Fibrinolytic System & DIC Test Kit

The fibrinolytic system is an important part of the coagulation system and plays a vital role in maintaining blood fluidity and vascular integrity.The fibrinolysis (fibrinolysis) system consists of four components, namely plasminogen (plasminogen, plasminogen), plasmin (plasmin, plasmin), Lysogen activator and fibrinolysis inhibitor. The basic process of fibrinolysis can be divided into two stages, namely activation of plasminogen and degradation of fibrin (or fibrinogen).

Products Details

Coagulation Solution

Series

Product Name

Abbr

Fibrinolytic System & DIC

Fibrinogen Degradation Products

FDP

D-Dimer

D-Dimer

Plasminogen

PLG

α2- antiplasminase

α2-AP

Plasminogen Activation Inhibitor

PAI

Von Willebrand Factor Antigen

vW Factor Antigen

The fibrinolytic system is an important part of the coagulation system and plays a vital role in maintaining blood fluidity and vascular integrity.The fibrinolysis (fibrinolysis) system consists of four components, namely plasminogen (plasminogen, plasminogen), plasmin (plasmin, plasmin), Lysogen activator and fibrinolysis inhibitor. The basic process of fibrinolysis can be divided into two stages, namely activation of plasminogen and degradation of fibrin (or fibrinogen) Plasminogen (PLG): PLG is synthesized by the liver. When blood clots, PLG is adsorbed on the fibrin web in large quantities. Under the action of T-PA or U-PA, PLG is activated into plasminase, promoting fibrin dissolution. Plasminogen is a single - chain β -globulin with a molecular weight of 80000 ~ 90000. It is synthesized in the liver, bone marrow, eosinophils, and kidneys and then enters the bloodstream. For adults, 10-20 mg/100ml plasma. It has a half-life in the bloodstream of 2 to 2.5 days. It is readily adsorbed to its substrate, fibrin . Plasminogen activator inhibitor (PAI) and α2 anti-plasminogen inhibitor (α2-AP). PAI can specifically bind to T-PA in a 1:1 ratio to inactivate it and activate PLG. The main forms are PAI-1 and PAI-2. α2-AP is synthesized by liver. The mechanism of action is as follows: α2-AP binds to PL in a 1:1 ratio to form complex, which inhibits PL activity. F ⅹ ⅲ makes α2-AP covalently bound to fibrin, which weakens the sensitivity of fibrin to PL. Fibrin degradation mechanism: PL degrades not only fibrin but also fibrinogen. PL degrades fibrinogen to produce X, Y, D and E fragments. Degradation of fibrin results in x', Y', D-D, E' fragments. All of these fragments are collectively called fibrin degradation products (FDP). Blood contains fibrin, which is activated and hydrolyzed to produce specific degradation products called "fibrin degradation products." D-dimer is the simplest product of fibrin degradation, and the increased level of D-dimer indicates the presence of hypercoagulability and secondary hyperfibrinolysis. Therefore, d-dimer mass concentration is of great significance in the diagnosis, efficacy evaluation and prognosis of thrombotic diseases. von Willebrand factor (factor VIII-related antigen) is a large glycoprotein that is present in the plasma and endothelium and binds to other proteins, particularly factor VIII, preventing its rapid degradation. It is absent in von Willebrand's disease. Von Willebrand factor/factor VIII concentrates play a key role in the treatment of patients with von Willebrand disease. The von Willebrand factor multimer fraction is very effective in achieving hemostasis. von Willebrand factor (VWF) is a large adhesive glycoprotein required for platelet adhesion to subendothelium at the site of vessel injury, platelet aggregation to form the platelet plug, and stabilization of factor VIII (FVIII) in the circulation. Deficiency or defect of VWF leads to von Willebrand disease (VWD). Accurate diagnosis and characterization of VWD require a panel of tests, including VWF antigen, a measure of VWF activity, FVIII activity, VWF multimers, and VWF binding measurements. Sequencing of specific VWF regions may also be useful in diagnosis. Type 1 (quantitative defects), type 2 (qualitative defects), and type 3 (complete deficiency) should be distinguished to provide appropriate therapy.

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