Iron deficiency anemia is the most prevalent nutritional problem in the world. Information on the metabolism of hepcidin and its possible significance as a biochemical parameter for assessment of iron deficiency anemia is reported in this review. A literature review was carried out in the databases PubMed and LILACS, between 2006-2010, assessing hepcidin as a parameter for the regulation of iron metabolism. During this period 35 studies were published in international journals and one study in a Brazilian journal. The production of hepcidin is homeostatically regulated by anemia and hypoxia. When oxygen supply is inadequate the level of hepcidin decreases. Therefore, more iron from the diet and from the stock of macrophages and hepatocytes becomes available. Hepcidin links to ferroportin, regulating iron release to plasma. When the hepcidin concentrations are low, the molecules of ferroportin are exposed on the plasmatic membrane and release iron. When hepcidin levels increase, hepcidin binds to molecules of ferroportin inducing its internalization and degradation and iron release gradually decreases. Apparently, development of diagnosis and therapy for anemia based on the parameter hepcidin may provide a more effective approach. Large-studies are needed to demonstrate the importance of hepcidin for the differential diagnosis of anemia, including sample protocols for analysis, with standards similar to those used in other biochemical evaluations, as well as the definition of cut-off points for the plasma and urinary expression of this peptide.
Anemia; Iron; Parameters
