Haema 2016; 7(3): 259-266
by Photis Beris
Professor of Haematology, Medical School, University of Geneva, Switzerland & Medical School, National and Kapodistrian University of Athens, Greece and Head of Haematology Department, UNILABS Coppet, Switzerland
Abstract
Iron absorption is done in the duodenum by DMT1 and ferroportin. The last one is also participating in the liberation of iron from the iron stores (macrophages). Regulation of absorption/liberation of iron is based on the levels of serum hepcidin. High hepcidin leads in decreased absorption/liberation of iron, while decreased hepcidin leads to increased iron absorption/liberation. Hepcidin is produced (mainly) in the liver. Regulation of hepcidin’s gene expression is done by iron stores (positive regulation), by the degree of inflammation (positive regulation) and by the degree of erythropoiesis (negative regulation). Recently erythroferrone has been described as the liaison between erythropoiesis and hepcidin secretion. Knowing almost in total the extracellular homeostasis of iron, we understood at a molecular level the basis of the 5 different forms of familial hemochromatosis, we described new hereditary diseases of the blood and we start developing new drugs against some, rather common forms of anemia.