In the 50 years since its first description (1), some aspects of the pathogenesis of thrombotic thrombocytopenic purpura have been clarified, but its etiologic definition and the development of effective therapy have remained elusive tasks. Instances of its occurrence in siblings (2) or marital partners (3) and its response in one case to hemodialysis (4) have suggested an environmental causative agent(s) (viral, bacterial, antigenic, or toxic) interacting with a genetically predisposed host. Various therapeutic regimens have been applied including adrenocorticosteriods and splenectomy (5, 6), heparin (7), exchange transfusion (8), and antiplatelet agents (9-23) (aspirin, dipyridamole, sulfinpyrazone, and dextran), but definitive