The most common<unk>  isotype involved in<unk>  is IgG, though sometimes IgA is found. The IgG<unk> es attach to a red blood cell, leaving their FC portion exposed with maximal reactivity at 37 °C (versus cold<unk>  induced<unk>  anemia whose<unk> es only bind red blood cells at low body temperatures, typically 28-31 °C). The FC region is recognized and grabbed onto by FC receptors found on monocytes and macrophages in the spleen. These cells will pick off portions of the red cell membrane, almost as if they are taking a bite. The loss of membrane causes the red blood cells to become spherocytes. Spherocytes are not as flexible as normal RBCs and will be singled-out for destruction in the red pulp of the spleen as well as other portions of the reticuloendothelial system. The red blood cells trapped in the spleen cause the spleen to enlarge, leading to the splenomegaly often seen in these patients. There are two models for this: the hapten model and the autoantibody model. The hapten model proposes that certain drugs, especially penicillin and cephalosporins, will bind to certain proteins on the red cell membrane and act as haptens (small molecules that can elicit an immune response only when attached to a large carrier such as a protein; the carrier may be one that also does not elicit an immune response by itself).<unk> es are created against the protein-drug complex, leading to the destructive sequence described above. The autoantibody model proposes that, through a mechanism not yet understood, certain drugs will cause<unk> es to be made against red blood cells which again leads to the same destructive sequence. It is possible for it to occur in an immunocompromised patient.
Warm antibody autoimmune hemolytic anemia
Cold autoimmune hemolytic anemia
Donath–Landsteiner hemolytic anemia
Mixed autoimmune hemolytic anemia
Auberger's blood group
symptom of Congenital dyserythropoietic anemia
Twin anemia-polycythemia sequence
Drug reaction with eosinophilia and systemic symptoms