Abstract
Multiple links between inflammation and iron homeostasis exist, the most important being centered on hepcidin, the master regulator of iron homeostasis, a defensin-like peptide that acts by binding and inactivating the cell iron exporter ferroportin. The pro-inflammatory cytokine IL-6 is one of the most powerful stimuli to hepcidin synthesis, which causes macrophage iron retention and a reduction of enterocyte iron absorption. This results in a reduction of extracellular iron, which is essential for many pathogens but also for immune cells. Inflammation perturbates the levels of classical laboratory markers of iron status, like ferritin, serum iron, and transferrin (and hence transferrin saturation [TSAT). Thus, they are often difficult to interpret during infections or other acute and chronic sterile inflammatory states. Other laboratory parameters, like hepcidin, soluble transferrin receptor (sTfR), percentage of hypochromic erythrocytes (%HYPO), and reticulocyte hemoglobin content (CHr), have been proposed to better assess iron status during inflammation. An accurate evaluation of iron status in the anemia of inflammation and anemia of chronic disorders (ACD) is key to establishing a possible indication to iron supplementation and represents an area of active research.
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