Anemia of chronic disease pathophysiology: Difference between revisions
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==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]]. | |||
==Pathophysiology== | ==Pathophysiology== | ||
* Inflammatory [[cytokines]] induce increased amounts of [[hepcidin]] by the liver. Hepcidin blocks [[ferroportin]] from releasing iron from the body stores.<ref name="pmid1391934">{{cite journal |vauthors=Means RT, Krantz SB |title=Progress in understanding the pathogenesis of the anemia of chronic disease |journal=Blood |volume=80 |issue=7 |pages=1639–47 |date=October 1992 |pmid=1391934 |doi= |url=}}</ref><ref name="pmid21239806">{{cite journal |vauthors=Roy CN |title=Anemia of inflammation |journal=Hematology Am Soc Hematol Educ Program |volume=2010 |issue= |pages=276–80 |date=2010 |pmid=21239806 |doi=10.1182/asheducation-2010.1.276 |url=}}</ref><ref name="pmid2784116">{{cite journal |vauthors=Moldawer LL, Marano MA, Wei H, Fong Y, Silen ML, Kuo G, Manogue KR, Vlassara H, Cohen H, Cerami A |title=Cachectin/tumor necrosis factor-alpha alters red blood cell kinetics and induces anemia in vivo |journal=FASEB J. |volume=3 |issue=5 |pages=1637–43 |date=March 1989 |pmid=2784116 |doi= |url=}}</ref> | * Inflammatory [[cytokines]] induce increased amounts of [[hepcidin]] by the liver. Hepcidin blocks [[ferroportin]] from releasing iron from the body stores.<ref name="pmid1391934">{{cite journal |vauthors=Means RT, Krantz SB |title=Progress in understanding the pathogenesis of the anemia of chronic disease |journal=Blood |volume=80 |issue=7 |pages=1639–47 |date=October 1992 |pmid=1391934 |doi= |url=}}</ref><ref name="pmid21239806">{{cite journal |vauthors=Roy CN |title=Anemia of inflammation |journal=Hematology Am Soc Hematol Educ Program |volume=2010 |issue= |pages=276–80 |date=2010 |pmid=21239806 |doi=10.1182/asheducation-2010.1.276 |url=}}</ref><ref name="pmid2784116">{{cite journal |vauthors=Moldawer LL, Marano MA, Wei H, Fong Y, Silen ML, Kuo G, Manogue KR, Vlassara H, Cohen H, Cerami A |title=Cachectin/tumor necrosis factor-alpha alters red blood cell kinetics and induces anemia in vivo |journal=FASEB J. |volume=3 |issue=5 |pages=1637–43 |date=March 1989 |pmid=2784116 |doi= |url=}}</ref> | ||
* Inflammatory cytokines also decrease [[ferroportin]] expression and stops [[erythropoiesis]] by increasing bone marrow [[erythropoietin]] resistance.<ref name="pmid10446488">{{cite journal |vauthors=Means RT |title=Advances in the anemia of chronic disease |journal=Int. J. Hematol. |volume=70 |issue=1 |pages=7–12 |date=July 1999 |pmid=10446488 |doi= |url=}}</ref><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> | * Inflammatory [[cytokines]] also decrease [[ferroportin]] expression and stops [[erythropoiesis]] by increasing [[bone marrow]] [[erythropoietin]] resistance.<ref name="pmid10446488">{{cite journal |vauthors=Means RT |title=Advances in the anemia of chronic disease |journal=Int. J. Hematol. |volume=70 |issue=1 |pages=7–12 |date=July 1999 |pmid=10446488 |doi= |url=}}</ref><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> | ||
* 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]] | ||
==References== | ==References== | ||
Revision as of 18:03, 28 September 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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
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.