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.