scholarly journals Evaluation of plasma levels of tissue factor and tissue factor pathway inhibitor in patients with psoriasis

2019 ◽  
Vol 36 (4) ◽  
pp. 442-448
Author(s):  
Anna Domagała ◽  
Elżbieta Wojtowicz-Prus ◽  
Joanna Dubis ◽  
Wojciech Witkiewicz ◽  
Anna Czarnecka
Keyword(s):  
Tissue Factor ◽  
Plasma Levels ◽  
Tissue Factor Pathway Inhibitor ◽  
Tissue Factor Pathway

Elevated Tissue Factor and Tissue Factor Pathway Inhibitor Circulating Levels in Ischaemic Heart Disease Patients

1998 ◽  
Vol 79 (03) ◽  
pp. 495-499 ◽  
Author(s):  
Anna Maria Gori ◽  
Sandra Fedi ◽  
Ludia Chiarugi ◽  
Ignazio Simonetti ◽  
Roberto Piero Dabizzi ◽  
...  
Keyword(s):  
Heart Disease ◽  
Ischaemic Heart Disease ◽  
Tissue Factor ◽  
Plasma Levels ◽  
Tissue Factor Pathway Inhibitor ◽  
Common Source ◽  
Previous Myocardial Infarction ◽  
Control Subjects ◽  
Tissue Factor Pathway ◽  
Circulating Levels

SummarySeveral studies have shown that thrombosis and inflammation play an important role in the pathogenesis of Ischaemic Heart Disease (IHD). In particular, Tissue Factor (TF) is responsible for the thrombogenicity of the atherosclerotic plaque and plays a key role in triggering thrombin generation. The aim of this study was to evaluate the TF/Tissue Factor Pathway Inhibitor (TFPI) system in patients with IHD.We have studied 55 patients with IHD and not on heparin [18 with unstable angina (UA), 24 with effort angina (EA) and 13 with previous myocardial infarction (MI)] and 48 sex- and age-matched healthy volunteers, by measuring plasma levels of TF, TFPI, Prothrombin Fragment 1-2 (F1+2), and Thrombin Antithrombin Complexes (TAT).TF plasma levels in IHD patients (median 215.4 pg/ml; range 72.6 to 834.3 pg/ml) were significantly (p<0.001) higher than those found in control subjects (median 142.5 pg/ml; range 28.0-255.3 pg/ml).Similarly, TFPI plasma levels in IHD patients were significantly higher (median 129.0 ng/ml; range 30.3-316.8 ng/ml; p <0.001) than those found in control subjects (median 60.4 ng/ml; range 20.8-151.3 ng/ml). UA patients showed higher amounts of TF and TFPI plasma levels (TF median 255.6 pg/ml; range 148.8-834.3 pg/ml; TFPI median 137.7 ng/ml; range 38.3-316.8 ng/ml) than patients with EA (TF median 182.0 pg/ml; range 72.6-380.0 pg/ml; TFPI median 115.2 ng/ml; range 47.0-196.8 ng/ml) and MI (TF median 213.9 pg/ml; range 125.0 to 341.9 pg/ml; TFPI median 130.5 ng/ml; range 94.0-207.8 ng/ml). Similar levels of TF and TFPI were found in patients with mono- or bivasal coronary lesions. A positive correlation was observed between TF and TFPI plasma levels (r = 0.57, p <0.001). Excess thrombin formation in patients with IHD was documented by TAT (median 5.2 μg/l; range 1.7-21.0 μg/l) and F1+2 levels (median 1.4 nmol/l; range 0.6 to 6.2 nmol/l) both significantly higher (p <0.001) than those found in control subjects (TAT median 2.3 μg/l; range 1.4-4.2 μg/l; F1+2 median 0.7 nmol/l; range 0.3-1.3 nmol/l).As in other conditions associated with cell-mediated clotting activation (cancer and DIC), also in IHD high levels of circulating TF are present. Endothelial cells and monocytes are the possible common source of TF and TFPI. The blood clotting activation observed in these patients may be related to elevated TF circulating levels not sufficiently inhibited by the elevated TFPI plasma levels present.

Recombinant Tissue Factor Pathway Inhibitor Prevents Lipopolysaccharide-induced Systemic Hypotension in Rats by Inhibiting Excessive Production of Nitric Oxide

2001 ◽  
Vol 86 (12) ◽  
pp. 1573-1577 ◽  
Author(s):  
Perenlei Enkhbaatar ◽  
Mitsuhiro Uchiba ◽  
Hirotaka Isobe ◽  
Hiroaki Okabe ◽  
Kenji Okajima
Keyword(s):  
Nitric Oxide ◽  
Tissue Factor ◽  
Plasma Levels ◽  
Tissue Factor Pathway Inhibitor ◽  
Factor Viia ◽  
Inos Mrna ◽  
Induced Hypotension ◽  
Inos Activity ◽  
Tnf Α ◽  
Tissue Factor Pathway

SummaryExcessive production of nitric oxide (NO) by the inducible form of NO synthase (iNOS) plays a key role in the development of endotoxin shock. Tumor necrosis factor-α (TNF-α) induces iNOS, thereby contributing to the development of shock. We recently reported that recombinant tissue factor pathway inhibitor (r-TFPI), an important inhibitor of the extrinsic pathway of the coagulation system, inhibits TNF-α production by monocytes. In this study, we investigated whether r-TFPI could ameliorate hypotension by inhibiting excessive production of NO in rats given lipopolysaccharide (LPS). Pretreatment of animals with r-TFPI prevented LPS-induced hypotension. Recombinant TFPI significantly inhibited the increases in both the plasma levels of NO2 -/NO3 - and lung iNOS activity 3 h after LPS administration. Expression of iNOS mRNA in the lung was also inhibited by intravenous administration of r-TFPI. However, neither DX-9065a, a selective inhibitor of factor Xa, nor an inactive derivative of factor VIIa (DEGR-F.VIIa) that selectively inhibits factor VIIa activity, had any effect on LPS-induced hypotension despite their potent anticoagulant effects. Moreover, neither the plasma levels of NO2 -/NO3 - nor lung iNOS activity were affected by administration of DX-9065a and DEGR-F.VIIa. These results suggested that r-TFPI ameliorates LPS-induced hypotension by reducing excessive production of NO in rats given LPS and this effect was not attributable to its anticoagulant effects, but to the inhibition of TNF-α production.

Genetic determinants of tissue factor pathway inhibitor plasma levels

2015 ◽  
Vol 114 (08) ◽  
pp. 245-257 ◽  
Author(s):  
Jessica Dennis ◽  
Irfahan Kassam ◽  
Pierre-Emmanuel Morange ◽  
David-Alexandre Trégouët ◽  
France Gagnon
Keyword(s):  
Risk Factors ◽  
Tissue Factor ◽  
Genetic Variants ◽  
Plasma Levels ◽  
Tissue Factor Pathway Inhibitor ◽  
Future Research ◽  
Genetic Determinants ◽  
Genome Wide ◽  
A Genome ◽  
Tissue Factor Pathway

SummaryTissue factor pathway inhibitor (TFPI) impedes early stages of the blood coagulation response, and low TFPI plasma levels increase the risk of thrombosis. TFPI plasma levels are heritable, but specific genetic determinants are unclear. We conducted a comprehensive review of genetic risk factors for TFPI plasma levels and identified 26 studies. We included 16 studies, as well as results from two unpublished genome-wide studies, in random effects meta-analyses of four commonly reported genetic variants in TFPI and its promoter (rs5940, rs7586970/rs8176592, rs10931292, and rs10153820) and 10 studies were summarised narratively. rs5940 was associated with all measures of TFPI (free, total, and activity), and rs7586970 was associated with total TFPI. Neither rs10931292 nor rs10153820 showed evidence of association. The narrative summary included 6 genes and genetic variants (P151L mutation in TFPI, PROS1, F5, APOE, GLA, and V617F mutation in JAK2) as well as a genome-wide linkage study, and suggested future research directions. A limitation of the systematic review was the heterogeneous measurement of TFPI. Nonetheless, our review found robust evidence that rs5940 and rs7586970 moderate TFPI plasma levels and are candidate risk factors for thrombosis, and that the regulation of TFPI plasma levels involves genetic factors beyond the TFPI gene.

scholarly journals Effects of Melatonin and Luzindole on Plasma Levels of Tissue Factor, Tissue Factor Pathway Inhibitor and Von Willebrand Factor in Rats

2015 ◽  
Vol 47 (1) ◽  
pp. 64
Author(s):  
Negrin Negrev ◽  
Yuri Nyagolov ◽  
Antoaneta Zarkova ◽  
Irina Ilieva Pashalieva ◽  
Emiliya Stancheva ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Von Willebrand Factor ◽  
Plasma Levels ◽  
Tissue Factor Pathway Inhibitor ◽  
Tissue Factor Pathway ◽  
Von Willebrand ◽  
Willebrand Factor

Decreased Plasma Tissue Factor Pathway Inhibitor Levels in Patients with Thrombotic Thrombocytopenic Purpura

1995 ◽  
Vol 73 (01) ◽  
pp. 010-014 ◽  
Author(s):  
Hideo Wada ◽  
Masayuki Kobayashi ◽  
Yoshihiro Wakita ◽  
Minori Shimura ◽  
Tutomu Nakase ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Healthy Volunteers ◽  
Tissue Factor ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Plasma Levels ◽  
Tissue Factor Pathway Inhibitor ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Thrombocytopenic Purpura ◽  
Tissue Factor Pathway

SummaryWe measured plasma levels of tissue factor (TF) and tissue factor pathway inhibitor (TFPI) in patients with thrombotic thrombocytopenic purpura (TTP) and disseminated intravascular coagulation (DIC) to examine the relationship between TFPI and vascular endothelial cell injury. TF antigen was detected in the plasma of healthy volunteers, and the levels were significantly increased in the patients with DIC, but decreased slightly in those with TTP. Plasma TFPI levels were significantly decreased in patients with TTP compared with those in healthy volunteers. The concentration of plasma thrombomodulin (TM) antigen was significantly higher in those with TTP than in normal volunteers. One month after treatment, TTP patients showed a significant decrease in plasma TM levels, and a significant increase, in plasma TFPI levels, but plasma levels of TF antigen were not significantly increased. As plasma TFPI/TF ratio was significantly increased after treatment, the hypercoagulable state was therefore improved after treatment. There was no significant difference in plasma TF and TFPI levels between those who achieved complete remission (CR) and those who died. However, plasma TM levels were significantly higher in those who died than in those who achieved CR. Plasma TFPI levels might reflect injury of vascular endothelial cells as do plasma TM levels, and decreased plasma TFPI/TF ratio and vascular endothelial cell injuries might play causative roles in TTP.

Tissue Factor Reduction and Tissue Factor Pathway Inhibitor Release after Heparin Administration

1999 ◽  
Vol 81 (04) ◽  
pp. 589-593 ◽  
Author(s):  
A. M. Gori ◽  
G. Pepe ◽  
M. Attanasio ◽  
M. Falciani ◽  
R. Abbate ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Plasma Levels ◽  
Tissue Factor Pathway Inhibitor ◽  
Day Treatment ◽  
Procoagulant Activity ◽  
Cytokine Gene Expression ◽  
Heparin Administration ◽  
Tissue Factor Pathway

SummaryElevated plasma levels of tissue factor (TF) and tissue factor pathway inhibitor (TFPI) and large amounts of monocyte procoagulant activity (PCA) have been documented in unstable angina (UA) patients. In in vitro experiments heparin is able to blunt monocyte TF production by inhibiting TF and cytokine gene expression by stimulated cells and after in vivo administration it reduces adverse ischemic outcomes in UA patients. TF and TFPI plasma levels and monocyte PCA have been investigated in 28 refractory UA patients before and during anticoagulant subcutaneous heparin administration (thrice daily weight- and PTT-adjusted for 3 days) followed by 5000 IU × 3 for 5 days. After 2-day treatment, immediately prior to the heparin injection, TF and TFPI plasma levels [(median and range): 239 pg/ml, 130-385 pg/ ml and 120 ng/ml, 80-287 ng/ml] were lower in comparison to baseline samples (254.5 pg/ml, 134.6-380 pg/ml and 135.5 ng/ml, 74-306 ng/ml). Four h after the heparin injection TF furtherly decreased (176.5 pg/ml, 87.5-321 pg/ml; -32.5%, p<0.001) and TFPI increased (240.5 ng/ml, 140-450 ng/ml; +67%, p<0.0001).After 7-day treatment, before the injection of heparin, TF and TFPI plasma levels (200 pg/ml, 128-325 pg/ml and 115 ng/ml, 70-252 ng/ml) significantly decreased (p<0.05) in comparison to the pre-treatment values. On the morning of the 8th day, 4 h after the injection of heparin TF plasma levels and monocytes PCA significantly decreased (156.5 pg/ml, 74-259 pg/ml and from 180 U/105 monocytes, 109-582 U/105 monocytes to 86.1 U/105 monocytes, 28-320 U/105 monocytes; - 38% and -55% respectively) and TFPI increased (235.6 ng/ml, 152-423 ng/ ml; +70%, p<0.001). In conclusion, heparin treatment is associated with a decrease of high TF plasma levels and monocyte procoagulant activity in UA patients. These actions of heparin may play a role in determining the antithrombotic and antiinflammatory properties of this drug.

Plasma levels of free tissue factor pathway inhibitor in patients with various thyroid disorders

2003 ◽  
Vol 110 (4) ◽  
pp. 243-247 ◽  
Author(s):  
Mehmet Ali Özcan ◽  
Abdurrahman Çömlekçi ◽  
Fatih Demirkan ◽  
Faize Yüksel ◽  
İsmail Sarı ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Plasma Levels ◽  
Tissue Factor Pathway Inhibitor ◽  
Thyroid Disorders ◽  
Tissue Factor Pathway

scholarly journals Tissue Factor Pathway Inhibitor and Thrombin Activatable Fibrinolytic Inhibitor Plasma Levels following Burnand Septic Injuries in Rats

2004 ◽  
Vol 10 (4) ◽  
pp. 379-385 ◽  
Author(s):  
Thyyar M. Ravindranath ◽  
Masakatsu Goto ◽  
Muzaffer Demir ◽  
Mahmut Tobu ◽  
M. Florian Kujawski ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Plasma Levels ◽  
Tissue Factor Pathway Inhibitor ◽  
Burn Injury ◽  
Coagulation Cascade ◽  
Clinical Model ◽  
Coagulation Status ◽  
Tissue Factor Pathway ◽  
Caecal Ligation And Puncture ◽  
Combined Injuries

Burn and septic injuries induce profound changes in coagulation status. This study examined the changes in plasma tissue factor pathway inhibitor (TFPI) and thrombin activatable fibrinolytic inhibitor (TAFI) levels in a rat model of burn and septic injuries. Rats underwent 30% TBSA cutaneous scald burn injury and septic insult was induced by caecal ligation and puncture (CLP). CLP was superimposed on burn injury to mimic the clinical model of sepsis complicating burn injury. Rats were pretreated with Cprofloxacin orally to colonize their gut with Enterococcus faecalis. TFPI and TAFI plasma levels were measured using functional activity assay kit with a chromogenic method at 24 and 72 hours following the injuries. TFPI levels decreased significantly at 24 hours in burn, CLP, and burn+CLP groups, followed by incomplete rebound recovery at 72 hours in all three groups. On the other hand, TAFI levels increased significantly at 24- and 72-hour time points in all three groups. These results suggest that burn, septic, and their combined injuries perturb coagulation cascade and thrombotic process toward the procoagulant pathway by impairing fibrinolysis.

Sign in / Sign up

Export Citation Format

Share Document