2. Immune Hemolytic Anemia
Immune Hemolytic Anemia (IHA) is characterized by destruction of red cells by antibodies acting against antigens on the erythrocyte membrane. Mediated by either IgG or IgM antibodies, IHA may be idiopathic, or secondary to infections, autoimmune diseases, lymphoproliferative disorders, or drugs. Patients present with anemia, reticulocytosis, indirect hyperbilirubinemia, elevated LDH with a positive Coombs test.
Drug-induced IHA may be associated with either drug-dependent or drug-independent antibodies [1]. Other drugs may cause nonimmunologic protein adsorption onto drug-treated red cells. With drug independent autoantibodies, typified by alpha-methyl DOPA, IHA can persist at length, even after the drug is withdrawn. IHA has been described with cephalosporins, nonsteroidal anti-inflammatory agents, levaquin, oxaliplatin, and teicoplanin, amongst others [1, 2].
Intravenous Rh (D) immune globulin, used for treatment of immune thrombocytopenic purpura in non-splenectomized Rh (D)-positive patients, intentionally induces a mild hemolysis, which likely accounts for its mechanism of action. However, severe hemolysis with renal insufficiency, disseminated intravascular coagulation, and death has been reported in a small number of cases [3].
Fludarabine, a purine nucleoside chemotherapeutic agent, has been reported to precipitate or exacerbate the auto-immune hemolytic anemia associated with chronic lymphocytic leukemia. However, combining fludarabine with rituximab and cyclophosphamide may reduce that risk [4].