[Anemia during inflammatory processes: pathogenesis and clinical and morphological manifestations]

Abstract

The review sums up the results of the current stage of studying the so-called anemia of inflammation (AI). The key mediator of AI is the polypeptide hepatic hormone hepcidin, the hepatocytic secretion of which is initiated by proinflammatory macrophageal cytokines (IL-6, IL-lalpha, and tumor necrosis factor-alpha) and T-lymphocyte gamma-interferon. Hepcidin has bactericidal properties and promotes iron retention in the enterocytes, macrophages, and hepatocytes through the internalization and degradation of ferroportin (a cell iron exporter into the plasma). The limited iron availability to microorganisms in AI is aimed at enhancing the body's natural resistance to infection. Therefore, AI serves as an example of fundamental reactions of innate immunity. The latent and manifest phases of AI can be identified. The major clinical and morphological manifestations of AI are a decreased functional iron stores and hepatic and splenic hemosiderosis.