fibrinolytit

Fibrinolytics, or fibrinolytit, refer to a group of enzymes and drugs that promote the breakdown of fibrin in blood clots. They are central to the body’s natural process of fibrinolysis, helping to dissolve thrombi after they have served their function. Endogenous fibrinolysis is tightly regulated to balance clot removal with the risk of excessive bleeding.

The core mechanism involves plasmin, an enzyme that degrades fibrin and other clot components. Plasmin is generated from its inactive zymogen, plasminogen, by plasminogen activators such as tissue plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA). Plasmin activity is limited by inhibitors including α2-antiplasmin and plasminogen activator inhibitors (PAI-1). The system is modulated to prevent unwarranted bleeding while allowing rapid clot dissolution when needed.

Fibrinolytics can be endogenous or pharmacologic. Endogenous factors include plasmin and the plasminogen activators. Pharmacologic fibrinolytics are drugs that accelerate plasmin formation or directly degrade fibrin. Common agents include streptokinase, alteplase (recombinant tPA), reteplase, tenecteplase (tPA variants), and urokinase. These agents are used in selected clinical scenarios to treat acute thromboembolism, such as myocardial infarction, certain types of ischemic stroke, and massive pulmonary embolism, but they carry a meaningful risk of bleeding and must be used under strict clinical guidelines.

Clinical use requires careful patient selection, monitoring for hemorrhage, and awareness of contraindications (such as active bleeding or recent intracranial hemorrhage). In some settings, antifibrinolytics like tranexamic acid are used to reduce bleeding, illustrating the balance within the fibrinolytic system between clot dissolution and hemostasis.