Abstract
Anemia of chronic disease (ACD), one of the most common syndromes in medicine, is observed in patients with chronic infections, inflammatory and neoplastic disorders. All of the factors involved in the development of ACD can be attributed to effects of cytokines, including shortened red cell survival, blunted erythropoietin response to anemia, impaired erythroid colony formation in response to erythropoietin and abnormal mobilization of reticuloendothelial iron stores. Tumor Necrosis Factor-alpha (TNF! ), which is important for the pathophysiology of ACD, may act directly on bone marrow erythroid precursors. Hepcidin is a liver-made peptide, and its synthesis is greatly stimulated by inflammation. The plasma level of erythropoietin (EPO) in anemic patients suffering from inflammation is often low in relation to the blood hemoglobin concentration. Interleukin 1 and TNF! suppress EPO gene expression. ACD is most effectively treated via approaches directed against the underlying cause. There are also some reports addressing that iron supplementation and iron chelation therapy may be useful. If this is not possible, supportive care is given through red cell transfusions or use of recombinant human EPO. Patients with inflammatory disorders showed remarkable hematologic responses to recombinant EPO, although a significant change in rheumatologic picture was not seen.
Keywords: anemia, chronic disease, connective tissue diseases, erythropoietin, inflammation, mediators
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