小儿特发性血小板减少性紫癜发病机制的研究

本文采用体外建立抗原—抗体—补体反应体系的试验方法,通过测定该反应体系的血小板~(51)Cr 释放量来进一步探讨特发性血小板减少紫癜(ITP)患儿血小板的破坏机制。结果45例ITP 惠儿其血小板~(51)Cr 释放量与正常值比较明显增高(P<0.01),急慢性之问无显著差异性。45例患儿中有31例血小板~(51)Cr释放量高出正常值上限。同时观察ITP 患儿血清对血小板超微形态和结构的影响,发现血小板表面有圆钝伪足形成,血小板聚集,血小板脱颗粒和空泡性变。正常儿血清对血小板超微形态和结构无明显影响。作者认为,ITP 患儿的血小板相关抗体,能介导血管内血小板的溶解与破坏,其既影响血小板数量,又改变血小板的结构,二者都是导致该病出血的重要原因。

STUDY ON EFFECT OF HOMOLOGOUS ANTIPLATELET ANTIBODIES IN IDIOPATHIC THROMBOCYTOPENIC PURPURA

By setting up in vitro an antibody-antigen-complement system andmeasuring platelet ~(51)Cr release in the system,we investigated the mecha-nism of platelet destruction in patients with idiopathic thrombocytopenicpurpura (ITP).The results showed that the values of ~(51)Cr release in 45patients with ITP were much higher than those in the 30 normals (P<0.01).There was no difference in the value between the patients of theacute and the chronic.In 31/45 cases the values of ~(51)Cr release were abovethe upper limit of the normal.We further studied the effect of ITP serumon the human platelet shape and ultrastructural changes.We discovered that the platelets developed a disk-to-sphere shape transformation and short,thick or bulbous pseudopodia on their surface.The results also showedthat ITP serum caused evident changes in the platelet ultrastructure,suchas agranulation,vauolation and long,thick plasma projections.Contraryto these changes,the normal serum had no evident effect on the plateletshape and the ultrastructure.We concluded that platelet associated immun-oglobin G (PAIgG) not only caused intravenous platelet destruction butinjured the platelet structure,which were responsible for bleeding in thepatients with ITP.