Figure 2.
Schematic representation of the regulation of iron metabolism in FID in CICs. Inflammation with increased cytokine production causes upregulation of liver hepcidin (H), which binds to ferroportin (F). Enterocytes are prevented from exporting absorbed iron (Fe) to transferrin (T) in the bloodstream. In hepatocytes and macrophages, iron is also trapped intracellularly and is stored as iron-rich ferritin, whereas macrophages increase iron-poor serum ferritin in circulation. High intracellular iron also downregulates transferrin production, lowering TIBC. Iron release is so restricted that the decrease in serum iron still lowers TSAT despite low TIBC. Iron restriction eventually leads to the anemia of inflammation. Both ID and FID have hypoferremia but low TIBC, and high ferritin characterizes FID.

Schematic representation of the regulation of iron metabolism in FID in CICs. Inflammation with increased cytokine production causes upregulation of liver hepcidin (H), which binds to ferroportin (F). Enterocytes are prevented from exporting absorbed iron (Fe) to transferrin (T) in the bloodstream. In hepatocytes and macrophages, iron is also trapped intracellularly and is stored as iron-rich ferritin, whereas macrophages increase iron-poor serum ferritin in circulation. High intracellular iron also downregulates transferrin production, lowering TIBC. Iron release is so restricted that the decrease in serum iron still lowers TSAT despite low TIBC. Iron restriction eventually leads to the anemia of inflammation. Both ID and FID have hypoferremia but low TIBC, and high ferritin characterizes FID.

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