Inhibitory effects of high doses of intravenous gamma-globulin on platelet interaction with the vessel wall in Kawasaki disease.

Clinical effects of high-dose gamma-globulin therapy in Kawasaki disease have been evaluated from the viewpoints of its inhibitory effects on platelet adhesion and thrombus formation on the vessel wall. Platelet adhesion to the subendothelium is the fist step of thrombosis as well as platelet interaction with the vessel wall, which can be observed experimentally by Baumgartner's method. Twelve patients with Kawasaki disease treated with intact intravenous gamma-globulin (IVGG) showed decreased platelet adhesion in contrast to ten patients treated with only aspirin (ASA) or flurbiprofen (FP). Addition of intact IVGG to normal blood in Baumgartner's method also resulted in decreasing platelet adhesion and thrombus formation; however, other pepsin-treated IVGG caused enhanced platelet adhesion and thrombus formation. Moreover, pretreatments of the vessel wall with both types of IVGG showed effects similar to those of addition. In conclusion, high-dose therapy with intact IVGG has inhibitory effects on platelet adhesion and thrombus formation. Although the mechanism of the effects is not yet clear, some competitive inhibition between intact IgG and adhesive protein such as von Willebrand factor is suggested, and Fc receptors of the platelet membrane and Fab and Fc receptors of the subendothelium of the vessel wall may have some role in the interaction.