scholarly journals Single nucleotide polymorphisms in an intergenic chromosome 2q region associated with tissue factor pathway inhibitor plasma levels and venous thromboembolism

2016 ◽  
Vol 14 (10) ◽  
pp. 1960-1970 ◽  
Author(s):  
J. Dennis ◽  
V. Truong ◽  
D. Aïssi ◽  
A. Medina-Rivera ◽  
S. Blankenberg ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Single Nucleotide Polymorphisms ◽  
Tissue Factor ◽  
Plasma Levels ◽  
Tissue Factor Pathway Inhibitor ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
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.

scholarly journals Elevated levels of tissue factor pathway inhibitor in patients with mild to moderate bleeding tendency

2021 ◽  
Vol 5 (2) ◽  
pp. 391-398
Author(s):  
Dino Mehic ◽  
Alexander Tolios ◽  
Stefanie Hofer ◽  
Cihan Ay ◽  
Helmuth Haslacher ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Tissue Factor Pathway Inhibitor ◽  
Genetic Alterations ◽  
Factor V ◽  
Bleeding Tendency ◽  
Healthy Controls ◽  
Single Nucleotide ◽  
Time To Peak ◽  
Coagulation Inhibitors ◽  
Tissue Factor Pathway

Abstract High levels of tissue factor pathway inhibitor (TFPI), caused by a longer TFPIα half-life after binding to a factor V splice variant and variants in the F5 gene, were recently identified in 2 families with an as-yet-unexplained bleeding tendency. This study aimed to investigate free TFPIα in a well-characterized cohort of 620 patients with mild to moderate bleeding tendencies and its association to genetic alterations in the F5 gene. TFPIα levels were higher in patients with bleeding compared with healthy controls (median [interquartile range], 8.2 [5.5-11.7] vs 7.8 [4.3-11.1]; P = .026). A higher proportion of patients had free TFPIα levels more than or equal to the 95th percentile compared with healthy controls (odds ratio [OR] [95% confidence interval (CI)], 2.82 [0.98-8.13]). This was pronounced in the subgroup of patients in whom no bleeding disorder could be identified (bleeding of unknown cause [BUC; n = 420]; OR [95% CI], 3.03 [1.02-8.98]) and in platelet function defects (PFDs) (n = 121; OR [95% CI], 3.47 [1.09-11.08]). An increase in free TFPIα was associated with a mild delay in thrombin generation (prolonged lag time and time to peak), but not with alterations in routinely used global clotting tests. We could neither identify new or known genetic variations in the F5 gene that are associated with free TFPIα levels, nor an influence of the single-nucleotide variant rs10800453 on free TFPIα levels in our patient cohort. An imbalance of natural coagulation inhibitors such as TFPIα could be an underlying cause or contributor for unexplained bleeding, which is most probably multifactorial in a majority of patients.

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

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.

Effects of Tissue Factor and Tissue Factor Pathway Inhibitor-1 on Lung Adenocarcinoma With Venous Thromboembolism

CHEST Journal ◽  
2016 ◽  
Vol 149 (4) ◽  
pp. A287
Author(s):  
Chaosheng Deng ◽  
Xiaoming Cao ◽  
Qi-Chang Lin ◽  
Zhihua Huang ◽  
Haibo Ding ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Lung Adenocarcinoma ◽  
Tissue Factor ◽  
Tissue Factor Pathway Inhibitor ◽  
Tissue Factor Pathway

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
Sign in / Sign up

Export Citation Format

Share Document