The fibrinolytic system is biologically designed to limit the extent of fibrin formation, to repair the injury, and to re-establish blood flow. Excessive local or systemic fibrinolysis may result in uncontrollable clinical bleeding. Antifibrinolytic therapy should rationally be considered in three groups of clinical situations.

1. When systemic fibrinolysis exists (or potentially may develop) due to primary hyperfibrinolysis such as that occurring in acute promyelocytic leukemia following initiation of chemotherapy or after specific thrombolytic therapy for an acute thrombotic event when bleeding complications develop.

2. Patients who have a decreased potential for hemostatic fibrin plug formation (such as hemophiliacs), so that any fibrin formed is not continually being lysed.

3. Certain circumstances when localized bleeding may be influenced by increased amounts of local fibrinolysis at potentially dangerous anatomical sites (i.e. pathological uterine bleeding, subarachnoid hemorrhage).

Antifibrinolytic agents overall limit fibrin degradation and can be categorized into the following groups of compounds.

1. The natural plasmin inhibitors, such as a2-antiplasmin, which to date have not been developed for human use.

2. Aprotinin and related inhibitory compounds for plasmin and other serine proteases.

3. The synthetic lysine analogs e-aminocaproic acid and trans-p-amino-methyl-cyclohexanecarboxylic acid (tranexamic acid). Both these compounds paradoxically accelerate plasminogen activation by inducing a conformational change in the molecule. However, they block the lysine binding site that is necessary for the binding of plasmin to fibrin (and fibrinogen), thus inhibiting overall fibrinolysis.

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