The relationship between anaemia and infection is complex. For example, it is important to distinguish between acute and chronic infection. In chronic infection, anaemia is usually mild or moderate and there is a common pathophysiological basis for the occurrence of anaemia in several chronic diseases, whether of an infectious, inflammatory or neoplastic nature (1). In the most frequent cases in which anaemia is associated with chronic infections the main underlying cause is an impaired release of iron by the reticuloendothelial system. This is brought on by the increased concentration of hepcidin – a regulatory hormone produced by liver cells – that rises with inflammation. Hepcidin induces the degradation of ferroportin, which is responsible for the transmembrane transfer of iron to plasma transferrin (2, 3).

When anaemia is present in acute infections, it can be due to several factors. The anaemia can be caused by the destruction of red blood cells (e.g. malaria) or it can be secondary to the inhibition of bone marrow erythropoiesis (e.g. parvovirus). Many other acute infections, both viral and bacterial, can cause anaemia through other mechanisms, such as mild idiopathic haemolysis (4). Moreover, the proliferative capability of many invasive pathogens is limited by the bioavailability of iron, and thus host defence strategies have evolved to sequester iron from invasive pathogens. Iron sequestration by ferritin in macrophages restricts iron availability for extracellular pathogens. The mechanism suppresses iron availability to erythropoietic progenitor cells by retaining iron inside the macrophages (5). The low plasma iron rapidly induces hypoferraemia and, as a consequence, decreased functional iron availability in the bone marrow, which leads to a decrease in the RET-He value and subsequently to the low-to-negative Delta-He value. The MicroR value – the percentage of microcytic red blood cells – would typically be normal-to-high since the proportion of microcytes would gradually rise due to iron-deficient erythropoiesis.

1. Marcos BV (2011): Anemia and infection: a complex relationship. Rev Bras Hematol Hemoter. 33(2): 90–92.
2. Darshan D et al. (2010): Severe iron deficiency blunts the response of the iron regulatory gene Hamp and pro-inflammatory cytokines to lipopolysaccharide. Haematologica. 95(10):1660-7.
3. Hentze MW et al. (2010): Two to tango: regulation of Mammalian iron metabolism. Cell. 142(1):24-38.
4. http://www.clinicaladvisor.com/hospital-medicine/infectious-hemolytic-anemias/article/601860/
5. Parrow NL et al. (2013): Sequestration and scavenging of iron in infection. Infect Immun. 81(10):3503-14.