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Mechanism for anemia of chronic disease/anemia of inflammation (ACD/AI)

Mechanism for anemia of chronic disease/anemia of inflammation (ACD/AI)
A proposed mechanism for ACD/AI is shown here. In the presence of infection, inflammation, or malignancy, the macrophage is stimulated to produce IL-6 and IL-1b, which induce the production of hepcidin by the liver. Hepcidin, in turn, through its interaction with the iron export protein ferroportin, inhibits iron absorption from the gastrointestinal tract and decreases release of iron from macrophages. Both effects lead to the reduced plasma iron levels (hypoferremia) characteristic of ACD/AI. Inflammatory cytokines such as IL-1b and TNF-a reduce erythropoietin production, decrease red blood cell lifespan, and reduce the efficiency of erythropoiesis, which are also components of ACD/AI.
ACD/AI: anemia of chronic disease/anemia of inflammation; GI: gastrointestinal; IL-1b: interleukin-1 beta; IL-16: interleukin-6; TNF-a: tumor necrosis factor-alpha.
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