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Thrombotic and hemorrhagic disorders due to abnormal fibrinolysis

William P Fay, MD
Section Editor
Lawrence LK Leung, MD
Deputy Editor
Jennifer S Tirnauer, MD


Hemorrhagic and thrombotic disorders are largely mediated by congenital or acquired abnormalities of blood coagulation, platelet number, or platelet function. (See "Overview of hemostasis".)

Congenital and acquired abnormalities of the fibrinolytic system, which are less common, can also be responsible for excessive bleeding or thrombosis, and will be discussed here.

Discussions of the fibrinolytic system as a prognostic factor in patients with breast cancer as well as in those with cardiovascular disease are presented separately. (See "Fibrinolytic markers and cardiovascular risk" and "Prognostic and predictive factors in early, nonmetastatic breast cancer".)


The key components of the blood fibrinolytic system are illustrated in the figure (figure 1) [1,2]. (See "Overview of hemostasis", section on 'Clot elimination and fibrinolysis'.)

Plasminogen — Plasminogen, the central zymogen of the fibrinolytic system, circulates in plasma at a concentration of approximately 2 microM. Under the action of plasminogen activators (t-PA and u-PA, described below), plasminogen is converted to plasmin, a serine protease that degrades fibrin and other proteins. The plasminogen molecule contains specific lysine binding sites, which mediate interaction with its target (fibrin) and major inhibitor (alpha-2-antiplasmin).


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Literature review current through: May 2017. | This topic last updated: May 26, 2017.
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