Abstract
Hepcidin is an essential iron regulatory protein encoded by human antimicrobial peptide gene. Structurally, hepcidin has three parts; the main structural framework, disulphide linkages and N-terminal region. Ferroportin, that allows the entry of iron into the blood, is degraded by hepcidin and inhibits this process. Transferrin receptor 1 and 2 play an important role along with hemochromatosis protein in sensing iron and increasing hepcidin expression. The role of hepcidin is instrumental in iron deficiency anemia. Iron-refractory iron deficiency anemia an autosomal recessive is associated with TMPRSS6 mutation that leads to increased concentration of serum hepcidin despite iron deficiency. In anemia of chronic disorder, hepcidin blocks the entry of iron from macrophages and duodenal enterocytes into blood, thus inhibiting the growth of microorganisms. In β-thalassemia major it has two effects; inhibitory and stimulatory. The inhibitory response is due to ineffective erythropoiesis and stimulatory response is due to multiple transfusions. In hereditary hemochromatosis type II hepcidin production is low due to gene mutation that leads to iron overload. This narrative review is compiled after relevant literature search from electronic databases. The key words used for searching relevant literature include iron, iron deficiency, iron deficiency anemia, iron metabolism, hepcidin, transferrin, causes of iron deficiency anemia and laboratory diagnosis of iron deficiency anemia. Reference hematology books were also consulted.

Key words: Hepcidin, iron deficiency anemia, iron, ferroportin