Effect of plasminogen activator inhibitor-1 4G/5G polymorphism in Turkish deep vein thrombotic patients with and without FV1691 G-A

A decreased fibrinolytic activity due to increased levels of plasminogen ac tivator inhibitor-1 has been shown in deep vein thrombosis patients. Elevat ed plasma plasminogen activator inhibitor-1 levels are associated with the 4G allele of a 4G/5G polymorphism located in the promoter region of the pla sminogen activator inhibitor-1 gene. Because there is no existing data in t he Turkish population, we aimed to study these mutations in patients with d eep vein thrombosis (n = 136) and normal controls (n = 113), consecutively selected among unrelated healthy subjects without personal and familial his tory of atherothrombosis from Ankara, Turkey. DNA was extracted by conventi onal methods, and polymerase chain reaction of the plasminogen activator in hibitor-1 4G/5G polymorphism was performed according to a previously descri bed method. Genotype distributions of FV 1691G-A and plasminogen activator inhibitor-1 4G/5G are as follows: plasminogen activator inhibitor-1 4G (pat ients) 0.562, plasminogen activator inhibitor-1 4G (controls) 0.50 (p = 0.6 ); FV1691A (patients) 0.147, FV1691A (controls) 0.035 (p = 0.005), Our data indicated that plasminogen activator inhibitor-1 4G/5G does not have an ef fect an the thrombotic risk. Carrying the 4G allele either in heterozygous or homozygous state increases the risk in the presence of FV1691A (odds rat io: 9.8 and 6.9, confidence interval 95% 2.9-32.7 and 1.3-35.8). FV1691A is an independent risk factor for thrombosis (odds ratio: 5.5, confidence int erval: 95% 2.5-12.1). We concluded that coexistence of FV1691A and plasmino gen activator inhibitor-1 4G allele leads to an increased risk for thrombos is leading a further evidence to another prothrombotic factor that may be n ecessary for the development of a manifest thrombotic event. (C) 2000 Elsev ier Science Ltd. All rights reserved.