Abstract
Immune haemolytic anaemia (IHA) is characterized by an increased breakdown of red blood cells (RBCs) due to allo‐ or auto‐antibodies directed to RBC antigens with or without complement activation. Based on the nature of the antibodies, IHA can be divided in three main categories: autoimmune, drug‐induced and alloimmune‐mediated IHA. There is growing evidence that the innate immune system plays an important role in the pathogenesis of IHA. Complement‐mediated haemolysis with the subsequent release of cell‐free haemoglobin and cell‐free haem resulting in the generation of reactive oxygen species and cytotoxicity as well as the production of anaphylatoxins induce a systemic inflammatory response, which contributes to morbidity and mortality in IHA. The natural plasma scavengers of cell‐free haemoglobin and cell‐free haem, haptoglobin and hemopexin, respectively, are depleted in cases of chronic or severe IHA. The inducible enzyme haem oxygenase 1 (HO‐1) is an efficient cellular scavenger degrading haem into anti‐inflammatory products to partially limit haem‐mediated oxidative damage in cases of saturated scavenging capacity. Complement‐targeted therapy and the therapeutic replenishment of haptoglobin and hemopexin as well as the induction of HO‐1 expression might be suitable targets in the treatment of IHA.
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