Background The multicenter, single-blind, randomized EU-PACT trial compared the safety and efficacy of genotype-guided and non-genetic dosing algorithms for acenocoumarol and phenprocoumon in patients with atrial fibrillation or deep vein thrombosis.
The aim of this study was to compare EQ-5D-5L against the pulmonary embolism (PE)-specific PEmb-QoL and the deep vein thrombosis (DVT)-specific VEINES-QOL/Sym, and PACT-Q2 (treatment-specific) questionnaires in five language settings.
Intravital microscopy showed that platelet and leukocyte recruitment in the early stages of DVT was dramatically higher in wild-type than in VWF(-/-) IVC.
The concentrations of free and total tissue factor pathway inhibitor, C-reactive protein, von Willebrand factor and D-Dimer were significantly higher in patients with deep venous thrombosis than in patients without deep venous thrombosis (P < 0.001 for all quantities).
Despite the tempting assumption that genetic factors that change ADAMTS13 activity might modulate the risk of DVT by altering vWF and FVIII levels, the polymorphisms analyzed in this study did not correlate with DVT risk among patients investigated.
These high levels are present in 25% of patients with a first episode of deep-vein thrombosis and in 11% of healthy controls. von Willebrand factor (VWF) and blood group are important determinants of the factor VIII level in plasma and therefore contribute to thrombotic risk, while factor VIII appears to be the final effector.
Basal plasma levels of von Willebrand factor and recruitment of platelets to the inferior vena cava wall after DVT induction were reduced in MC-deficient mice.
Comparison of activated partial thromboplastin time, antithrombin III, D-dimer, lupus anticoagulant, free S protein (PS), C protein, and antiphospholipid and PS antibodies was performed on children with acute VZV and DVT (group I), acute uncomplicated VZV (group II), and 30 healthy controls of both sexes (15 boys and 15 girls, mean age 7.5 ± 2.6 years, group III).
Identification of the VKORC1 -1639 (A/G) and CYP2C9 (*1/*2/*3) allelic variants was performed using the PGX-Thrombo Strip in 41 patients with warfarin resistance compared with 30 patients with normal warfarin response out of 352 diagnosed cases of deep vein thrombosis.
To investigate the correlations between three vascular endothelial growth factor 2 (VEGFR2) gene polymorphisms, +1192C>T, +1719T>A, and -604T>C, and deep venous thrombosis (DVT) in Chinese Han population.
Tissue Factor (TF), Vascular Cell Adhesion Molecule-1 (VCAM-1), Interleukin-6 (IL-6) and D-dimer levels were not associated with development deep vein thrombosis in patients with acute foot and ankle injury.
On the contrary, an improvement in GCS (on presentation versus discharge) was associated with starting chemical DVT prophylaxis in ICH patients within 24 hours post-procedure.
Anti-tubulin-α-1c antibody is a promising biomarker in diagnosis and severity evaluation of BD and in indicating the risk of deep venous thrombosis and erythema nodosum.
This was a single-center retrospective review of patients with acute iliofemoral or central DVT treated with the Indigo continuous aspiration mechanical thrombectomy 8 system (Penumbra, Inc, Alameda, Calif) from 2016 to 2017.
Tspan18-knockout mice have 60% reduced thrombus size in a deep vein thrombosis model, and 50% reduced platelet deposition in the microcirculation following myocardial ischemia-reperfusion injury.
Factors significantly associated with positive duplex scans for any (proximal and/or distal) DVT include more severe neurological injury (AIS A, B or C versus AIS D: χ<sup>2</sup> = 7.1791, df = 1, P = 0.007) and older age (age ≥50 years old: χ<sup>2</sup> = 14.9410, df = 1, P = 0.000).
Together, these studies define mechanisms by which p53 regulates thrombus resolution by increasing inflammatory vascular remodeling of venous thrombi in vivo, and the potential therapeutic application of a p53 agonist as a treatment to accelerate this process in patients with DVT.
In ultrasonography-negative cases, TRANCE-MRI detected four additional cases (16%, 4/25) of DVT; three cases (12%, 3/25) of venous compression caused by pelvic lymphadenopathy, hip prosthesis or knee joint effusion; one case (4%, 1/25) of vena cava anomaly; two cases (8%, 2/25) of occult peripheral artery disease (PAD); and one case (4%, 1/25) of an occluded bypass graft.