Gralnick H R, Williams S B, Shafer B C, Corash L
Blood. 1982 Aug;60(2):328-32.
A form of von Willebrand's disease has been described with enhanced ristocetin-induced platelet aggregation and anodal migration of the factor VIII/von Willebrand factor protein (type IIb). We studied two families with this form of von Willebrand's disease and macrothrombocytopenia. We have found that these platelets bind more of the normal and intermediate-sized multimers of the factor VIII/von Willebrand factor than normal platelets. Analysis of the binding data show an increased affinity of these vWd platelets for the factor VIII/von Willebrand factor. These findings are consistent with an increased number of platelet receptors, which, either by their native topography or migration on the platelet surface, bind factor VIII/von Willebrand factor protein with greater affinity than normal platelets, platelets of other vWd patients, and large platelets of other etiologies.
一种血管性血友病已被描述,其瑞斯托霉素诱导的血小板聚集增强,且因子VIII/血管性血友病因子蛋白呈阳极迁移(IIb型)。我们研究了两个患有这种血管性血友病和大血小板减少症的家族。我们发现,这些血小板比正常血小板结合更多的因子VIII/血管性血友病因子的正常和中等大小多聚体。结合数据的分析表明,这些血管性血友病血小板对因子VIII/血管性血友病因子的亲和力增加。这些发现与血小板受体数量增加一致,这些受体要么因其天然拓扑结构,要么因其在血小板表面的迁移,比正常血小板、其他血管性血友病患者的血小板以及其他病因导致的大血小板,以更高的亲和力结合因子VIII/血管性血友病因子蛋白。