Anemia of inflammation
Open accessAbstract
Anemia of inflammation (AI), also known as anemia of chronic disease (ACD), is regarded as the most frequent anemia in hospitalized and chronically ill patients. It is prevalent in patients with diseases that cause prolonged immune activation, including infection, autoimmune diseases, and cancer. More recently, the list has grown to include chronic kidney disease, congestive heart failure, chronic pulmonary diseases, and obesity. Inflammation-inducible cytokines and the master regulator of iron homeostasis, hepcidin, block intestinal iron absorption and cause iron retention in reticuloendothelial cells, resulting in iron-restricted erythropoiesis. In addition, shortened erythrocyte half-life, suppressed erythropoietin response to anemia, and inhibition of erythroid cell differentiation by inflammatory mediators further contribute to AI in a disease-specific pattern. Although the diagnosis of AI is a diagnosis of exclusion and is supported by characteristic alterations in iron homeostasis, hypoferremia, and hyperferritinemia, the diagnosis of AI patients with coexisting iron deficiency is more difficult. In addition to treatment of the disease underlying AI, the combination of iron therapy and erythropoiesis-stimulating agents can improve anemia in many patients. In the future, emerging therapeutics that antagonize hepcidin function and redistribute endogenous iron for erythropoiesis may offer additional options. However, based on experience with anemia treatment in chronic kidney disease, critical illness, and cancer, finding the appropriate indications for the specific treatment of AI will require improved understanding and a balanced consideration of the contribution of anemia to each patient's morbidity and the impact of anemia treatment on the patient's prognosis in a variety of disease settings.
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During infections, increased cytokine concentrations activate the production of myeloid cells important for host defense.
“activate the production of myeloid cells important for host defense [55]”
From Hepcidin-Ferroportin Interaction Controls Systemic Iron Homeostasis (2021) · cites this paper as [55]
The Introduction says microbial molecules trigger inflammatory cytokine release and that IFN-γ promotes production, differentiation, and activation of leukocytes important for host defense. It does not specifically identify those cells as myeloid or establish that increased cytokine concentrations generally drive their production during infections. (LLM, conf=0.84)
Experimental — accuracy not yet measuredBased on real-life evidence, determination of iron status by using serum ferritin and transferrin saturation is the most commonly deployed strategy used in clinical and public health settings.
“Although many laboratory indexes may be helpful for the ID differential diagnostic workup, such as the mean corpuscular volume (MCV), the reticulocyte count and reticulocyte Hb content, the soluble transferrin receptor and its correlation with SF, and hepcidin measurement, based on the real-life evidence, the determination of iron status by using SF and TSAT is the most commonly deployed strategy”
From Defining Global Thresholds for Serum Ferritin: A Challenging Mission in Establishing the Iron Deficiency Diagnosis in This Era of Striving for Health Equity (2025) · cites this paper as [17]
The Introduction (page unavailable) uses transferrin saturation and serum ferritin to distinguish anemia of inflammation from iron-deficiency anemia, and discusses limitations of alternative tests. It does not establish that this is the most commonly deployed strategy, cite real-life evidence for its frequency of use, or address its use in public health settings. (LLM, conf=0.84)
Experimental — accuracy not yet measuredIt is usual practice in many specialties and guidelines to assume that, regardless of the lower normality value of the ferritin test used, SF <30 ng/mL (irrespective of TSAT) or SF <100 ng/mL and TSAT <20% are the hallmarks of absolute iron deficiency; while SF >100 ng/mL and TSAT <20% usually indicate anemia of inflammation in the context of infection or inflammation.
“It is a usual practice in many specialties and guidelines to assume that, regardless of the lower normality value of the ferritin test used, SF <30 ng/mL (irrespective of the TSAT value) or SF <100 ng/mL and TSAT <20% are the hallmarks of absolute ID; while SF >100 ng/mL and TSAT <20% usually indicate AI in the context of infection or inflammation [1,2,15,16,17,18,19,20].”
From Defining Global Thresholds for Serum Ferritin: A Challenging Mission in Establishing the Iron Deficiency Diagnosis in This Era of Striving for Health Equity (2025) · cites this paper as [17]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredHepcidin contributes to innate immunity by decreasing plasma iron levels, providing an iron-restricted internal milieu inhospitable to microbes.
“Hepcidin contributes to innate immunity by decreasing plasma iron levels, providing an iron-restricted internal milieu inhospitable to microbes (6).”
From Epidermal hepcidin is required for neutrophil response to bacterial infection (2019) · cites this paper as [6]
During infections, increased cytokine concentrations inhibit erythropoiesis.
“During infections, increased cytokine concentrations inhibit erythropoiesis”
From Hepcidin-Ferroportin Interaction Controls Systemic Iron Homeostasis (2021) · cites this paper as [55]
In functional iron deficiency (e.g., in inflammation) total body iron is not decreased, but iron is sequestered in stores by the high hepcidin levels.
“In functional iron deficiency (e.g., in inflammation) total body iron is not decreased, but iron is sequestered in stores by the high hepcidin levels.84,97”
From Iron metabolism and iron disorders revisited in the hepcidin era (2020) · cites this paper as [84]
High hepcidin levels lead to a phenotype opposite to that of hemochromatosis, reminiscent of anemia of inflammation.
“High hepcidin levels lead to a phenotype opposite to that of hemochromatosis, reminiscent of anemia of inflammation.84”
From Iron metabolism and iron disorders revisited in the hepcidin era (2020) · cites this paper as [84]
Proinflammatory cytokines such as IL-6 and IL-1β, produced in chronic infections, autoimmunity, cancer, renal failure and other chronic disorders, activate hepcidin expression leading to iron-restricted erythropoiesis and anemia of inflammation.
“Proinflammatory cytokines such as IL-6 and IL-1β, produced in chronic infections, autoimmunity, cancer, renal failure and other chronic disorders activate hepcidin expression leading to iron-restricted erythropoiesis and anemia of inflammation, once named anemia of chronic diseases.84,97,98”
From Iron metabolism and iron disorders revisited in the hepcidin era (2020) · cites this paper as [84]
Anemia of inflammation largely results from inflammation-driven retention of iron in certain immune cells, resulting in iron-limited erythropoiesis.
“The second most frequent anemia, anemia of inflammation (also called anemia of chronic disease), largely results from inflammation-driven retention of iron in certain immune cells, resulting in iron-limited erythropoiesis (Weiss et al., 2019).”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Weiss et al., 2019
Prolonged activation of the hepcidin defense mechanism can restrict iron availability to developing erythrocytes in the bone marrow, leading to the development of AI.
“However, prolonged activation of this defense mechanism can eventually restrict the availability of iron not only to the invading pathogens, but also to developing erythrocytes in the bone marrow, leading to the development of AI (Kim et al., 2014; Weiss et al., 2019).”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Weiss et al., 2019
Inflammation or infection invariably lead to changes in iron homeostasis and usually to hypoferremia and hyperferritinemia.
“However, inflammation or infection lead invariably to changes in iron homeostasis and usually to hypoferremia and hyperferritinemia [150,151].”
From Iron in immune cell function and host defense (2021) · cites this paper as [151]
Inflammation causes alterations of iron homeostasis hallmarked by functional iron deficiency, high serum ferritin, and low circulating iron.
“Inflammation, therefore, causes alterations of iron homeostasis hallmarked by functional iron deficiency (ID) as reflected by high iron content in reticuloendothelial cells and consequently high serum ferritin levels whereas circulating iron levels are low.”
Inflammation limits iron availability for erythropoiesis, causing anemia of inflammation.
“Subsequently, inflammation limits this metal’s availability for erythropoiesis, thus causing anemia, termed as anemia of inflammation (AI) [7].”
Inflammation-driven dysregulation of iron homeostasis is well established.
“It has been suggested that the COVID-19 related inflammation may be the main cause of COVID-19 associated iron disorders, as an inflammation-driven dysregulation of iron homeostasis is well established [4, 6, 7].”
Some studies define ID using only ferritin levels <100 μg/mL, while others also take a low transferrin saturation into account.
“The definition of ID in general may also play a role because some studies only use ferritin levels <100 μg/mL as definition of ID whereas others also take a low transferrin saturation into account”
From Anaemia, iron status, and gender predict the outcome in patients with chronic heart failure (2020) · cites this paper as [14]
Low transferrin saturation reflects iron availability for the bone marrow and tissue.
“because the latter parameter reflects iron availability for the bone marrow and tissue. 12 , 13 , 14 , 15”
From Anaemia, iron status, and gender predict the outcome in patients with chronic heart failure (2020) · cites this paper as [14]
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Targeting Hepcidin with Antisense Oligonucletides Improves Anemia Endpoints in Mice.
Crosby, J. R., Gaarde, W. A., Egerston, J., et al. (2006) · Blood · doi:10.1182/blood.v108.11.269.269 · Cited by 4 · see citing works
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Iron metabolism and iron disorders revisited in the hepcidin era
Camaschella, C., Nai, A., & Silvestri, L. (2020) · Haematologica · doi:10.3324/haematol.2019.232124 · Cited by 734 · see citing works
“84,97,98 By withholding iron in macrophages, extra-cellular Gram-negative microorganisms are deprived of this essential nutrient.”
InfluentialGardner, W. M., Razo, C., McHugh, T. A., Hagins, H., Vilchis-Tella, V. M., Hennessy, C., Taylor, H. J., Perumal, N., Fuller, K., Cercy, K. M., et al. (2023) · The Lancet Haematology · doi:10.1016/s2352-3026(23)00160-6 · Cited by 642 · see citing works
Hepcidin-Ferroportin Interaction Controls Systemic Iron Homeostasis
Nemeth, E., & Ganz, T. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22126493 · Cited by 540 · see citing works
Self-citationThe Role of Iron Regulation in Immunometabolism and Immune-Related Disease
Cronin, S. J. F., Woolf, C. J., Weiss, G., & Penninger, J. M. (2019) · Frontiers in Molecular Biosciences · doi:10.3389/fmolb.2019.00116 · Cited by 299 · see citing works
Self-citationBellmann-Weiler, R., Lanser, L., Barket, R., Rangger, L., Schapfl, A., Schaber, M., Fritsche, G., Wöll, E., & Weiss, G. (2020) · Journal of Clinical Medicine · doi:10.3390/jcm9082429 · Cited by 244 · see citing works
Self-citationIron in immune cell function and host defense
Haschka, D., Hoffmann, A., & Weiss, G. (2021) · Seminars in Cell & Developmental Biology · doi:10.1016/j.semcdb.2020.12.005 · Cited by 188 · see citing works
Sonnweber, T., Boehm, A., Sahanic, S., Pizzini, A., Aichner, M., Sonnweber, B., Kurz, K., Koppelstätter, S., Haschka, D., Petzer, V., et al. (2020) · Respiratory Research · doi:10.1186/s12931-020-01546-2 · Cited by 177 · see citing works
Self-citationThe Role of Nutrition in COVID-19 Susceptibility and Severity of Disease: A Systematic Review
James, P. T., Ali, Z., Armitage, A. E., Bonell, A., Cerami, C., Drakesmith, H., Jobe, M., Jones, K. S., Liew, Z., Moore, S. E., et al. (2021) · The Journal of Nutrition · doi:10.1093/jn/nxab059 · Cited by 147 · see citing works
Lactoferrin in aseptic and septic inflammation
Lepanto, M. S., Rosa, L., Paesano, R., Valenti, P., & Cutone, A. (2019) · Molecules · doi:10.3390/molecules24071323 · Cited by 147 · see citing works
Bolondi, G., Russo, E., Gamberini, E., Circelli, A., Meca, M. C. C., Brogi, E., Viola, L., Bissoni, L., Poletti, V., & Agnoletti, V. (2020) · World Journal of Emergency Surgery · doi:10.1186/s13017-020-00323-2 · Cited by 82 · see citing works
Anaemia, iron status, and gender predict the outcome in patients with chronic heart failure
Kurz*†, K., Lanser†, L., Seifert, M., Kocher, F., Pölzl, G., & Weiss*, G. (2020) · ESC Heart Failure · doi:10.1002/ehf2.12755 · Cited by 77 · see citing works
Mehta, U., Dey, S., Chowdhury, S., Ghosh, S., Hart, J. E., & Kurpad, A. (2021) · Environmental Epidemiology · doi:10.1097/ee9.0000000000000125 · Cited by 62 · see citing works
Interleukin-6 triggers toxic neuronal iron sequestration in response to pathological α-synuclein
Sterling, J. K., Kam, T.-I., Guttha, S., Park, H., Baumann, B., Mehrabani-Tabari, A. A., Schultz, H., Anderson, B., Alnemri, A., Chou, S.-C., et al. (2022) · Cell Reports · doi:10.1016/j.celrep.2022.110358 · Cited by 58 · see citing works
Morales-Ancajima, V. C., Tapia, V., Vu, B. N., Liu, Y., Alarcón-Yaquetto, D. E., & Gonzales, G. F. (2019) · Journal of Environmental and Public Health · doi:10.1155/2019/6127845 · Cited by 57 · see citing works
Epidermal hepcidin is required for neutrophil response to bacterial infection
Malerba, M., Louis, S., Cuvellier, S., Shambat, S. M., Hua, C., Gomart, C., Fouet, A., Ortonne, N., Decousser, J.-W., Zinkernagel, A. S., et al. (2019) · Journal of Clinical Investigation · doi:10.1172/jci126645 · Cited by 55 · see citing works
“Hepcidin contributes to innate immunity by decreasing plasma iron levels, providing an iron-restricted internal milieu inhospitable to microbes (6).”
BackgroundFu, Y.-K., Liu, H.-M., Lee, L.-H., Chen, Y.-J., Chien, S.-H., Lin, J.-S., Chen, W.-C., Cheng, M.-H., Lin, P.-H., Lai, J.-Y., et al. (2021) · Diagnostics · doi:10.3390/diagnostics11091725 · Cited by 38 · see citing works
Effects of PM2.5 and its constituents on hemoglobin during the third trimester in pregnant women
Xie, G., Yue, J., Yang, W., Yang, L., Xu, M., Sun, L., Zhang, B., Guo, L., & Chung, M. C. (2022) · Environmental Science and Pollution Research · doi:10.1007/s11356-022-18693-2 · Cited by 34 · see citing works
Iron status and the risk of sepsis and severe COVID-19: a two-sample Mendelian randomization study
Mohus, R. M., Flatby, H., Liyanarachi, K. V., DeWan, A. T., Solligård, E., Damås, J. K., Åsvold, B. O., Gustad, L. T., & Rogne, T. (2022) · Scientific Reports · doi:10.1038/s41598-022-20679-6 · Cited by 28 · see citing works
The <i>Staphylococcus aureus</i> non-coding RNA IsrR regulates TCA cycle activity and virulence
Rios-Delgado, G., McReynolds, A. K. G., Pagella, E. A., Norambuena, J., Briaud, P., Zheng, V., Munneke, M. J., Kim, J., Racine, H., Carroll, R. K., et al. (2025) · Nucleic Acids Research · doi:10.1093/nar/gkae1243 · Cited by 19 · see citing works
“Hosts further limit Fe availability during infection by reducing the absorption of dietary Fe in a process referred to as anemia of inflammation ( 12 ).”
Cancado, R. D., Leite, L. A. C., & Muñoz, M. (2025) · Diagnostics · doi:10.3390/diagnostics15030289 · Cited by 19 · see citing works
Swellam, M., Gabal, K. M. A., & Youssef, S. S. (2013) · IUBMB Life · doi:10.1002/iub.1205 · Cited by 14 · see citing works
- Authors
- Weiss, G., Ganz, T., & Goodnough, L. T.
- Affiliations
- Department of Internal Medicine II and
- University of California, Los Angeles (US)
- Stanford Medicine (US)
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2019-01-03
- Volume
- 133
- Issue
- 1
- Pages
- 40-50
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- PMC
- PMC6536698
- OpenAlex
- W2900365689
- Cited by
- 1,219
- References
- 166
- Citations by year
- 2026: 172 · 2025: 181 · 2024: 185 · 2023: 178 · 2022: 161 · 2021: 171 · 2020: 111 · 2019: 51 · 2018: 2 · 2015: 1 · 2014: 3 · 2013: 1
- FWCI
- 13.79
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Blood (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK065029)
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
- Health Sciences › Medicine › Emergency Medicine › Hematological disorders and diagnostics
- Keywords
- anemia of chronic disease, hepcidin, iron homeostasis, iron limitation, erythropoiesis, cytokines, erythropoietin, erythrocyte survival, iron deficiency, hyperferritinemia, hypoferremia, erythropoiesis-stimulating agents, iron therapy, chronic kidney disease, cancer
- MeSH terms
- Anemia, Humans, Inflammation, Prognosis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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