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Iron absorption, transport, storage

  • Iron absorption & transport: IOL may occur by inappropriately increased GI absorption and/or through RBC transfusions. IOL leads to disorders in many organ systems. In BTM, ICT attenuates organ failure & improves survival1,2. In MDS, hepcidin levels & therefore GI iron absorption & possibly susceptibility to IOL toxicity varies between MDS subtypes3.
    • Iron is transported in the circulation bound to transferrin. Once transferrin is saturated, non-transferrin bound iron (NTBI) & oxidative species are seen4.
    • The regulation of ferritin metabolism is complex, therefore there is a good but not perfect association between SF level & iron load in organs measured by MRI. The association between SF level and clinical outcomes is not always associated with liver iron content (LIC) info
    • SF level of 1000-2500ng/mL &/or actual/anticipated transfusion of 25-50 RBC units may be considered as a threshold for starting ICT. IOL should be verified by serial SF levels & a fasting transferrin saturation of ≥0.54.

Graphic - Iron absorption, transport, & storage
Figure. Regulators of iron balance. Dietary iron enters the enterocyte after being reduced to the ferrous (Fe2+) state by duodenal cytochrome B and transported by divalent metal transporter1. Hephaestin (Heph) facilitates iron export by ferroportin (FPN). Hepatocytes take up either free (non-transferrin bound iron/NTBI, which enters cells in an unregulated manner) or transferrin (Tf)-bound iron (by receptor mediated endocytosis) and release it back into the circulation via ferroportin. Iron is also released from macrophages via ferroportin. Ferroportin-mediated release of iron is inhibited by hepcidin. Hepcidin is inhibited by erythroferrone, produced by erythroblasts under conditions of erythropoietic activity. Cp, ceruloplasmin; Fe, iron; RBC, red blood cell; TfR, transferrin receptor.