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Abstract |
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Intravenous immunoglobulin (IVIG) has been an important therapy of immune thrombocytopenic purpura (ITP) for more than 20 years; however, questions still remain regarding the mechanisms of IVIG action in ITP. Recent reviews have focused on the hypotheses that IVIG effects are mediated via inhibition of Fc-receptor mediated platelet phagocytosis, suppression of anti-platelet antibody production, and anti-idiotypic inhibition of anti-platelet antibodies; however, new research suggests that a significant portion of IVIG benefit may be due to IVIGmediated acceleration of the elimination of anti-platelet antibodies. It is anticipated that promising new therapies of ITP, and other autoimmune conditions, will be developed based on a better understanding of IVIG mechanism of action. |