Abstract
Thrombotic thrombocytopenic purpura (TTP) has been recognized as a clinical entity for more than 50 years.1 The classic histologic lesions of this remarkable disease are "microthrombi" consisting mainly of platelets and fibrin, which can be found in the small vessels of virtually any tissue. These lesions appear to explain most of the clinical findings in TTP, but their origin has thus far defied explanation.Until about 1965, TTP was regarded as a fulminant, almost invariably fatal disease. Since then, increasing numbers of survivors have been reported. Most of them have been treated with some combination of corticosteroids, splenectomy, heparin and . . .

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