What is the role of intravenous immunoglobulin (IVIG) in the treatment of ITP?

Updated: Jul 05, 2018
  • Author: Jessica Katz, MD, PhD, FACP; Chief Editor: Emmanuel C Besa, MD  more...
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Platelet destruction occurs in the spleen. The spleen contains large numbers of Fc receptor (Fc-gamma-R)–bearing phagocytic cells, such as monocytes and macrophages. These cells can bind and destroy opsonized platelets. Although platelets are destroyed in many different organs, splenectomy is a successful treatment for many cases of ITP. In 1982, Fehr et al demonstrated that in cases of ITP without splenectomy, the infusion of IVIG prolonged the clearance of radiolabeled, antibody-sensitized RBCs in vivo. [31]

In 1983, Salama et al suggested that the success of IVIG in the treatment of ITP was due to competitive inhibition of Fc receptors on phagocytic cells within the reticuloendothelial system by sensitized erythrocytes. [32] Possible mechanisms that underlie this are (1) IVIG dimers and multimers, which are present in low but significant levels in preparations of IVIG, bind to Fc receptors and block platelet clearance and (2) IVIG contains IgG molecules that have a multitude of host antigenic reactivities. These IgG molecules likely bind to host antigens, form immune complexes, and compete with antibody-sensitized platelets for Fc receptors in the reticuloendothelial system, resulting in prolonged platelet survival. [33]

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