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Coagulation factor XIIIa is the activated form of factor XIII, a transglutaminase enzyme essential for the physiologic stabilization of blood clots. Activated by thrombin and calcium, FXIIIa catalyzes the formation of covalent cross-links between fibrin monomers and between fibrin and antifibrinolytic proteins (such as α2-antiplasmin), thereby enhancing the mechanical strength and resistance of the clot to fibrinolysis. FXIIIa is crucial for hemostasis, wound healing, and protection against premature clot breakdown. Deficiency results in bleeding diatheses with defective clot stability. Therapeutic replacement of FXIII is curative for deficiency; other drugs interact indirectly through effects on the broader coagulation or fibrinolytic pathways[1][2][3][5][8].
Replacement therapy (for deficiency, via recombinant or plasma factor XIII to restore clot stability); Inhibition of fibrinolysis (through cross-linking of antifibrinolytic proteins)
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