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Cited by 146Iron Metabolism and DisordersErythropoietin and Anemia TreatmentRheumatoid Arthritis Research and Therapies

Anaemia in inflammatory rheumatic diseases

Weiss, Günter, Schett, Georg·2013·Nature Reviews Rheumatology
DOI 10.1038/nrrheum.2012.183
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Abstract

Anaemia is frequently observed in patients with inflammatory rheumatic diseases. Depending on its severity, anaemia negatively affects cardiovascular performance, physical activity and the quality of life of patients. However, anaemia is considered to be a symptom of the underlying inflammatory disease and, thus, neglected as a complex medical condition that warrants specific diagnosis and treatment. Although inflammation-induced alterations in iron homeostasis and erythropoiesis have a dominant role in the pathogenesis of this type of anaemia, multiple other factors such as chronic blood loss, haemolysis, disease and treatment-associated adverse effects or vitamin deficiencies can also take part in the development of anaemia. Accordingly, the prevalence of anaemia is positively associated with the severity of the underlying disease. This Review will summarize epidemiological data on anaemia in inflammatory rheumatic diseases, along with a detailed description of underlying pathophysiological pathways, available diagnostic tools and practical diagnostic strategies. Discussion of established and newly emerging treatment regimens, as well as the need for further research in this clinically relevant field, will also be included.

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Crossref · 10.1038/nrrheum.2012.183

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125 of 125 references verified0 citation errors · 0 not checkable

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  • The underlying pathophysiology of ACD involves mainly iron retention within the monocyte/macrophage system, a blunted formation and activity of erythropoietin (Epo), and an impaired proliferation and differentiation of erythroid progenitor cells.

    “The underlying pathophysiology involves mainly (i) iron retention within the monocyte/macrophage system, (ii) a blunted formation and activity of the red blood cell hormone erythropoietin (Epo), and (iii) an impaired proliferation and differentiation of erythroid progenitor cells (Weiss and Schett, 2013).”

    From Iron at the interface of immunity and infection (2014) · cites this paper as Weiss and Schett, 2013

  • Iron restriction in monocytes and macrophages is achieved by the activity of cytokines such as TNF-α, IL-1, IL-6, and IL-10 on iron transport and storage proteins and by hepcidin, which binds ferroportin, resulting in its internalization and degradation, thereby blocking macrophage iron egress.

    “Iron restriction in monocytes and MΦs is achieved by the activity of different cytokines, such as TNF-α, IL-1, IL-6, and IL-10, on iron transport and storage proteins of macrophages and most importantly by the action of the liver-derived acute phase protein hepcidin, which binds to the only known cellular iron exporter ferroportin, resulting in its internalization and degradation, thereby blocking”

    From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [170]

  • Alterations of iron traffic are thought to result from a defense strategy of the body to limit the availability of iron for invading pathogens, leading to retention of iron in macrophages and impaired iron absorption from the diet.

    “These alterations of iron traffic are thought to result from defense strategy of the body to limit the availability of iron for invading pathogens (167–169), which lead to retention of iron in MΦs and an impaired iron absorption from the diet (170).”

    From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [170]

  • Alterations of iron homeostasis result in limited availability of iron for erythropoiesis, a cornerstone for the development of anemia of infection or anemia of chronic disease.

    “However, these alterations of iron homeostasis result also in a limited availability of iron for erythropoiesis, which is a cornerstone for the development of anemia, termed anemia of infection or anemia of chronic disease (170).”

    From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [170]

  • IL-4, IL-10, and IL-13 promote TfR-mediated iron uptake and intracellular retention by ferritin.

    “Other cytokines such as IL-4, IL-10, and IL-13 promote TfRmediated Fe uptake and intracellular retention by ferritin [113].”

    From The Iron age of host–microbe interactions (2015) · cites this paper as [113]

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Authors
Weiss, G., & Schett, G.
Affiliations
  • Innsbruck Medical University (AT)
  • Friedrich-Alexander-Universität Erlangen-Nürnberg (DE)
Corresponding author
Weiss, Günter
ORCID
Venue
Nature Reviews Rheumatology
Publisher
Springer Science and Business Media LLC
Published
2012-11-13
Volume
9
Issue
4
Pages
205-215
ISSN
  • 1759-4790 (ISSN-L)
  • 1759-4804
DOI
10.1038/nrrheum.2012.183
OpenAlex
W2096011394
Cited by
146
References
128
Citations by year
2026: 9 · 2025: 12 · 2024: 12 · 2023: 10 · 2022: 14 · 2021: 9 · 2020: 11 · 2019: 9 · 2018: 10 · 2017: 12 · 2016: 8 · 2015: 11 · 2014: 12 · 2013: 6
FWCI
1.47
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Nature Reviews Rheumatology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
  • Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
  • Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
Keywords
anemia, inflammatory rheumatic diseases, chronic inflammation, iron homeostasis, erythropoiesis, anemia of chronic disease, chronic blood loss, hemolysis, vitamin deficiency, anemia diagnosis, anemia treatment, disease severity, quality of life
MeSH terms
Adult, Aged, Avitaminosis, Erythropoiesis, Female, Hematologic Tests, Hemoglobins, Humans, Inflammation, Male, Middle Aged, Prognosis, Rheumatic Diseases, Severity of Illness Index, Comorbidity, Prevalence, Risk Assessment, Anemia, Iron-Deficiency

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