ABSTRACT
Immunoglobulin preparations extracted from human blood have been used since the early 1950s to treat immunodeficiency diseases1. Intravenous immunoglobulin (IVIG) therapy has also been shown to be effective in treating immune deficiency states2,3, bacterial/viral infections4 and immune regulatory disorders, particularly immunohematological disorders such as autoimmune neutropenia, autoimmune hemolytic anemia and autoimmune thrombocytopenia5-7. While the mechanisms of action of the antiinflammatory nature of IVIG are complex and not fully elucidated, several theories have been postulated. In autoimmune thrombocytopenic purpura (AITP), four non-mutually exclusive major theories have evolved to explain IVIG’s mechanism(s) of action. First, IVIG may cause competitive reticuloendothelial system (RES) blockade of activating Fc receptors on macrophages8; second, IVIG may act through interactions with the inhibitory FcγRIIB which result in paralysis of phagocytes9; third, IVIG may initiate FcγR-mediated cytokine alterations which shut off RES function10; and/or fourth, antiidiotypic antibodies present in IVIG may neutralize/regulate antiplatelet autoantibodies11. This chapter focuses primarily on these four theories, and discusses how different IVIG products can utilize both FcγR-and non-FcγR-mediated events to affect platelet counts.
