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__NOTOC__ | __NOTOC__ | ||
{{Anemia of chronic disease}} | {{Anemia of chronic disease}} | ||
{{CMG}} {{AE}}{{OK}} | {{CMG}} {{shyam}} {{AE}}{{OK}} | ||
==Overview== | ==Overview== | ||
Inflammatory [[cytokines]] induce increased amounts of [[hepcidin]] by the liver. Hepcidin blocks [[ferroportin]] from releasing iron from the body stores. Inflammatory [[cytokines]] also decrease [[ferroportin]] expression and stops [[erythropoiesis]] by increasing bone marrow [[erythropoietin]] resistance. Apart from [[iron]] sequestration, [[white blood cells]] production is promoted by inflammatory [[cytokines]]. [[Bone marrow]] [[stem cells]] produce both [[red blood cells]] and [[white blood cells]] [[Stem cells|cells]]. Therefore, the upregulation of [[white blood cells]] causes fewer [[stem cells]] to differentiate into [[red blood cells]]. This may also have a role in inhibition of [[erythropoiesis]] ,even when [[erythropoietin]] levels are normal, and aside from the effects of [[hepcidin]]. | Inflammatory [[cytokines]] induce increased amounts of [[hepcidin]] by the liver. Hepcidin blocks [[ferroportin]] from releasing iron from the body stores. Inflammatory [[cytokines]] also decrease [[ferroportin]] expression and stops [[erythropoiesis]] by increasing bone marrow [[erythropoietin]] resistance. Apart from [[iron]] sequestration, [[white blood cells]] production is promoted by inflammatory [[cytokines]]. [[Bone marrow]] [[stem cells]] produce both [[red blood cells]] and [[white blood cells]] [[Stem cells|cells]]. Therefore, the upregulation of [[white blood cells]] causes fewer [[stem cells]] to differentiate into [[red blood cells]]. This may also have a role in inhibition of [[erythropoiesis]], even when [[erythropoietin]] levels are normal, and aside from the effects of [[hepcidin]]. | ||
==Pathophysiology== | ==Pathophysiology== | ||
| Line 10: | Line 10: | ||
* Apart from iron sequestration, white blood cells production is promoted by inflammatory cytokines. [[Bone marrow]] stem cells produce both [[red blood cells]] and [[white blood cells]] [[stem cells|cells]]. Therefore, the upregulation of [[white blood cells]] causes fewer [[stem cells]] to differentiate into [[red blood cells]]. This may also have a role in inhibition of [[erythropoiesis]] , even when [[erythropoietin]] levels are normal, and aside from the effects of hepcidin.<ref name="pmid11861275">{{cite journal |vauthors=Papadaki HA, Kritikos HD, Gemetzi C, Koutala H, Marsh JC, Boumpas DT, Eliopoulos GD |title=Bone marrow progenitor cell reserve and function and stromal cell function are defective in rheumatoid arthritis: evidence for a tumor necrosis factor alpha-mediated effect |journal=Blood |volume=99 |issue=5 |pages=1610–9 |date=March 2002 |pmid=11861275 |doi= |url=}}</ref><ref name="pmid12091338">{{cite journal |vauthors=Papadaki HA, Kritikos HD, Valatas V, Boumpas DT, Eliopoulos GD |title=Anemia of chronic disease in rheumatoid arthritis is associated with increased apoptosis of bone marrow erythroid cells: improvement following anti-tumor necrosis factor-alpha antibody therapy |journal=Blood |volume=100 |issue=2 |pages=474–82 |date=July 2002 |pmid=12091338 |doi=10.1182/blood-2002-01-0136 |url=}}</ref> | * Apart from iron sequestration, white blood cells production is promoted by inflammatory cytokines. [[Bone marrow]] stem cells produce both [[red blood cells]] and [[white blood cells]] [[stem cells|cells]]. Therefore, the upregulation of [[white blood cells]] causes fewer [[stem cells]] to differentiate into [[red blood cells]]. This may also have a role in inhibition of [[erythropoiesis]] , even when [[erythropoietin]] levels are normal, and aside from the effects of hepcidin.<ref name="pmid11861275">{{cite journal |vauthors=Papadaki HA, Kritikos HD, Gemetzi C, Koutala H, Marsh JC, Boumpas DT, Eliopoulos GD |title=Bone marrow progenitor cell reserve and function and stromal cell function are defective in rheumatoid arthritis: evidence for a tumor necrosis factor alpha-mediated effect |journal=Blood |volume=99 |issue=5 |pages=1610–9 |date=March 2002 |pmid=11861275 |doi= |url=}}</ref><ref name="pmid12091338">{{cite journal |vauthors=Papadaki HA, Kritikos HD, Valatas V, Boumpas DT, Eliopoulos GD |title=Anemia of chronic disease in rheumatoid arthritis is associated with increased apoptosis of bone marrow erythroid cells: improvement following anti-tumor necrosis factor-alpha antibody therapy |journal=Blood |volume=100 |issue=2 |pages=474–82 |date=July 2002 |pmid=12091338 |doi=10.1182/blood-2002-01-0136 |url=}}</ref> | ||
* However, the combined effects of all the process are likely be in favor as it will allow the body to keep iron away from [[bacteria]] while the body boost the [[immune cell]] production.<ref name="pmid16434484">{{cite journal |vauthors=Theurl I, Mattle V, Seifert M, Mariani M, Marth C, Weiss G |title=Dysregulated monocyte iron homeostasis and erythropoietin formation in patients with anemia of chronic disease |journal=Blood |volume=107 |issue=10 |pages=4142–8 |date=May 2006 |pmid=16434484 |doi=10.1182/blood-2005-08-3364 |url=}}</ref><ref name="pmid15758012">{{cite journal |vauthors=Weiss G, Goodnough LT |title=Anemia of chronic disease |journal=N. Engl. J. Med. |volume=352 |issue=10 |pages=1011–23 |date=March 2005 |pmid=15758012 |doi=10.1056/NEJMra041809 |url=}}</ref> | * However, the combined effects of all the process are likely be in favor as it will allow the body to keep iron away from [[bacteria]] while the body boost the [[immune cell]] production.<ref name="pmid16434484">{{cite journal |vauthors=Theurl I, Mattle V, Seifert M, Mariani M, Marth C, Weiss G |title=Dysregulated monocyte iron homeostasis and erythropoietin formation in patients with anemia of chronic disease |journal=Blood |volume=107 |issue=10 |pages=4142–8 |date=May 2006 |pmid=16434484 |doi=10.1182/blood-2005-08-3364 |url=}}</ref><ref name="pmid15758012">{{cite journal |vauthors=Weiss G, Goodnough LT |title=Anemia of chronic disease |journal=N. Engl. J. Med. |volume=352 |issue=10 |pages=1011–23 |date=March 2005 |pmid=15758012 |doi=10.1056/NEJMra041809 |url=}}</ref> | ||
* Sometimes, [[HIV]] infection and chronic kidney disease can lead to [[inflammation]] that can ultimately produce [[cytokines]] that can cause [[anemia of chronic disease]] | * Sometimes, [[HIV]] infection and chronic kidney disease can lead to [[inflammation]] that can ultimately produce [[cytokines]] that can cause [[anemia of chronic disease]]. | ||
=== '''Cytokines''' === | === '''Cytokines''' === | ||
Latest revision as of 23:03, 29 November 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Shyam Patel [2] Associate Editor(s)-in-Chief: Omer Kamal, M.D.[3]
Overview
Inflammatory cytokines induce increased amounts of hepcidin by the liver. Hepcidin blocks ferroportin from releasing iron from the body stores. Inflammatory cytokines also decrease ferroportin expression and stops erythropoiesis by increasing bone marrow erythropoietin resistance. Apart from iron sequestration, white blood cells production is promoted by inflammatory cytokines. Bone marrow stem cells produce both red blood cells and white blood cells cells. Therefore, the upregulation of white blood cells causes fewer stem cells to differentiate into red blood cells. This may also have a role in inhibition of erythropoiesis, even when erythropoietin levels are normal, and aside from the effects of hepcidin.
Pathophysiology
- Inflammatory cytokines induce increased amounts of hepcidin by the liver. Hepcidin blocks ferroportin from releasing iron from the body stores.[1][2][3]
- Inflammatory cytokines also decrease ferroportin expression and stops erythropoiesis by increasing bone marrow erythropoietin resistance.[4][5]
- Apart from iron sequestration, white blood cells production is promoted by inflammatory cytokines. Bone marrow stem cells produce both red blood cells and white blood cells cells. Therefore, the upregulation of white blood cells causes fewer stem cells to differentiate into red blood cells. This may also have a role in inhibition of erythropoiesis , even when erythropoietin levels are normal, and aside from the effects of hepcidin.[6][7]
- However, the combined effects of all the process are likely be in favor as it will allow the body to keep iron away from bacteria while the body boost the immune cell production.[5][8]
- Sometimes, HIV infection and chronic kidney disease can lead to inflammation that can ultimately produce cytokines that can cause anemia of chronic disease.
Cytokines
Activated monocytes release cytokines like the interleukins (eg, IL-1 and IL-6) and tumor necrosis factor (TNF-alpha). These cytokines activate a cascade of reactions leading to the secretion of interferon (IFN)-beta and IFN-gamma by T lymphocytes leading to increased resistance of bone marrow to EPO.[9][10]
Hepcidin
Hepcidin is directly involved in iron metabolism and a component of the innate immune response to acute infection. It decreases the absorption of iron from small intestine, from placenta and from macrophages as well, secondary to its effect on internalization and degradation of the iron export protein ferroportin.[11][12][13][14]
References
- ↑ Means RT, Krantz SB (October 1992). "Progress in understanding the pathogenesis of the anemia of chronic disease". Blood. 80 (7): 1639–47. PMID 1391934.
- ↑ Roy CN (2010). "Anemia of inflammation". Hematology Am Soc Hematol Educ Program. 2010: 276–80. doi:10.1182/asheducation-2010.1.276. PMID 21239806.
- ↑ Moldawer LL, Marano MA, Wei H, Fong Y, Silen ML, Kuo G, Manogue KR, Vlassara H, Cohen H, Cerami A (March 1989). "Cachectin/tumor necrosis factor-alpha alters red blood cell kinetics and induces anemia in vivo". FASEB J. 3 (5): 1637–43. PMID 2784116.
- ↑ Means RT (July 1999). "Advances in the anemia of chronic disease". Int. J. Hematol. 70 (1): 7–12. PMID 10446488.
- ↑ 5.0 5.1 Theurl I, Mattle V, Seifert M, Mariani M, Marth C, Weiss G (May 2006). "Dysregulated monocyte iron homeostasis and erythropoietin formation in patients with anemia of chronic disease". Blood. 107 (10): 4142–8. doi:10.1182/blood-2005-08-3364. PMID 16434484.
- ↑ Papadaki HA, Kritikos HD, Gemetzi C, Koutala H, Marsh JC, Boumpas DT, Eliopoulos GD (March 2002). "Bone marrow progenitor cell reserve and function and stromal cell function are defective in rheumatoid arthritis: evidence for a tumor necrosis factor alpha-mediated effect". Blood. 99 (5): 1610–9. PMID 11861275.
- ↑ Papadaki HA, Kritikos HD, Valatas V, Boumpas DT, Eliopoulos GD (July 2002). "Anemia of chronic disease in rheumatoid arthritis is associated with increased apoptosis of bone marrow erythroid cells: improvement following anti-tumor necrosis factor-alpha antibody therapy". Blood. 100 (2): 474–82. doi:10.1182/blood-2002-01-0136. PMID 12091338.
- ↑ Weiss G, Goodnough LT (March 2005). "Anemia of chronic disease". N. Engl. J. Med. 352 (10): 1011–23. doi:10.1056/NEJMra041809. PMID 15758012.
- ↑ Boutou AK, Pitsiou GG, Stanopoulos I, Kontakiotis T, Kyriazis G, Argyropoulou P (July 2012). "Levels of inflammatory mediators in chronic obstructive pulmonary disease patients with anemia of chronic disease: a case-control study". QJM. 105 (7): 657–63. doi:10.1093/qjmed/hcs024. PMID 22355163.
- ↑ Raj DS (April 2009). "Role of interleukin-6 in the anemia of chronic disease". Semin. Arthritis Rheum. 38 (5): 382–8. doi:10.1016/j.semarthrit.2008.01.006. PMID 18336871.
- ↑ Nemeth E, Valore EV, Territo M, Schiller G, Lichtenstein A, Ganz T (April 2003). "Hepcidin, a putative mediator of anemia of inflammation, is a type II acute-phase protein". Blood. 101 (7): 2461–3. doi:10.1182/blood-2002-10-3235. PMID 12433676.
- ↑ Armitage AE, Eddowes LA, Gileadi U, Cole S, Spottiswoode N, Selvakumar TA, Ho LP, Townsend AR, Drakesmith H (October 2011). "Hepcidin regulation by innate immune and infectious stimuli". Blood. 118 (15): 4129–39. doi:10.1182/blood-2011-04-351957. PMID 21873546.
- ↑ Ganz T (April 2011). "Hepcidin and iron regulation, 10 years later". Blood. 117 (17): 4425–33. doi:10.1182/blood-2011-01-258467. PMC 3099567. PMID 21346250.
- ↑ Drakesmith H, Prentice AM (November 2012). "Hepcidin and the iron-infection axis". Science. 338 (6108): 768–72. doi:10.1126/science.1224577. PMID 23139325.