Abstract
Hepcidin controls the systemic level of iron as well as the transfer of tissue iron by binding ferroportin to the iron exporter, which allows it to be depleted. Iron is an important element needed by all organisms because of its role in a range of critical cellular biochemical pathways such as DNA production and respiration. Iron is available to both host and pathogen during Mycobacterium tuberculosis (TB) infection. Tuberculosis may have an influence on the contagious result. Both the host and M. tuberculosis require iron, TB should be capable of trapping iron from the host, and the host must modify its iron spread in consequence to infection. This reallocation could act as a protection mechanism against some infectious agents. Even so, hepcidin exquisites the iron intracellular macrophage and the reticuloendothelial system as a protection mechanism for TB infection. Anemia of chronic disease (ACD) is anemia that occurs in acute or chronic immune disorders such as TB and is the second most common in iron deficiency anemia. Several research has reported the prevalence of anemia in patients with TB, and there is some indication that anemia in the diagnosis of TB is correlated with a higher risk of death, and it is also necessary to identify the factors that lead to TB-related anemia.