Summary
Many subjects carrying inherited thrombophilic defects will never experience venous
thromboembolism (VTE) while other individuals developed recurrent VTE with no known
additional risk factors. High levels of circulating microparticles (MP) have been
associated with increased risk of VTE in patients with factor V Leiden and prothrombin
G20210A mutation, suggesting a possible contribution of MP in the hypercoagulability
of mild genetic thrombophilia. The role of MP as additional risk factor of VTE in
carriers of natural clotting inhibitors defects (severe thrombophilia) has never been
assessed. Plasma levels of annexin V-MP, endothelial-derived MP (EMP), platelet-derived
MP (PMP), tissue factor-bearing MP (TF+) and the MP procoagulant activity (PPL) were
measured in 132 carriers of natural anticoagulant deficiencies (25 antithrombin, 63
protein C and 64 protein S defect) and in 132 age and gender-matched healthy controls.
Carriers of natural anticoagulant deficiencies, overall and separately considered,
presented with higher median levels of annexin V-MP, EMP, PMP, TF+MP and PPL activity
than healthy controls (p< 0.001, < 0.001, < 0.01, 0.025 and 0.03, respectively). Symptomatic
carriers with a previous episode of VTE had significantly higher median levels of
annexin-V MP than those without VTE (p=0.027). Carriers with high levels of annexin
V-MP, EMP and PMP had an adjusted OR for VTE of 3.36 (95 % CI, 1.59 to 7.11), 9.26
(95 % CI, 3.55 to 24.1) and 2.72 (95 %CI, 1.16 to 6.38), respectively. Elevated levels
of circulating MP can play a role in carriers of mild and severe inherited thrombophilia.
The clinical implications of this association remain to be defined.
Keywords
Coagulation inhibitors - hypercoagulability - microparticles - thrombophilia - venous
thrombosis