Abstract
One factor that has been proposed to explain the pathogenesis of thrombosis is the existence of a hypercoagulable state that favours intravascular clotting. Evidence in support of such a construct is convincing in only a few situations. Patients with neoplasm may have intravascular coagulation because the blood is exposed to clot-promoting agents; thrombosis after the transfusion of preparations of the vitamin K-dependent clotting factors may have a similar origin. In a few instances, thrombosis has been related to decreasedtitres of antithrombin III, the presence of an abnormal form of plasminogen, or the presence of increased titres of inhibitors of the generation or action of plasmin. In the majority of cases, no present data relate a hypercoagulable state to the evolution of thrombi. We need a fresh paradigm.
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