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.

A hepcidina como parâmetro bioquímico na avaliação da anemia por deficiência de ferro / Hepcidin as a biochemical parameter for the assessment of iron deficiency anemia

A anemia por deficiência de ferro caracteriza-se como o mais prevalente problema nutricional em todo o mundo. Nesta revisão reuniu-se informações a respeito do metabolismo da hepcidina, avaliando-se seu valor como parâmetro bioquímico na anemia por deficiência de ferro. Realizou-se um levantamento bibliográfico nas bases de dados PUBMED e LILACS, período 2006-2010, referentes à hepcidina como um biomarcador para a regulação do metabolismo do ferro. Foram localizados 35 estudos publicados em revistas internacionais e um estudo sobre o assunto em revista nacional. A produção de hepcidina é regulada homeostaticamente pela anemia e hipóxia. Quando a oferta de oxigênio está inadequada ocorre diminuição do nível de hepcidina. Consequentemente, maior quantidade de ferro proveniente da dieta e dos estoques dos macrófagos e hepatócitos se tornam disponíveis. A hepcidina possui a função de se ligar à ferroportina, regulando a liberação do ferro para o plasma. Quando as concentrações de hepcidina estão baixas, as moléculas de ferroportina são expostas na membrana plasmática e liberam o ferro. Quando os níveis de hepcidina aumentam, a hepcidina liga-se às moléculas de ferroportina induzindo sua internalização e degradação, e o ferro liberado diminui progressivamente. Aparentemente o desenvolvimento do diagnóstico e terapia da anemia baseados no bioindicador hepcidina pode oferecer uma abordagem mais efetiva. Estudos epidemiológicos são necessários para comprovar o valor da hepcidina no diagnóstico diferencial das anemias, incluindo protocolos de amostragem para análise, com padronização similar às utilizadas em outras avaliações bioquímicas, e estabelecimento de pontos de corte para a expressão urinária e plasmática desse peptídeo.

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.