload, extra-hepatic iron distribution differs, depending on the underlying condition. Relative mechanisms of plasma non-transferrin bound iron (NTBI) generation may account for these differences. Markers of iron metabolism (plasma NTBI, labile iron, hepcidin, transferrin, monocyte SLC40A1 [ferroportin]), erythropoiesis (growth differentiation factor 15, soluble transferrin receptor) and tissue hypoxia (erythropoietin) were compared in patients with Thalassaemia Major (TM), Sickle Cell Disease and Diamond-Blackfan Anaemia (DBA), with matched transfusion histories. The most striking differences between these conditions were relationships of NTBI to erythropoietic markers, leading us to propose three mechanisms of NTBI generation: iron overload (all), ineffective erythropoiesis (predominantly TM) and low transferrin-iron utilization (DBA). |
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