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Editorial
. 2010 Feb;95(2):175-8.
doi: 10.3324/haematol.2009.017046.

Pathogenesis and treatment of anemia in inflammatory bowel disease

Günter Weiss, Christoph Gasche
Editorial

Pathogenesis and treatment of anemia in inflammatory bowel disease

Günter Weiss et al. Haematologica. 2010 Feb.
No abstract available

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Figures

Figure 1.
Figure 1.
Pathophysiological mechanisms contributing to anemia in patients with IBD. Cytokines induce the formation of hepcidin which then blocks cellular iron (Fe2+) export via ferroportin (FPN) from macrophages and inhibits the transfer of absorbed iron from enterocytes to the circulation. This results in a reduction of circulating iron and limited availability of the metal for erythroid progenitors, thus blocking erythropoiesis. Cytokines, such as tumor necrosis factor (TNF)-agr; and interferon (IFN)-γ, also aggravate iron restriction in macrophages by stimulating iron uptake and promoting erythrophagocytosis while inhibiting iron export via repression of ferroportin transcription. In addition, TNF-α further contributes to blockage of iron absorption. Iron deficiency can also be aggravated by chronic blood loss from intestinal lesions caused by active IBD. Erythropoiesis is further impaired as a consequence of a cytokine-mediated reduction of the formation and/or the biological activity of erythropoeitin (Epo) along with direct anti-proliferative effects of these cytokines on erythroid progenitor cells. Finally, vitamin deficiencies can impair erythroid differentiation.
See this image and copyright information in PMC

Comment on

References

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