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- W2005496663 endingPage "525" @default.
- W2005496663 startingPage "519" @default.
- W2005496663 abstract "In chronic inflammatory conditions increased endogenous release of specific cytokines (TNFα, IL-1, IL-6, IFNγ and others) is presumed. It has been shown that those of monocyte lineage play a key role in cytokine expression and synthesis. This may be associated with changes in iron metabolism and impaired erythropoiesis and may lead to development of anaemia in patients with rheumatoid arthritis. Firstly, increased synthesis of acute phase proteins, like ferritin, during chronic inflammation is proposed as the way by which the toxic effect of iron and thereby the synthesis of free oxy-radicals causing the damage on the affected joints, may be reduced. This is associated with a shift of iron towards the mononuclear phagocyte system which may participate in the development of anaemia of chronic disease. Secondly, an inhibitory action of inflammatory cytokines (TNFα, IL-1), on proliferation and differentiation of erythroid progenitors as well as on synthesis of erythropoietin has been shown, thereby also contributing to anaemia. Finally, chronic inflammation causes multiple, complex disturbances in the delicate physiologic equilibrium of interaction between cytokines and cells (erythroid progenitors, cells of mononuclear phagocyte system and erythropoietin producing cells) leading to development of anaemia of chronic disease (Fig. 1)." @default.
- W2005496663 created "2016-06-24" @default.
- W2005496663 creator A5004718384 @default.
- W2005496663 creator A5011248329 @default.
- W2005496663 creator A5031506026 @default.
- W2005496663 creator A5033811992 @default.
- W2005496663 date "1995-09-01" @default.
- W2005496663 modified "2023-09-27" @default.
- W2005496663 title "Interaction of inflammatory cytokines and erythropoeitin in iron metabolism and erythropoiesis in anaemia of chronic disease" @default.
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- W2005496663 doi "https://doi.org/10.1007/bf02208148" @default.
- W2005496663 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8549089" @default.