Iron is an essential element for human and bacteria, including mycobacterium tuberculosis. Over review includesthe literature on the problem of iron metabolism in patients with tuberculosis and with comorbid pathology HIV infection and tuberculosis. The literature was searched for when writing this review using the RSCI, CyberLeninka, Scopus, Web of Science, MedLine, PubMed databases using the following keywords: iron, ferritin, hepsidin, lactoferrin, tuberculosis, pneumonia, HIV infection. Iron compounds are involved in many redox reactions: oxygen transport, cellular respiration, the trichloroacetic acid cycle, DNA biosynthesis, and others. The ratio of intracellular and extracellular iron in the body is regulated by the low molecular weight hormone hepcidin, the mechanism of action of which is to block the function of ferroportin, an exporter of iron from cells, which leads to the accumulation of the intracellular iron pool and the prevention of the toxic effect of free iron. The role of iron in the interaction of the human body with ferro-dependent bacteria has been established. Iron is necessary for the growth and development of bacterial cells, and the methods for its production from the host are different. Information on the effect of iron metabolism on pulmonary tuberculosis is scarce and contradictory: some authors have identified a decrease in hemoglobin and transferrin in combination with elevated levels of ferritin in patients with tuberculosis; according to other sources, hyperferritinemia in tuberculosis cannot be predictive, but is a marker inflammation. At the same time, there are studies that indicate a significant increase in ferritin in patients with disseminated tuberculosis relative to other clinical forms. Currently, the incidence of tuberculosis in patients with HIV infection is increasing, while diagnostic tests are not very informative. The search for diagnostic markers in terms of iron metabolism may open up new possibilities for the diagnosis of pulmonary tuberculosis.