Fibrinolysis in patients with the 1691 G-A mutation in factor V gene and history of deep vein thrombosis
Stegnar, Mojca ...
It was observed that cosegregation of two inherited risk factors for deep veinthrombosis (DVT), e.g. resistance to activated protein C (APC) with protein C or protein S deficiency increases clinical ...manifestation of DVT. Theaim was to establish if there exists cosegreagtaion of the 1691 G-A mutation in factor V gene, the major cause of resistance to APC and impairmentof fibrinolysis, and if possible cosegregation of both defects effects severity of the disease. Eighty-eight consecutive patients (37 females, 51 males, aged 19-60, mean 42 years) were investigated 18 +- 10 months after acute DVT. In 15 patients (16%), the 1691 G-A mutation in factor V gene was observed. These patients did not differ from other DVT patients by clinical characteristics, age, body mass index, fasting glucose and cholesterol, or by resting levels of tissue-type plasminogen activator (t-PA),plasminogen activator inhibitor 1 (PAI-1) and euglobulin activity (t-PAantigen: 7.5 vs 7.1 ng/mL; t-PA activity: 0.9 IU/mL; PAI-1 antigen: 18.1 vs 13.6 ng/mL; PAI activity 13.8 vs 13.9 IU/mL, all values medians; euglobulinclot lysis time: 308 +- 32 vs 298 +- 78 min, mean +- SD). Moreover, frequncies of abnormal levels of t-PA, PAI-1 (t-PA antigen > 13 ng/mL, t-PA activity < 0.1 IU/mL, PAI-1 antigen > 37 ng/mL, PAI activity > 35 IU/mL) and euglobulin activity (euglobulin clot lysis time > 410 min) were similar in both subgroups of patients. Recurrent DVT was not more frequent in patients with both defectsL the 1691 G-A mutation in factor V gene and impared fibrinolysis. It was concluded that altered fibrinolysis is not an aggrevatingfactor for DVT in patients with the 1691 G-A mutation in factor V gene.
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