Anemia of chronic disease: A unique defect of iron recycling for many different chronic diseases

Poggiali, Erika; Amicis, Margherita Migone De; Motta, Irene

doi:10.1016/j.ejim.2013.07.011

Cited by 78 publications

(62 citation statements)

References 78 publications

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“…Conversely, a low transferrin saturation with high ferritin (>100 ng/ml) is peculiar of anemia of chronic disease (ACD) 27 . Frequently these two entities coexist, presenting with low transferrin saturation and a moderate increase in serum ferritin (Table 8).…”

Section: Anemia and Agingmentioning

confidence: 99%

Anemia in Clinical Practice—Definition and Classification: Does Hemoglobin Change With Aging?

Cappellini

Motta

2015

Seminars in Hematology

Self Cite

326

116

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Section: Anemia and Agingmentioning

confidence: 99%

Anemia in Clinical Practice—Definition and Classification: Does Hemoglobin Change With Aging?

Cappellini

Motta

2015

Seminars in Hematology

Self Cite

326

116

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“…Considering the characteristic of anemia of inflammation, blood transfusion, erythropoietin, and iron supplementation are the main strategies to ameliorate the diseases in clinical practice; however, these interventions may be accompanied by the risk of secondary iron overload. 77 …”

Section: Iron Disorders Due To Deregulation Of Hepcidinmentioning

confidence: 99%

Hepcidin

et al. 2016

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Iron is required for most forms of organisms, and it is the most essential element for the functions of many iron-containing proteins involved in oxygen transport, cellular respiration, DNA replication, and so on. Disorders of iron metabolism are associated with diverse diseases, including anemias (e.g., iron-deficiency anemia and anemia of chronic diseases) and iron overload diseases, such as hereditary hemochromatosis and β-thalassemia. Hepcidin (encoded by Hamp gene) is a peptide hormone synthesized by hepatocytes, and it plays an important role in regulating the systematic iron homeostasis. As the systemic iron regulator, hepcidin, not only controls dietary iron absorption and iron egress out of iron storage cells, but also induces iron redistribution in various organs. Deregulated hepcidin is often seen in a variety of iron-related diseases including anemias and iron overload disorders. In the case of iron overload disorders (e.g., hereditary hemochromatosis and β-thalassemia), hepatic hepcidin concentration is significantly reduced.Since hepcidin deregulation is responsible for iron disorder-associated diseases, the purpose of this review is to summarize the recent findings on therapeutics targeting hepcidin.Continuous efforts have been made to search for hepcidin mimics and chemical compounds that could be used to increase hepcidin level. Here, a literature search was conducted in PubMed, and research papers relevant to hepcidin regulation or hepcidin-centered therapeutic work were reviewed. On the basis of literature search, we recapitulated recent findings on therapeutic studies targeting hepcidin, including agonists and antagonists to modulate hepcidin expression or its downstream signaling. We also discussed the molecular mechanisms by which hepcidin level and iron metabolism are modulated.Elevating hepcidin concentration is an optimal strategy to ameliorate iron overload diseases, and also to relieve β-thalassemia phenotypes by improving ineffective erythropoiesis. Relative to the current conventional therapies, such as phlebotomy and blood transfusion, therapeutics targeting hepcidin would open a new avenue for treatment of iron-related diseases.

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“…This is a protective mechanism during times of acute infection to reduce bioavailable iron necessary for growth of invading microorganisms, in which iron absorption through enterocytes is decreased and iron release from macrophages in the process of iron recycling is diminished [15]. However, in chronic diseases which may carry a prolonged inflammatory stimulus, iron is pathologically sequestered within cells of the reticuloendothelial system and despite adequate iron stores, anemia may result due to impairments in iron recycling yielding insufficient iron available for erythropoiesis and hemoglobin synthesis [16]. …”

Section: Mechanism Of Action In the Vitamin D – Anemia Associationmentioning

confidence: 99%

Vitamin D and anemia

Smith

Tangpricha

2015

Current Opinion in Endocrinology, Diabetes &Amp; Obesity

128

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Purpose of review This review highlights recent findings in the emerging association between vitamin D and anemia through discussion of mechanistic studies, epidemiologic studies, and clinical trials. Recent findings Vitamin D has previously been found to be associated with anemia in various healthy and diseased populations. Recent studies indicate that the association may differ between race and ethnic groups and is likely specific to anemia of inflammation. The mechanism underlying this association involves the reduction of pro-inflammatory cytokines by vitamin D as well as the direct suppression of hepcidin mRNA transcription. There is also evidence that vitamin D may be protective against anemia by supporting erythropoiesis. Other calciotropic hormones, fibroblast growth factor 23 (FGF-23) and parathyroid hormone (PTH) have also been found to be involved in iron homeostasis and erythropoiesis. Summary Recent advances in our understanding the association between vitamin D and anemia suggest that maintenance of sufficient vitamin D status may be important in preventing anemia, particularly in diseases characterized by inflammation. Early clinical trials have been promising, but further research is needed to define the efficacy of vitamin D as a future approach for the treatment of anemia.

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Anemia of chronic disease: A unique defect of iron recycling for many different chronic diseases

Cited by 78 publications

References 78 publications

Anemia in Clinical Practice—Definition and Classification: Does Hemoglobin Change With Aging?

Anemia in Clinical Practice—Definition and Classification: Does Hemoglobin Change With Aging?

Hepcidin

Vitamin D and anemia

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