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The activated protein C resistance (APCR) test is a coagulation test used in the evaluation and diagnosis of activated protein C (APC) resistance, a form of hypercoagulability. [ 1 ] [ 2 ] Hereditary APC resistance is usually caused by the factor V Leiden mutation, whereas acquired APC resistance has been linked to antiphospholipid antibodies ...
Activated protein C resistance (APCR) Protein C Anticoagulant Pathway: Thrombin escaping from a site of vascular injury binds to its receptor thrombomodulin (TM) on the intact cell surface. As a result, thrombin loses its procoagulant properties and instead becomes a potent activator of protein C. Activated protein C (APC) functions as a ...
Blood clotting tests are the tests used for diagnostics of the hemostasis system. Coagulometer is the medical laboratory analyzer used for testing of the hemostasis system. Modern coagulometers realize different methods of activation and observation of development of blood clots in blood or in blood plasm
Protein C, also known as autoprothrombin IIA and blood coagulation factor XIV, [5]: 6822 [6] is a zymogen, that is, an inactive enzyme.The activated form plays an important role in regulating anticoagulation, inflammation, and cell death and maintaining the permeability of blood vessel walls in humans and other animals.
Activated protein C–protein C inhibitor (APC-PCI) is a complex of activated protein C (APC) and protein C inhibitor (PCI). [1] [2] [3] It has been measured in coagulation testing to evaluate coagulation, thrombosis, and other cardiovascular complications. [2] [3] [4] It is a marker of thrombin generation and indicates hypercoagulability.
The thrombin time (TT), also known as the thrombin clotting time (TCT), is a blood test that measures the time it takes for a clot to form in the plasma of a blood sample containing anticoagulant, after an excess of thrombin has been added. [1] It is used to diagnose blood coagulation disorders and to assess the effectiveness of fibrinolytic ...
There have also been cases in patients with other deficiency, including protein S deficiency, [6] [7] activated protein C resistance (Factor V Leiden) [8] and antithrombin III deficiency. [ 9 ] Although the above hypothesis is the most commonly accepted, others believe that it is a hypersensitivity reaction or a direct toxic effect.
The "lupus anticoagulant paradox" [6] may be explained by platelet activation as described above, as well as enhancement of activated protein C resistance and suppression of the anticoagulant activity of TFPIα. Another proposed mechanism is the antibody-mediated destruction of Annexin A5 on the membranes of endothelial cells and trophoblast cells.