Service d'Hématologie Clinique et de Thérapie Cellulaire, Hôpital Saint Antoine, APHP, Paris, France.
Sorbonne Universités, UPMC Univ. Paris 06, Centre de recherche Saint-Antoine, UMR-S938, Paris, France.
Am J Hematol. 2021 Aug 1;96(8):1008-1016. doi: 10.1002/ajh.26189. Epub 2021 May 14.
The role of iron in the formation and functioning of erythrocytes, and to a lesser degree of white blood cells, is well established, but the relationship between iron and platelets is less documented. Physiologically, iron plays an important role in hematopoiesis, including thrombopoiesis; iron levels direct, together with genetic factors, the lineage commitment of megakaryocytic/erythroid progenitors toward either megakaryocyte or erythroid progenitors. Megakaryocytic iron contributes to cellular machinery, especially energy production in platelet mitochondria. Thrombocytosis, possibly favoring vascular thrombosis, is a classical feature observed with abnormally low total body iron stores (mainly due to blood losses or decreased duodenal iron intake), but thrombocytopenia can also occur in severe iron deficiency anemia. Iron sequestration, as seen in inflammatory conditions, can be associated with early thrombocytopenia due to platelet consumption and followed by reactive replenishment of the platelet pool with possibility of thrombocytosis. Iron overload of genetic origin (hemochromatosis), despite expected mitochondrial damage related to ferroptosis, has not been reported to cause thrombocytopenia (except in case of high degree of hepatic fibrosis), and iron-related alteration of platelet function is still a matter of debate. In acquired iron overload (of transfusional and/or dyserythropoiesis origin), quantitative or qualitative platelet changes are difficult to attribute to iron alone due to the interference of the underlying hematological conditions; likewise, hematological improvement, including increased blood platelet counts, observed under iron oral chelation is likely to reflect mechanisms other than the sole beneficial impact of iron depletion.
铁在红细胞的形成和功能中起着重要作用，在一定程度上也对白血细胞起着重要作用，但铁与血小板之间的关系则记录较少。从生理学上讲，铁在造血过程中起着重要作用，包括巨核细胞生成；铁水平与遗传因素一起，决定巨核细胞/红细胞祖细胞向巨核细胞或红细胞祖细胞的谱系定向。巨核细胞铁有助于细胞机制，特别是血小板线粒体中的能量产生。血小板增多症可能有利于血管血栓形成，是观察到的异常低的全身铁储存（主要是由于失血或十二指肠铁摄入减少）的经典特征，但严重缺铁性贫血也可发生血小板减少症。炎症状态下的铁蓄积可能由于血小板消耗而导致早期血小板减少症，随后血小板池可能会出现反应性补充，从而导致血小板增多症。遗传性铁过载（血色病），尽管与铁死亡相关的预期线粒体损伤，但尚未报道会引起血小板减少症（除了在高度肝纤维化的情况下），并且铁相关的血小板功能改变仍然存在争议。在获得性铁过载（输血和/或红细胞生成异常）中，由于潜在的血液学状况的干扰，很难将血小板的数量或质量变化归因于铁；同样，在铁口服螯合治疗下观察到的血液学改善，包括血小板计数增加，可能反映了除铁耗竭的单纯有益影响以外的机制。
