BACKGROUND: Plasminogen activator inhibitor-1 (PAI-1) is the most importantinhibitor of plasminogen activator. The functional 4G/5G polymorphism of the genecoding for PAI-1 may affect PAI-1 plasmatic activity, influencing the imbalancebetween coagulation and fibrinolysis cascades. In this prospective cohortanalytic study, we investigated the role of this single nucleotide polymorphismin the persistence of thrombotic lesion and the occurrence of post-thromboticsyndrome.PATIENTS/METHODS: In a group of 168 patients with post-surgical deep veinthrombosis of the legs, we analyzed the 4G/5G polymorphism in the promoter ofPAI-1 gene and plasmatic PAI-1 activity. Enrolled patients were divided in twogroups: patients with 4G/5G polymorphism and increased PAI-1 activity (n=85) and patients without 4G/5G polymorphism and normal PAI-1 activity (n=83). Allpatients were treated according to current protocols and re-examined after 3, 12 and 36months in order to evaluate the persistence of thrombotic lesion and theoccurrence of post-thrombotic syndrome.RESULTS: We found a significantly increased PAI activity in carrier of the 4Gallele, who experienced much more frequently a persistence of thrombosis after 3,12 and 36months and/or the development of post-thrombosis syndrome, in spite ofthe anticoagulant treatment.CONCLUSIONS: These data not only confirm the role played by PAI-1 activity and bythe 4G/5G SNP of the PAI-1 gene, but also suggest that current therapeuticprotocols, recommending the administration of low weight molecular heparin andoral anticoagulant for the treatment of deep vein thrombosis, could be nonsufficient for patients genetically predisposed to a less efficient clot lysis.
|Number of pages||4|
|Publication status||Published - 2014|
All Science Journal Classification (ASJC) codes