scholarly journals Thrombus precursor protein, endogenous thrombin potential, von-Willebrand factor and activated factor VII in suspected deep vein thrombosis: is there a place for new parameters?

2002 ◽  
Vol 120 (1) ◽  
pp. 123-128 ◽  
Author(s):  
Robert A. Bucek ◽  
Markus Reiter ◽  
Peter Quehenberger ◽  
Ansgar Weltermann ◽  
Paul A. Kyrle ◽  
...  
Keyword(s):  
Deep Vein Thrombosis ◽  
Von Willebrand Factor ◽  
Precursor Protein ◽  
Factor Vii ◽  
Endogenous Thrombin Potential ◽  
Vein Thrombosis ◽  
Activated Factor Vii ◽  
Von Willebrand ◽  
Deep Vein ◽  
Willebrand Factor

Synergic effect of GPIBA and von Willebrand factor in pathogenesis of deep vein thrombosis

Vascular ◽  
2020 ◽  
Vol 28 (3) ◽  
pp. 309-313
Author(s):  
Da Li ◽  
Xiaosong Zhang ◽  
Honggang Zhang ◽  
Xiaoqiang Li
Keyword(s):  
Cardiovascular Disease ◽  
Deep Vein Thrombosis ◽  
Membrane Protein ◽  
Von Willebrand Factor ◽  
Integrin Subunit ◽  
Dynamic Changes ◽  
Vein Thrombosis ◽  
Von Willebrand ◽  
Deep Vein ◽  
Willebrand Factor

Objectives In cardiovascular disease, deep vein thrombosis is one of the vital symptoms causing pulmonary thromboembolism. However, the pathogenesis of deep vein thrombosis is still not clear. One of the critical factors leading to deep vein thrombosis is the platelet aggregation that is mediated by a set of key genes including platelet membrane protein coded by platelet glycoprotein Ib alpha chain (GPIBA). Methods Deep vein thrombosis model was established according to the previous protocol, and venous blood and thrombi were collected for further analysis. Results The dynamic changes of GPIBA and coagulation factor, von Willebrand factor, were observed in deep vein thrombosis models. Meanwhile, critical proteins participating in adhesion and binding of platelets such as epithelial membrane protein 2 (EMP2), vascular cell adhesion protein 1 (VCAM1), immunoreceptor tyrosine-based activation motif 1 (ITAM1), integrin subunit alpha M (ITGAM), or fibronectin were also differentially expressed in deep vein thrombosis models. Conclusions Application of heparin could reverse these dynamic changes in deep vein thrombosis models. Thus, we explained the potential synergic role of GPIBA and von Willebrand factor in regulating the occurrence of deep vein thrombosis and provide therapeutic target against cardiovascular disease.

Role of clotting factor VIII in effect of von Willebrand factor on occurrence of deep-vein thrombosis

The Lancet ◽  
1995 ◽  
Vol 345 (8943) ◽  
pp. 152-155 ◽  
Author(s):  
T. Koster ◽  
J.P. Vandenbroucke ◽  
F.R. Rosendaal ◽  
E. Briët ◽  
F.R. Rosendaal ◽  
...  
Keyword(s):  
Deep Vein Thrombosis ◽  
Factor Viii ◽  
Von Willebrand Factor ◽  
Clotting Factor ◽  
Vein Thrombosis ◽  
Von Willebrand ◽  
Deep Vein ◽  
Willebrand Factor

scholarly journals von Willebrand factor–mediated platelet adhesion is critical for deep vein thrombosis in mouse models

Blood ◽  
2011 ◽  
Vol 117 (4) ◽  
pp. 1400-1407 ◽  
Author(s):  
Alexander Brill ◽  
Tobias A. Fuchs ◽  
Anil K. Chauhan ◽  
Janie J. Yang ◽  
Simon F. De Meyer ◽  
...  
Keyword(s):  
Deep Vein Thrombosis ◽  
Von Willebrand Factor ◽  
Platelet Adhesion ◽  
Wild Type ◽  
Flow Disturbance ◽  
Vein Thrombosis ◽  
Flow Restriction ◽  
Von Willebrand ◽  
Deep Vein ◽  
Willebrand Factor

Abstract Deep vein thrombosis (DVT) and its complication, pulmonary embolism, are frequent causes of disability and mortality. Although blood flow disturbance is considered an important triggering factor, the mechanism of DVT initiation remains elusive. Here we show that 48-hour flow restriction in the inferior vena cava (IVC) results in the development of thrombi structurally similar to human deep vein thrombi. von Willebrand factor (VWF)–deficient mice were protected from thrombosis induced by complete (stasis) or partial (stenosis) flow restriction in the IVC. Mice with half normal VWF levels were also protected in the stenosis model. Besides promoting platelet adhesion, VWF carries Factor VIII. Repeated infusions of recombinant Factor VIII did not rescue thrombosis in VWF−/− mice, indicating that impaired coagulation was not the primary reason for the absence of DVT in VWF−/− mice. Infusion of GPG-290, a mutant glycoprotein Ibα-immunoglobulin chimera that specifically inhibits interaction of the VWF A1 domain with platelets, prevented thrombosis in wild-type mice. Intravital microscopy showed that platelet and leukocyte recruitment in the early stages of DVT was dramatically higher in wild-type than in VWF−/− IVC. Our results demonstrate a pathogenetic role for VWF-platelet interaction in flow disturbance-induced venous thrombosis.

scholarly journals Von Willebrand Factor: Antigen and Adamts-13 Level, but not Soluble P-Selectin, are Risk Factors for the First Asymptomatic Deep Vein Thrombosis in Cancer Patients Undergoing Chemotherapy

2020 ◽  
Author(s):  
Budi Setiawan ◽  
Cecilia Oktaria Permatadewi ◽  
Baringin de Samakto ◽  
Ashar Bugis ◽  
Ridho M. Naibaho ◽  
...  
Keyword(s):  
Risk Factors ◽  
Logistic Regression ◽  
Deep Vein Thrombosis ◽  
Cancer Patients ◽  
Von Willebrand Factor ◽  
Plasma Levels ◽  
Vein Thrombosis ◽  
Von Willebrand ◽  
Deep Vein ◽  
Willebrand Factor

Abstract Background There is a high incidence of deep vein thrombosis (DVT) among cancer patients undergoing chemotherapy. Chemotherapy-induced vascular endothelial cell activation (VECA) is characterized by increased plasma levels of von Willebrand factor (vWF) and soluble P-selectin (sP-selectin), leading to the activation of endothelial cells and signaling cascades. The biological role of a disintegrin-like and metalloproteinase with thrombospondin type 1 motif, member 13 (ADAMTS-13) is to control the activity of vWF and consequently the risk of thrombosis. The objective of this study was to investigate the roles of sP-selectin, vWF, and ADAMTS-13 as risk factors for the first episode of DVT in cancer patients undergoing chemotherapy.Methods This prospective cohort study was conducted at Dr. Kariadi Hospital, Indonesia, on 40 cancer patients. Prechemotherapy (baseline) and postchemotherapy sP-selectin, vWF antigen (vWF:Ag), and ADAMTS-13 plasma levels were determined with ELISAs before and 3 months after chemotherapy. The clinical characteristics of the patients, cancer type, cancer stage, chemotherapy regimen, ABO blood type, D-dimer level and Khorana risk score were also analyzed using logistic regression. Patients were observed for the possibility of developing DVT during chemotherapy.Results DVT was confirmed in 5 patients (12.5%) after a period of 3 months. In patients with DVT, sP-selectin and vWF were significantly higher while ADAMTS-13 was lower than in their counterparts. The levels of baseline vWF:Ag and ADAMTS-13, with cut-off points ≥ 2.35 IU/mL and ≤ 1.03 IU/mL, respectively, were found to independently predict the incidence of DVT. In the multivariate logistic regression analysis, the relative risk (RR) for DVT in patients with high vWF:Ag was 3.80 (95% CI 1.15-12.48, p=0.028), and that for patients with low ADAMTS-13 was 2.67 (95% CI 1.22-23.82, p=0.005). The vWF:Ag/ADAMTS-13 ratio and both vWF:Ag and ADAMTS-13 dynamics during treatment were also able to differentiate those with prospective DVT. However, sP-selectin and other covariates showed no statistical significance.Conclusion We found that prechemotherapy plasma levels of vWF:Ag ≥ 2.35 IU/mL and ADAMTS-13 ≤ 1.03 IU/mL are independent risk factors for DVT incidence among cancer patients.

Hemostasis Abnormalities in Patients with Vascular Dementia and Alzheimer’s Disease

1996 ◽  
Vol 75 (02) ◽  
pp. 216-218 ◽  
Author(s):  
D Mari ◽  
L Parnetti ◽  
R Coppola ◽  
B Bottasso ◽  
G P Reboldi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vascular Dementia ◽  
Vascular Disease ◽  
Von Willebrand Factor ◽  
Plasminogen Activator Inhibitor ◽  
Factor Vii ◽  
Activated Factor Vii ◽  
Von Willebrand ◽  
Willebrand Factor

SummarySince it has not been established to what extent abnormalities of hemostasis contribute to the occurrence and development of dementia, selected measurements of coagulation and fibrinolysis were obtained in elderly patients with Alzheimer’s disease (n = 22) or vascular dementia (n = 29), compared with healthy individuals in the same age range (n = 61). Hemostasis abnormalities were more frequent and marked in vascular dementia, being expressed as significant increases of plasminogen activator inhibitor type 1, von Willebrand factor, D-dimer. and activated factor VII. However, some hemostasis measurements (von Willebrand factor, activated factor VII) were abnormally high also in the patients with Alzheimer’s disease, a condition in which vascular damage is not considered to play a major pathogenetic role. It could not be established in this study whether or not these hemostatic abnormalities play a causal role in the pathogenesis of dementia, or whether they are secondary to inflammation and chronic vascular disease. Nevertheless, their presence may contribute to aggravating vascular disease.

Decreased plasma levels of activated factor VII in patients with deep vein thrombosis

2015 ◽  
Vol 13 (7) ◽  
pp. 1320-1324 ◽  
Author(s):  
A. M. Schut ◽  
J. C. M. Meijers ◽  
Y. Lisman- van Leeuwen ◽  
M. L. van Montfoort ◽  
M. Roest ◽  
...  
Keyword(s):  
Deep Vein Thrombosis ◽  
Plasma Levels ◽  
Factor Vii ◽  
Vein Thrombosis ◽  
Activated Factor Vii ◽  
Deep Vein

scholarly journals Activated αIIbβ3 on platelets mediates flow-dependent NETosis via SLC44A2

2018 ◽  
Author(s):  
Adela Constantinescu-Bercu ◽  
Luigi Grassi ◽  
Mattia Frontini ◽  
Isabelle I. Salles-Crawley ◽  
Kevin J Woollard ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Von Willebrand Factor ◽  
Neutrophil Extracellular Trap ◽  
Cell Binding ◽  
Vein Thrombosis ◽  
Von Willebrand ◽  
Deep Vein ◽  
Willebrand Factor ◽  
Insight Into ◽  
Impaired Binding

AbstractPlatelet-neutrophil interactions are important for innate immunity, but also contribute to the pathogenesis of deep vein thrombosis, myocardial infarction and stroke. Here we report that, under flow, von Willebrand factor/glycoprotein Ibα-dependent platelet ‘priming’ induces integrin αIIbβ3 activation that, in turn, mediates neutrophil and T-cell binding. Binding of platelet αIIbβ3 to SLC44A2 on neutrophils leads to mechanosensitive-dependent production of highly prothrombotic neutrophil extracellular traps. A polymorphism in SLC44A2 (rs2288904-A) present in 22% of the population causes an R154Q substitution in an extracellular loop of SLC44A2 that is protective against venous thrombosis results in severely impaired binding to both activated αIIbβ3 and VWF-primed platelets. This was confirmed using neutrophils homozygous for the SLC44A2 R154Q polymorphism. Taken together, these data reveal a previously unreported mode of platelet-neutrophil cross-talk, mechanosensitive NET production, and provide mechanistic insight into the protective effect of the SLC44A2 rs2288904-A polymorphism in venous thrombosis.SummaryPlatelets that are primed following interaction with von Willebrand factor under flow mediated direct interactions with neutrophils via activated platelet integrin, αIIbβ3, and SLC44A2 on neutrophils. This interaction initiates signaling in a mechanosensitive manner that promotes neutrophil extracellular trap formation.

scholarly journals Soluble P-Selectin, Von Willebrand Factor, And Adamts13 Levels As Risk Factors Of Deep Vein Thrombosis In Cancer Patients Undergoing Chemotherapy

2020 ◽  
Author(s):  
Budi Setiawan ◽  
Cecilia Oktaria Permatadewi ◽  
Baringin de Samakto ◽  
Ashar Bugis ◽  
Eko Adhi Pangarsa ◽  
...  
Keyword(s):  
Risk Factors ◽  
Deep Vein Thrombosis ◽  
Cancer Patients ◽  
Plasma Levels ◽  
Vein Thrombosis ◽  
Soluble P ◽  
Von Willebrand ◽  
Deep Vein ◽  
Willebrand Factor

Abstract Background There is a high number of deep vein thrombosis (DVT) incidence among cancer patients undergoing chemotherapy. Chemotherapy-induced vascular endothelial cell activation (VECA) is marked with increasing plasma levels of von Willebrand Factor (VWF) and soluble P-selectin (sP-selectin) leading to activation of endothelial cells and coagulation cascade. The biological role of a disintegrin-like and metalloproteinase with thrombospondin type 1, motif 13 (ADAMTS13) is to control the activity of VWF. The objectives of this study is to investigate the role of sP-selectin, VWF, and ADAMTS13 as risk factors for the incidence of DVT in cancer patients undergoing chemotherapy. Methods This prospective cohort study was conducted in Dr. Kariadi hospital, Semarang Indonesia, on 40 cancer patients. Soluble P-selectin, VWF, and ADAMS13 plasma levels were determined with enzyme-linked immunosorbent assay (ELISA) method, examined before and after chemotherapy. These patients were observed for the possibility of developing DVT during three months. Results Deep vein thrombosis was confirmed in 5 patients (12.5%) after a median period of 8 weeks. In patients with DVT, sP-selectin and VWF were significantly higher, while ADAMTS13 were significantly lower compared in cancer patients without DVT. Pre- and post-chemotherapy concentration of sP selectin, VWF, and ADAMTS13 could effectively predict the incidence of DVT in cancer patients undergoing chemotherapy. The levels of sP-selectin, VWF and ADAMTS13 pre-chemotherapy with cut-off point >106.7 ng/mL, >2.99 U/mL and <0,80 U/mL, respectively, had relative risk (RR) for DVT incidence being 16 (95% CI 2,06-124,25, p=0,001); 36 (95% CI 5,21-248,65, p=0,000) and 10,5 (95% CI 1,31-84,28, p=0,015), respectively, whereas the levels of sP-selectin, VWF and ADAMTS13 post-chemotherapy with cut-off point >111.7 ng/mL, >3,06 U/mL and <0,49 U/mL, respectively, had RR for DVT incidence being 8.7 (95% CI 1,01-74,39, p=0,045); 20,4 (95% CI 2,60-159,94, p=0,004) and 26,25 (95% CI 3,50-196,48, p=0,002), respectively. Pre-chemotherapy vWF levels (cut-off value >2.99 U/mL) was found to be independently predict DVT incidence with RR 11.1 (95% CI, 1.95-62.74, p=0.007). Conclusions Plasma levels of VWF more than 2.99 U/mL pre-chemotherapy was an independent risk factor for DVT incidence, which could be performed early and helpful for thromboprophylaxis therapy.

Sign in / Sign up

Export Citation Format

Share Document