Such coagulopathy often leads to a hyperfibrinolytic phenotype where hemostatic clots become unstable because of upregulated tissue plasminogen activator (tPA) activity.
A profibrinolytic coagulopathy phenotype was demonstrated in all subgroups with increased tissue plasminogen activator levels and decreased plasminogen activator inhibitor-1 levels.
Finally, new approaches to develop procoagulant aptamers to control bleeding associated with hemophilia and other coagulopathies involve targeting activated protein C and tissue plasminogen activator.
We evaluated the effects of different doses, including a very high dose of FXIII (3.6-32.4 IU/mL) on tissue-plasminogen activator-induced hyperfibrinolysis and the combined condition of dilutional coagulopathy and tissue-plasminogen activator-induced hyperfibrinolysis in vitro.
In addition, we simulate the efficacy of tranexamic acid treatment on coagulopathy initiated through endothelial t-PA release, and are able to reproduce the time-sensitive nature of the efficacy of this treatment as observed in clinical studies.
The authors describe a patient with a life-long bleeding diathesis who demonstrated evidence of excess t-PA. One of two daughters also had a bleeding tendency and demonstrated excess t-PA.