 Hepcidin is the master regulator of iron metabolism and hence, a modulator of anemia in states of inflammation. Hepcidin is an acute phase protein synthetised in the liver and which acts as an hyposideremia inducing hormone. It binds to ferroportin an iron exporter and prevents the release of iron from the cells: prevents the absorption of dietary iron from enterocytes and prevents iron release from macrophages, where it is stored. Thus, the effect of hepcidin would be iron sequestration, lowering the serum iron concentrations. The beneficial result would be a low availability of iron for bacterial growth thus, a direct antimicrobial effect and less oxidative stress. The detrimental result is the limited possibility for the synthesis of new haemoglobin molecules and the occurrence of anemia. The up-regulation of hepcidin, as a pro-inflammatory biomarker, characterises both acute and chronic inflammatory conditions. The induction of hepcidin synthesis may be the cause for the iron-restricted erythropoiesis in the surgical population and in patients with sepsis. The induction of hepcidin synthesis may contribute to the development of anemia, which is detrimental for tissue oxygenation and might increase transfusion requirements and the aggravation of immune suppression after blood transfusion. In animal models of anemia due to inflammation, hepcidin knockout mice had milder anemia and faster recovery. 