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Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
Published on: May 23, 2025
Decreased procoagulant phospholipids in patients treated by vitamin K antagonists
Aurélie Rousseau1, Barry Woodhams, Michèle Paunet-Bobo
1Diagnostica Stago, 125 avenue Louis Roche, 92635 Gennevilliers cedex, France.
Introduction:
The stimulation of cells by thrombin is associated with the release of microparticles (MPs) from cell membranes. These MPs can express procoagulant activity. As vitamin K antagonists (VKA) decrease the generation of thrombin, we compared plasma procoagulant phospholipids (PPL) levels in patients with a previous history of venous thrombosis who were being treated with VKA and compared them with an untreated group.
Materials And Methods:
Plasma PPL were measured using a factor Xa-based coagulation assay. sGPV, a marker of platelet activation by thrombin, was measured by ELISA. Platelet MPs were also evaluated using standard flow cytometric techniques. Ninety-six VKA-treated patients and 80 patients not undergoing VKA therapy were tested and the results compared.
Results:
PPL activity was significantly reduced (p<0.0001) in VKA-treated patients compared with the untreated group. PPL were correlated with platelet and white blood cell count and with sGPV levels in the untreated group, but not in VKA-treated patients. PPL were correlated with fibrinogen levels in both groups, but not with C-reactive protein. Polymorphonuclear neutrophils (PMN) were significantly lower (p=0.01) in VKA-treated patients than in untreated patients.
Conclusion:
The difference between PPL levels in VKA-treated patients and patients without treatment could be related to the decrease in PMN count. It remains to be established if this decrease of PPL is directly related to the capacity of activated PMN to generate MPs, or indirectly by reducing the amount of pro-inflammatory cytokines or reactive oxygen species produced by PMN.
Insights
Vitamin K antagonist (VKA) therapy significantly reduces plasma procoagulant phospholipids (PPL) in patients with a history of venous thrombosis. This reduction may be linked to decreased polymorphonuclear neutrophil (PMN) counts in VKA-treated individuals.
Area of Science:
- Hematology
- Thrombosis Research
- Pharmacology
Background:
- Thrombin stimulation releases procoagulant microparticles (MPs) from cell membranes.
- Vitamin K antagonists (VKA) inhibit thrombin generation.
- This study investigates VKA's effect on plasma procoagulant phospholipids (PPL).
Purpose of the Study:
- To compare plasma PPL levels in VKA-treated patients versus untreated patients with a history of venous thrombosis.
- To explore potential correlations between PPL, platelet activation markers, and inflammatory markers.
Main Methods:
- Plasma PPL measured using a factor Xa-based coagulation assay.
- Soluble glycoprotein V (sGPV) assessed by ELISA as a marker of platelet activation.
- Platelet MPs evaluated by flow cytometry.
- Ninety-six VKA-treated and 80 untreated patients analyzed.
Main Results:
- PPL activity was significantly lower in VKA-treated patients (p<0.0001).
- PPL correlated with platelet, white blood cell, and sGPV levels in untreated patients only.
- Polymorphonuclear neutrophil (PMN) counts were significantly lower in VKA-treated patients (p=0.01).
Conclusions:
- Reduced PPL levels in VKA-treated patients may be associated with decreased PMN counts.
- Further research is needed to determine if PPL reduction is directly or indirectly mediated by PMN activity.
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