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Mechanisms of plasma non‐transferrin bound iron generation: insights from comparing transfused diamond blackfan anaemia with sickle cell and thalassaemia patients
- Porter, John B;
- Walter, Patrick B;
- Neumayr, Lynne D;
- Evans, Patricia;
- Bansal, Sukhvinder;
- Garbowski, Maciej;
- Weyhmiller, Marcela G;
- Harmatz, Paul R;
- Wood, John C;
- Miller, Jeffery L;
- Byrnes, Colleen;
- Weiss, Guenter;
- Seifert, Markus;
- Grosse, Regine;
- Grabowski, Dagmar;
- Schmidt, Angelica;
- Fischer, Roland;
- Nielsen, Peter;
- Niemeyer, Charlotte;
- Vichinsky, Elliott
- et al.
Published Web Location
https://doi.org/10.1111/bjh.13081Abstract
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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