ANALYSIS OF MICROPARTICLES IN DEEP VENOUS THROMBOSIS AND ANTIPHOSPHOLIPID SYNDROME PATIENTS AND CARRIERS OF LEIDEN FACTOR V
Abstract number: P-S-523
Flores-Nascimento1 M.C., Beltrame2 M.P., Pereira1 F.G., Lorand-Metze1 I., Biro3 E., Berckmans3 R.J., Nieuwland3 R., de Paula1 E.V., Annichino-Bizzacchi1 J.M.
11Hematology-Hemotherapy Center, UNICAMP, Campinas 22Hematology-Hemotherapy Center, UFPR, Curitiba, Brazil 33Department of Clinical Chemistry, University of Amsterdam, Amsterdam, Netherlands
How-to-cite Flores-Nascimento MC, Beltrame MP, Pereira FG, Lorand-Metze I, Biro E, Berckmans RJ, Nieuwland R, de Paula EV, Annichino-Bizzacchi JM. ANALYSIS OF MICROPARTICLES IN DEEP VENOUS THROMBOSIS AND ANTIPHOSPHOLIPID SYNDROME PATIENTS AND CARRIERS OF LEIDEN FACTOR V. J Thromb Haemost 2007; 5 Supplement 2: P-S-523
Abstract
Introduction: Venous thrombosis is a multicausal disease but many risk factors are not well defined. Microparticles (MPs) are small blebs released from cellular surfaces during activation and apoptosis. In vitro MPs can initiate and diffuse the coagulation, and clinical studies revealed increased number of MPs in arterial occlusion. We determined MPs in a group of patients with Deep Venous Thrombosis (DVT), Antiphospholipid Syndrome (AFS) and asymptomatic heterozygous carriers of Factor V Leiden (FVLeiden) to investigate any role with disease.
Methods: MPs were isolated from citrate-anticoagulated blood by differential centrifugation from 10 patients with comproved diagnosis of spontaneous DVT of lower limbs (7F/3M; mean age=32.9; without anticoagulation), 11 patients with DVT and AFS (9F/2M; mean age=33.6; under warfarin therapy) and 5 FVLeiden (5F/0M; mean age=32), and their matched controls (CTR). The flow cytometry was performed using the antibodies: CD235, CD61, CD45, CD31, CD14, CD45, anti-TF, Anexin V and IgGs. Statistical test: U de Mann-Whitney, a= 0.05.
Results: The MPs were defined based on forward/side scatter characteristics and biding with Anexin V. The other populations were defined from that one. The number of MPs was significantly increased in AFS patients (mean= 45% vs. CTR= 29.12%; p=0.016) predominantly from platelet origin (CD61: mean= 91.9% vs. CTR= 82.69%; p=0.01), and erythrocyte-originated MPs were significantly lower (mean= 2.79% vs. CTR= 10.57%; p=0.016) in these patients. Although the MPs number was different between spontaneous DVT and FVLeiden and theirs controls, this was not statistically significant. MPs CD235+ were lower in DVT and MPs CD61+ were higher in FVLeiden group.
Conclusions: Our results demonstrated that, like in arterial disease, MPs could play a role on venous thrombosis, particularly in presence of AFS. Patients with AFS are at increased risk of thrombosis, and the increased number of MPs could contribute to this risk.
