The Science Journal of the Lander College of Arts and Sciences


Anemia of chronic disease (ACD) is the result of altered iron metabolism, blunted erythropoiesis, and shortened red blood cell survival caused by inflammatory cytokines. Hepcidin plays a key role in anemia of chronic disease by inducing endocytosis of the iron exporter ferroportin. Iron is trapped in enterocytes, hepatocytes, and macrophages, and is unavailable for hemoglobin synthesis. When treating the underlying disease is not an option, or anemia is severe, ACD should be treated. While oral iron supplementation is not suitable for ACD, intravenous iron may be effective. Erythropoiesis stimulating agents are a common approach to treating ACD, but a large percentage of ACD patients are refractory to ESAs. Additionally, there are many safety issues associated with ESA therapy. Concomitant IV iron supplementation increases patient response to ESAs and may reduce safety concerns as well. Several new, more targeted approaches to ACD treatment are being studied. Isocitrate supplements have been shown to improve ACD by minimizing the iron restriction response to increase erythropoiesis. Antibodies such as infliximab and tocilizumab, which neutralize the inflammatory cytokines TNF-α and IL-6, respectively, decrease hepcidin expression and improve hemoglobin levels. Finally, antibodies and speigelmers that target hepcidin directly are being developed. These new therapies, alone or in combination with IV iron or ESAs, show promise in alleviating anemia of chronic disease.



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