PubMed · 13274457
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E V Z SCOTT. 1955. Prostatic enzymes and abnormal bleeding.. https://pubmed.ncbi.nlm.nih.gov/13274457/
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Thrombolytic drugs do not only stimulate the plasmin system but also induce thrombin activation additionally to the preexisting hypercoagulative state in patients with acute myocardial infarction. Testing the in vitro-derived hypothesis of a plasmin-mediated activation of the contact phase of the coagulation leading to the procoagulant effect, several thrombolytic regimen have been evaluated. Paradoxical thrombin activation (referred to as "thrombolytic paradox") was related to absence of fibrin specificity. Highly fibrin-specific drugs like tenecteplase did not cause additional thrombin activation, while non-fibrin-specific drugs like streptokinase caused a marked additional activation of the contact phase and of thrombin. It could be shown that the thrombolytic paradox was related to the extent of systemic plasmin activation confirming the hypothesis of a plasmin-mediated factor XII/kallikrein system activation as cause of the thrombolytic paradox.
This article briefly describes some important aspects of the fibrinolytic system, its regulation, and possible disturbances of this system in connection with deep vein thrombosis and myocardial infarction.
Thrombolytic agents directly or indirectly activate plasminogen into plasmin, the true thrombolytic being plasmin. Streptokinase is a non-enzyme protein which has occupied the reference position so far. Streptokinase is immunogenic and its activity is neutralised by pre-existing antistreptococcal antibodies. Its administration provokes a systemic activation of fibrinolysis. Urokinase and anisoylated streptokinase-plasminogen complex have no clear advantages when compared with streptokinase. More fibrin specific agents (tissue plasminogen activator, prourokinase) do not improve the risk of bleeding (0.75% in brain). Haemostasis survey does not allow bleeding prediction, but contributes to its control by quantifying the systemic fibrinolytic activity of the drug and checking the anticoagulation level induced by heparin (which is often associated to thrombolysis).