Hepcidin as a biochemical parameter for the assessment of iron deficiency anemia

Iron deficiency anemia is the most prevalent nutritional disorder in the world. Information on the metabolism of hepcidin and its possible significance as a biochemical parameter in iron deficiency anemia is reported in this review, which was based on a survey of the databases PubMed and LILACS for articles published between 2006 and 2010 on hepcidin as a biomarker for the regulation of iron metabolism. The literature search returned 35 studies published in international journals and one study on the subject in a Brazilian journal. Hepcidin production is homeostatically regulated by anemia and hypoxia. When oxygen delivery is inadequate, hepcidin levels decrease. Consequently, more iron is made available from the diet and from the storage pool in macrophages and hepatocytes. Hepcidin binds to ferroportin, regulating iron release into plasma. When hepcidin concentrations are low, ferroportin molecules are displayed on the plasma membrane and release iron. When hepcidin levels increase, hepcidin binds to ferroportin molecules inducing their internalization and degradation, and iron release is decreased progressively. Apparently, the development of diagnosis and therapy for anemia based on the bioindicator hepcidin may provide a more effective approach. Epidemiological studies are needed to demonstrate the relevance of hepcidin to the differential diagnosis of anemia, including sampling protocols for analysis, with standardization similar to that used in other biochemical assessments, and establishment of cutoff points for urinary and plasma expression of this peptide.