A significant association was found between the possession of the AA or GA genotypes of FVL polymorphism among patients with BD and the presence of any thrombosis (OR=2.51; 95% CI: 1.68, 3.74; P<0.00001).
Two hundred consecutive Italian patients satisfying the International Study Group criteria for BD who were followed up for seven years and 241 healthy Italian age- and gender-matched blood donors were molecularly genotyped for the PlA1/A2 polymorphism of the platelet GpIIIa gene; 118 and 117 of the 200 BD patients were also respectively genotyped for factor V Leiden and prothrombin gene G20210A polymorphisms.
The present study was designed to analyse the role of the factor V Leiden and the prothrombin G20210A mutations and plasminogen activator inhibitor-1 4G/5G polymorphism on the thrombotic risk of patients with Behcet's disease.
The present study was designed to analyse the role of the factor V Leiden and the prothrombin G20210A mutations and plasminogen activator inhibitor-1 4G/5G polymorphism on the thrombotic risk of patients with Behcet's disease.
Strong family history of BD, clinical course, and laboratory results (no evidence of disseminated intravascular coagulation, normal levels of protein C and S, absence of factor V Leiden and anticardiolipin antibodies) suggested neurological manifestations of BD as the most probable diagnosis.
These findings suggest that homozygosity or heterozygosity for factor V Leiden is not always associated with occurrence of venous thrombosis in BD, but it may be a contributing risk factor for venous thromboembolic events in these patients.