Reduced plasma fibrinolytic potential is a risk factor for venous thrombosis

Lisman, Ton; Groot, Philip G. de; Meijers, Joost C. M.; Rosendaal, Frits R.

doi:10.1182/blood-2004-08-3253

Cited by 253 publications

(247 citation statements)

References 30 publications

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“…We have recently shown in these same individuals that TAFI antigen levels and clot lysis times were only weakly associated (Lisman et al, 2005). The present study showed an increased risk of DVT in carriers of …”

Section: Discussionsupporting

confidence: 59%

“…It was shown that clot lysis times were associated with both TAFI antigen and activity levels in a group of 20 healthy volunteers. However, recently we showed in a much larger group of healthy subjects (n ¼ 469), which is the control group of the study we report on here, that the association between the clot lysis time and TAFI antigen levels was, at most, very weak (0AE188 increase in clot lysis time (in min) per 1 U/dl increase in TAFI, after age-adjustment) (Lisman et al, 2005). In the total study population, 403 (43%) were men, 540 (57%) women and the mean age in patients and control subjects was 45AE0 years (range 15-69 years) and 44AE7 years (15-72 years), respectively.…”

Section: Discussionmentioning

confidence: 96%

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The effect of genetic variants in the thrombin activatable fibrinolysis inhibitor (TAFI) gene on TAFI‐antigen levels, clot lysis time and the risk of venous thrombosis

et al. 2006

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SummaryThrombin activatable fibrinolysis inhibitor (TAFI) is an important inhibitor of fibrinolysis. High TAFI antigen levels are associated with an increased risk of deep venous thrombosis (DVT). Because TAFI levels are partly determined genetically, we assessed the association between three TAFI gene polymorphisms (−438 G/A, 505 A/G and 1040 C/T), TAFI antigen levels and clot lysis times and the risk of DVT. Carriers of the 505G allele, which is associated with lower TAFI antigen levels than the 505A allele, showed an increased risk of DVT. This indicates that the relationship between TAFI and venous thrombosis is more complex than previously suggested.

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 96%

The effect of genetic variants in the thrombin activatable fibrinolysis inhibitor (TAFI) gene on TAFI‐antigen levels, clot lysis time and the risk of venous thrombosis

et al. 2006

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“…by comparing the thrombin and reptilase-induced polymerisation profiles to identify the mechanisms of the defective conversion of fibrinogen to fibrin [30]. The clot lysis time has been widely used to assess the plasma fibrinolytic potential in a broad range of diseases [31][32][33][34][35]. In the setting of congenital dysfibrinogenaemia, fibrinogen variants with a well-identified thrombotic phenotype have been associated with hypofibrinolysis [36].…”

Section: Discussionmentioning

confidence: 99%

Fibrin clot structure in patients with congenital dysfibrinogenaemia

Casini

Duval

Pan

et al. 2016

Thrombosis Research

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Article:Casini, A, Duval, C orcid.org/0000-0002-4870-6542, Pan, X et al. (3 more authors) (2016) Fibrin clot structure in patients with congenital dysfibrinogenaemia. Thrombosis Research, https://doi.org/10.1016/j.thromres. 2015.11.008 © 2016. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/ eprints@whiterose.ac.uk https://eprints.whiterose.ac.uk/ Reuse Unless indicated otherwise, fulltext items are protected by copyright with all rights reserved. The copyright exception in section 29 of the Copyright, Designs and Patents Act 1988 allows the making of a single copy solely for the purpose of non-commercial research or private study within the limits of fair dealing. The publisher or other rights-holder may allow further reproduction and re-use of this version -refer to the White Rose Research Online record for this item. Where records identify the publisher as the copyright holder, users can verify any specific terms of use on the publisher's website. TakedownIf you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing eprints@whiterose.ac.uk including the URL of the record and the reason for the withdrawal request. ABSTRACTThe clinical phenotype of patients with congenital dysfibrinogenaemia is highly heterogeneous, from absence of symptoms to mild bleeding, or thrombosis. A few mutations are associated with a specific phenotype, but generally the clinical course is not predictable. We investigated whether fibrin clot properties are correlated with the patient's phenotype and/or genotype. Ex vivo plasma fibrin clot characteristics, including turbidity, fibrinolysis, clot permeability and fibrin fibre density assessed by laser scanner confocal microscopy were investigated in 24 genotyped patients with congenital dysfibrinogenaemia compared to normal pool plasma. Compared to normal pool plasma, the patients were characterised by slower fibrin polymerisation (lag time, 345.10 ± 22.98 vs. 166.00 s), thinner fibrin fibres (maximum absorbance, 0.15 ± 0.01 vs. 0.31), prolonged clot lysis time (23.72 ± 0.97 vs. 20.32 min) and larger clot pore size (21.5 × 10−9 ± 4.48 × 10−9 vs. 7.96 × 10−9 cm2). Laser scanning confocal microscopy images confirmed disorganised fibrin networks in all patients. Patients with tendency to bleed showed an increased permeability compared to asymptomatic patients (p=0.01) and to patients with a thrombotic history (p=0.02) while patients with thrombotic history had a tendency to have a prolonged clot lysis time. Fibrin clot properties were similar among hotspot mutations. Further studies including a larger number of patients are needed to evaluate whether analysis of permeability and clot lysis time may help to distinguish the clinical phenotype in these patients and to assess differences according to the genotype.

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“…Plasma fibrinolytic potential of tissue factor induced clots, lysed by exogenous tissue plasminogen activator (tPA) [23][24][25] were determined for control plasma and plasma with different concentrations of 17β-estradiol (30,60,140, 220, 300 pg/ml and 1ng/ml) and progesterone (30, 60, …”

Section: Sample Preparation For Turbidimetric Analysismentioning

confidence: 99%