Abstract
Anemia of inflammation (AI), also known as anemia of chronic inflammation or anemia of chronic disease was described over 50 years ago as anemia in association with clinically overt inflammatory disease, and the findings of low plasma iron, decreased bone marrow sideroblasts and increased reticuloendothelial iron. Pathogenic features underlying AI include a mild shortening of red cell survival, impaired erythropoietin production, blunted responsiveness of the marrow to erythropoietin, and impaired iron metabolism mediated by inflammatory cytokines and the iron regulatory peptide, hepcidin. Despite marked recent advances in understanding AI, gaps remain, including understanding of the pathogenesis of AI associated with “noninflammatory” or mildly inflammatory diseases, the challenge of excluding iron deficiency anemia in the context of concomitant inflammation, and understanding more precisely the contributory role of hepcidin in the development of AI in human inflammatory diseases.
Highlights
Anemia of inflammation (AI), known as anemia of chronic inflammation or anemia of chronic disease, was described over 50 years ago as a normo to microcytic anemia, typically of mild severity, characterized biochemically by a low plasma iron, decreased total ironbinding capacity, decreased transferrin saturation, and, on bone marrow examination, decreased sideroblasts and increased reticuloendothelial iron [1]
Despite the heterogeneity of underlying infectious, malignant and inflammatory diseases described in conjunction with this type of anemia, there was a remarkable degree of similarity in terms of the severity of the anemia, correlating directly with the degree of inflammation present, and its stability over time, features which remain characteristic of AI today [1]
Despite advances in understanding the underlying mechanisms leading to AI, several key clinical issues remain, including understanding of mechanisms of AI in “noninflammatory” diseases, optimal methods for distinguishing AI from iron deficiency anemia, and understanding the contributory role of various pathologic mechanisms in individual human diseases that lead to AI
Summary
Anemia of inflammation (AI), known as anemia of chronic inflammation or anemia of chronic disease, was described over 50 years ago as a normo to microcytic anemia, typically of mild severity, characterized biochemically by a low plasma iron, decreased total ironbinding capacity, decreased transferrin saturation, and, on bone marrow examination, decreased sideroblasts and increased reticuloendothelial iron [1]. Despite the heterogeneity of underlying infectious, malignant and inflammatory diseases described in conjunction with this type of anemia, there was a remarkable degree of similarity in terms of the severity of the anemia, correlating directly with the degree of inflammation present, and its stability over time, features which remain characteristic of AI today [1]. Despite advances in understanding the underlying mechanisms leading to AI, several key clinical issues remain, including understanding of mechanisms of AI in “noninflammatory” diseases, optimal methods for distinguishing AI from iron deficiency anemia, and understanding the contributory role of various pathologic mechanisms in individual human diseases that lead to AI
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