Our results indicate that hypothermia leads to platelet activation in the spleen via the upregulation of vWF, and this activation causes hypercoagulability after rewarming.
A disintegrin-like and metalloproteinase with thrombospondin type-1 motifs 13 (ADAMTS13) and von Willebrand factor (VWF) are associated with the pathophysiology of liver cirrhosis and HCC through their roles in hypercoagulability; they are also associated with angiogenesis <i>via</i> vascular endothelial growth factor (VEGF).
These results suggest that the imbalance between VWF secretion and ADAMTS-13 may play a critical role in the hypercoagulability state in advanced NSCLC.
This study is a prospective observational cohort study; Hypercoagulability and inflammatory biomarkers including:(1) Coagulation and fibrinolysis activation Markers (D-dimer, Fibrinogen, Antithrombin, plasminogen activator inhibitor 1 [PAI-1]);(2) Endothelium and platelet activation Markers (von Willebrand Factor [vWF], soluble P-selectin); and (3) Inflammation Markers (Tumor necrosis factor alpha [TNF-α], Interleukin-6 [IL-6]) were assayed on a group of 171 patients with hematological malignancies at time of diagnosis.
Recent studies have shown that increased plasma levels of Von Willebrand factor (VWF) and reduced plasma levels of enzyme ADAMTS13 are associated with diabetic nephropathy and an increased risk of developing cardiovascular disease, suggesting that these markers of hypercoagulability may contribute to an increased risk of cardiovascular disease in diabetic patients with impaired renal function.
Five patients showed at least one risk factor for hypercoagulability: lupus anti-coagulant (one patient), increased von Willebrand factor (2 patients) or homocysteine levels (4 patients).
von Willebrand factor (vWF) gene promoter polymorphism at nucleotide positions -2659 and -2525 influences corticosteroid-mediated increase in vWF level and possibly hypercoagulability of the blood.
Cushing syndrome (CS) features high-glucocorticoid secretion and an associated hypercoagulable state often involving an increase in von Willebrand factor (VWF).
We investigated the effect of ABO genotypes on VWF and factor VIII (FVIII) levels and on the degree to which VWF is loaded with A- and B-antigens, expressed as normalized ratios, nA-ratio and nB-ratio, respectively, in the Leiden Thrombophilia Study, a large case-control study on venous thrombosis.
We hypothesized differences in the hypercoagulable state [as assessed by tissue factor (TF), fibrinogen and D-dimer], endothelial function [markers soluble E-selectin (sE-sel) and von Willebrand factor (vWf)], and inflammation [markers interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hsCRP)] in these two SCD genotypes.
Purported mechanisms for migraine-associated stroke include involvement of the vasculature (including vasospasm, arterial dissection and small vessel arteriopathy), hypercoagulability (elevated von Willebrand Factor, platelet activation) and elevated risk of cardioembolism (patent foramen ovale, atrial septal aneurysm).