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Markers Of Cascade & Hemostasis Activation
F1+2 - T/AT Complexes - SFM
The generation of fibrin is the end result of activation of the coagulation cascade. This process may occur from vascular accidents (normal response) or activation from low level stimuli, such as, Immune System Activation of Coagulation (ISAC) from viral or bacterial infections, or response to tissue factor generation from chemical exposure or chemotherapy. Whatever the source of activation, the process can be monitored by methodologies for these specific markers: Fibrinogen, Prothrombin Fragment 1+2 (F1+2), Thrombin/AntiThrombin Complexes (TATs) and Soluble Fibrin Monomer (SFM). (See diagram on back)
Thrombin itself is impossible to quantitate because it lasts only seconds in the blood circulation. Thus, it is necessary to use a surrogate marker. Fragment1+2 is generated when prothrombin is converted to thrombin by activation of factor Xa. This peptide is released into the plasma and has a half life of 90 minutes, compared to the half life of thrombin which is 30 seconds. This longer half life makes Fragment 1+2 a useful marker for the generation of thrombin in vivo.
As thrombin is generated, natural inhibitors attempt to prevent clot formation by complexing with thrombin to remove it from the circulation. The primary inhibitor is Antithrombin (AT) which forms TAT complexes. Activated Protein C/AntiTrypsin (APCAT) complex is a secondary inhibitor to thrombin generation. Thus, in a compensated system, small amounts of thrombin are removed appropriately. Elevated TATs indicates thrombin generation and an attempt to remove excess thrombin. Low TAT levels may indicate that this system is compromised by lack of heparin exposure on the endothelial cell (EC) surfaces inside capillaries, whether the decrease is due to down regulation of the EC surface by viral or bacterial insult or by fibrin deposition covering the EC.
When excess thrombin is generated, fibrinogen is cleaved to Soluble Fibrin Monomer with the release of Fibrinopeptides A & B (Fpa, Fpb). With the consumption of fibrinogen, the body may compensate by increasing fibrinogen levels slightly above the normal range. Elevated SFM levels increases blood viscosity, is seen as “fibrin deposition” on endothelial cells in the micro-circulation, and lead to chronic illnesses. When there is a burst of Thrombin, Factor XIII is activated to XIIIa, which crosslinks SFM into insoluble cross-linked fibrin strands, leading to a blood clot. Increased SFM indicates that the normal removal of thrombin is saturated or no longer working properly and that there is enough activation of the clotting mechanism to generate fibrin or potentially form a blood clot, ie, the hypercoagulable or prethrombotic state.
If you want the vascular activation profile, request JAVA: vWF Antigen, Platelet Activation (PA by Flow), PAI-1 & D-Dimer (quantitative). Or order both: MOCHA JAVA - Markers Of Cascade & Hemostasis Activation, Juxtaposed Against Vascular Activation.
These tests and panels are available through HEMEX Laboratories and may by ordered as the MOCHA or JAVA panels or may be ordered individually. They can be ordered through any hospital or on an outpatient basis. Two 2 ml frozen aliquots of platelet free citrated plasma are needed for these assays and 1 Yellow top tube for the PA Score.
