The role of hepcidin in iron metabolism in inflammatory bowel diseases

Abstract

Hepcidin is a 25-amino-acid peptide synthesized predominantly in hepatocytes, which plays an essential role in the regulation of systemic iron homeostasis. As a result of inflammation, hepcidin binds to ferroportin resulting in its internalization and degradation in enterocytes and macrophages. Thus iron is trapped in both enterocytes and macrophages, leading to functional hypoferremia. In iron deficiency or enhanced erythropoiesis, hepcidin expression is reduced. That fact results in increase of iron absorption and releasing iron storage from macrophages. The discovery of the biological properties of hepcidin clarified the relationship between iron homeostasis, immune response, and anaemia of chronic disease. Anaemia is the most common extra intestinal manifestation of inflammatory bowel disease. Anaemia significantly reduces the quality-of-life among patients and can lead to a number of serious complications, even life-threatening. The main types of anaemia in inflammatory bowel diseases are iron deficiency anaemia and anaemia of chronic disease. These two types of anaemia coexist commonly. The key issue is differentiation these types of anaemia to implement a proper management. Commonly used parameters as iron concentration, ferritin and transferrin, are rather unreliable indices for the evaluation of anaemia in inflammatory bowel diseases. In recent studies the important role of hepcidin as a potential alternative marker of anemia and iron status has been shown. Moreover, there are data that antihepcidin treatment may be an effective treatment of anaemia of chronic disease in inflammatory bowel disease. This paper presents hepcidin structure, mechanism of action and regulation, and highlights hepcidin function in anaemia in inflammatory bowel disease.