Objective – to study the features of iron metabolism and the pathogenetic mechanisms of anemia development in rheumatoid arthritis. Methods. The studies were conducted in 121 women with anemia in rheumatoid arthritis. The control group consisted of 79 practically healthy women. The study included an assessment of peripheral blood parameters, iron metabolism parameters (serum iron, total iron binding capacity, latent iron binding capacity, transferrin saturation coefficient), acute phase inflammatory proteins (CRP, α1-acid glycoprotein, neopterin). The assessment of iron reserves was carried out by the level of serum ferritin, which was studied by the enzyme immunoassay using test systems. The content of hepcidin-25 was determined by the enzyme immunoassay using test systems. The concentration of cytokines (IL-6, TNF-α, IFN-γ) was determined on a Lazurite enzyme immunoassay analyzer. Results.The revealed anemia in RA patients was hypochromic, microcytic with reduced serum iron levels against a background of high ferritin content. In the study of hepcidin, its high level was determined, correlating with the level of pro-inflammatory cytokines (IL6, TNF-α, IFN-γ). Conclusions. Induced by pro-inflammatory cytokines, hepcidin promotes increased iron sequestration in macrophages, disrupting iron export from cells by blocking the activity of the ferroportin protein. The modulation of the biological activity of hepcidin, which is a key factor in the regulation of iron homeostasis, causes the formation of anemic syndrome in RA. Anemia in RA occurs as a result of functional iron deficiency, as opposed to true iron deficiency in iron deficiency anemia.