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Published on: March 14, 2017
Advances in the anemia of chronic disease
1Hematology/Oncology Division, Ralph H. Johnson VA Medical Center, Charleston, South Carolina, USA. meansr@musc.edu
Insights
Anemia of chronic disease (ACD) is common in inflammatory conditions. Cytokines drive ACD by affecting red blood cells, erythropoietin response, and iron stores, impacting diagnosis and treatment.
Area of Science:
- Hematology
- Immunology
- Internal Medicine
Background:
- Anemia of chronic disease (ACD) is a prevalent clinical syndrome.
- It is associated with chronic infectious, inflammatory, and neoplastic disorders.
- ACD pathogenesis involves increased pro-inflammatory cytokines.
Purpose of the Study:
- To review advances in understanding the diagnosis of ACD.
- To summarize the pathophysiologic mechanisms of ACD.
- To discuss therapeutic strategies for ACD.
Main Methods:
- Literature review of diagnostic criteria for ACD.
- Analysis of cytokine involvement in ACD pathophysiology.
- Evaluation of current and emerging ACD treatments.
Main Results:
- Cytokines like TNF-α, IL-1, and interferons are central to ACD development.
- ACD mechanisms include reduced red blood cell lifespan and impaired erythropoiesis.
- Abnormal iron metabolism and blunted erythropoietin response are key features.
Conclusions:
- Understanding cytokine-driven mechanisms is crucial for ACD management.
- Advances in diagnostics and therapeutics offer improved patient outcomes.
- Targeting inflammatory pathways holds promise for ACD treatment.
Abstract:
The anemia found in patients with chronic infectious, inflammatory, and neoplastic disorders, known as the anemia of chronic disease (ACD), is one of the most common syndromes in medicine. A characteristic finding of the disorders associated with ACD is increased production of the cytokines that mediate the immune or inflammatory response, such as tumor necrosis factor, interleukin-1, and the interferons. All the processes involved in the development of ACD can be attributed to these 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. In this review, advances in the understanding of the diagnostic, pathophysiologic, and therapeutic aspects of this syndrome are summarized.
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