HEPCIDIN PADA ANEMIA OF CHRONIC DISEASE

Abstract

Anemia of chronic disease (ACD) induce dysregulation of iron homeostasis. A hallmark of anemia of chronic disease is the
development of disturbances of iron homeostasis, with increased uptake and retention of iron within cells of the
reticuloendothelial system (RES), that leads to a diversion of iron from the circulation into storage sites of RES, and decreased
intestinal iron absorption, subsequent limitation of the availability of iron for erythroid progenitor cells, and iron-restricted
erythropoiesis. A new small peptide called hepcidin was found. It is strongly suggest that hepcidin play role on the pathogenesis
of ACD. Hepcidin expression is induced by inflammation/infection (by lipopolysaccharide and interleukin-6) and iron overload
condition, it is strongly suggest that hepcidin induced dysregulation of iron homeostasis by inhibit iron efflux from macrophage
dan RES (causing iron retention in turn) and decrease intestinal iron absorption. In the aggregate, the increase of hepcidin
production suppress erythropoiesis by iron starvation strongly suggest that hepcidin is the key mediator of ACD. If hepcidin
follows the pattern of other peptide hormones or cytokines, its actions will be mediated by cell surface receptors. Elucidation of
the receptor and its transduction pathways should lead to the development of hepcidin antagonists, some of which could be useful
in treatment of ACD, along with it's underlying disease.