LAUSR

The accelerated clearance of platelets is a central feature of immune thrombocytopenia (ITP) pathophysiology. The Harrington-Hollingsworth experiment provided evidence that accelerated platelet clearance may be due to factors present in ITP patient circulation. Harrington et al. demonstrated that the transfusion of ITP patient blood or plasma can produce a precipitous platelet count decrease in non-ITP recipients.1 It was hypothesized that circulating "thrombocytopenic factors" were responsible for the platelet count decreases and thus also in ITP.1 Overall, the transfusion of ITP blood or its plasma equivalent produced a >50% recipient platelet count decrease in 16 of 26 (61.5%) of such instances.2 Subsequent work by Shulman et al. provided more direct evidence that anti-platelet immunoglobulin G (IgG) autoantibodies are a thrombocytopenic factor in ITP.3 Anti-platelet autoantibodies are thought to opsonize platelets and trigger clearance by macrophage phagocytosis,4,5 particularly in the spleen which is the dominant site of platelet clearance in ITP.6 It is now appreciated that IgG autoantibodies in ITP target multiple platelet antigens including glycoprotein (GP)IIb/IIIa, GPIb/IX, GPV, and GPIa/IIa.7-10 More recently, it has been demonstrated that C-reactive protein can enhance the phagocytosis of blood cells such as erythrocytes11 and platelets,12 and may potentially be a thrombocytopenic factor in ITP.