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Anaemia of chronic disease (ACD), sometimes referred to as anaemia of inflammation, is the second most frequent type of anaemia after iron deficiency and is typically observed in people with chronic inflammatory, viral, malignant or autoimmune diseases. That’s because immunological stimulation leads to the release of cytokines (such as IL-6) that cause the liver to make more hepcidin. Hepcidin at high levels prevents iron absorption in the gut and sequesters iron in macrophages, causing a functional iron deficit in the presence of normal or increasing iron reserves. At the same time, inflammatory mediators down-regulate erythropoietin (EPO) production and degrade the marrow response to EPO and promote shortened red blood cell survival.

Clinically, ACD is frequently normocytic and normochromic (or weakly microcytic) with low serum iron, low transferrin/TIBC and normal to high ferritin – differentiating it from iron-deficient anaemia. Symptoms are usually modest (fatigue, weakness, pallor) and may be masked by the underlying condition.

Management is targeted at the underlying problem (e.g., treatment of infection, optimisation of autoimmune therapy, management of cancer or CKD). For substantial and symptomatic anaemia, choices are erythropoiesis-stimulating drugs (particularly in CKD or cancer) and, specifically, intravenous iron if there is a genuine or mixed deficiency. In difficult symptomatic situations, blood transfusion is reserved. New techniques are aimed at blocking hepcidin to restore iron mobilisation.