Extem is a specific reagent for assessing the
extrinsic coagulation pathway. The conventional coagulation parameter (PT) is also specific for the
extrinsic coagulation pathway and is a standard assay for monitoring rivaroxaban (9).
In the
extrinsic coagulation pathway, which we examined using ExTEM, we found that 20% mannitol significantly decreased CFT values compared with the control group.
Inappropriate expression of TF within the vasculature upon atherosclerotic plaque rupture leads to interaction with circulating FVIIa resulting in the formation of the TF/FVIIa complex that initiates the
extrinsic coagulation pathway through a cascade of enzymatic reactions driving the conversion of FX to FXa and the production of thrombin, ultimately leading to thrombosis [9].
Among markers of activation of the
extrinsic coagulation pathway, prothrombin fragment 1 + 2, D-dimer, and CRP are increased in CSU patients and seem to correlate with disease severity.
The level of TFPI, a specific inhibitor of the
extrinsic coagulation pathway, in the blood of the rats in the SW group was elevated from 2 hours after seawater exposure and was 2.11-fold greater than that in the rats of the control group at 4 hours.
Exposure of the blood to tissue factor triggers the
extrinsic coagulation pathway whose function is monitored by the prothrombin time (PT) through interaction of tissue factor with activated coagulation factor.
[sup][5] These factors could trigger the
extrinsic coagulation pathway. Third, respiratory efforts can lead to sleep fragmentation, which may activate the sympathetic nervous system and increase arterial blood pressure, leading to hemodynamic disturbances.
We aim to evaluate coagulation and fibrinolytic status during COH through detection of plasma HCY, FVIII, and FX as well as D-dimer, of which HCY is an endothelial injury marker, FVIII is a key procoagulant factor, FX plays an important part in the common pathway of intrinsic and
extrinsic coagulation pathway, and D-dimer is the specific degradation products of fibrin indicating the formation of thrombosis.
In addition, all patients were screened by several laboratory tests, including measurement of the complete blood count (CBC), including platelet count; prothrombin time (PT) to evaluate the
extrinsic coagulation pathway (factor II, V, VII, and X activity), which were converted to calculate the International Normalized Ratio (INR) (7); and activated partial thromboplastin rime (aPTT) to evaluate the intrinsic coagulation pathway (factor VIII, IX, XI, and XII activity).
This fibrin clot forms via (1) the intrinsic coagulation pathway, when activated factor XII (FXIIa) binds to the exposed endothelial cells at the site of injury and (2) the
extrinsic coagulation pathway, when small amounts of circulating FVIIa bind to tissue factor released from injured endothelial tissues.
The pathogenesis of acute disseminated intravascular coagulation is believed to involve the liberation of thromboplastins produced by the tumor cells, with resultant activation of the
extrinsic coagulation pathway. This course eventually leads to a consumptive coagulopathy with thrombocytopenia and removal of coagulation factors from the circulation.
And our study also demonstrated that TFPI-1 levels were positively and negatively correlated with AT, D-D, Fbg, and FVIII:C levels, respectively, which further indicated that decreased TFPI-1 was closely associated with blood coagulation abnormalities in NSCLC patients, and lower TFPI-1 may have a lower inhibitory power on initial activation of
extrinsic coagulation pathway. Therefore, as a result of lower TFPI-1 levels, the risk of thrombotic complications would be increased.