Anemia of Inflammation – Pathophysiology

Pathophysiology of anemia of inflammation. Systemic inflammation results in the release of multiple inflammatory cytokines (especially interleukin-6) from cells of the immune system, which stimulate hepcidin production by liver hepatocytes. Hepcidin binds to the only known transmembrane iron exporter, ferroportin, causing cellular ferroportin internalization and degradation. As a result, the iron efflux ferroportin “gates” are shut closed, resulting in reduced delivery of iron into the circulation from duodenal enterocytes (dietary iron) and tissue macrophages (iron from breakdown of senescent red blood cells). Impaired dietary iron absorption and retention of iron in macrophages cause decreased iron delivery for erythropoiesis. Other less important mechanisms underlying anemia for inflammation include inflammatory suppression of erythropoietic activity and decreased red cell survival (not shown). Learn more here.
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