Hepcidin in turn causes increased internalisation of ferroportin molecules on cell membranes which prevents release from iron stores.
Before the recent discovery of hepcidin and its function in iron metabolism, anemia of chronic disease was seen as the result of a complex web of inflammatory changes.
Nonetheless, there are other mechanisms that also contribute to the lowering of hemoglobin levels during inflammation: (i) Inflammatory cytokines suppress the proliferation of erythroid precursors in the bone marrow.
;[9] (ii) inflammatory cytokines inhibit the release of erythropoietin (EPO) from the kidney; and (iii) the survival time of circulating red cells is shortened.
However, if inflammation continues, the effect of locking up iron stores is to reduce the ability of the bone marrow to produce red blood cells.
[citation needed] Because anemia of chronic disease can be the result of non-infective causes of inflammation, future research is likely to investigate whether hepcidin antagonists might be able to treat this problem.
[14] The risk of serious side effects such as bleeding, electrolyte depletion and cardiac arrest could be greater with ferric carboxymaltose therapy, however the certainty of this evidence is low.
[citation needed] Blood transfusion to patients with anemia of chronic disease is associated with a higher mortality, supporting the concept.