Altered Fibrinolysis in DVT: Influence of Site of Sampling

Summary

Alteration of the fibrinolytic system is considered to be important in the development of deep venous thrombosis (DVT). Using specific assays for tissue plasminogen activator (t-PA) activity, t-PA inhibitor (PAI) and t-PA antigen, we measured these activities in 16 women who developed DVT during their pregnancies. A group of 24 healthy females of comparable age was studied as controls. PAI was increased in 87% of these patients compared to the healthy controls. In some of these patients a defect in release of t-PA from vascular endothelium was found as well. The site at which blood was sampled for analysis appeared to be an important criterion in the ex vivo assessment of functional t-PA reserve and PAI levels, though relatively less so for the latter measurement. The unaffected lower limbs, relative to the unaffected upper limbs, showed an increase in PAI and a demonstrable decrease in t-PA release, both representing increased risk factors for rethrombosis. The affected lower limbs showed similar but more accentuated changes in these parameters.

Key words

Altered fibrinolysis - Deep vein thrombosis - Sampling site

• References

• 1 Bertina RM, Broekmans AW, Van der Linden IK, Mertens K. Protein C deficiency in a Dutch family with thrombotic disease. Thromb Haemostas 1982; 48: 1-5
• 2 Broekmans AW, Veitkamp JJ, Bettina RM. Congenital protein C deficiency and venous thromboembolism. A study of three Dutch families N Engl J Med 1983; 309: 340-344
• 3 Egeberg O. Inherited antithrombin deficiency causing thrombophilia. Thromb Diath Haemorrh 1965; 13: 516-530
• 4 Von Kaulla E, Von Kaulla KN. Deficiency of antithrombin III activity associated with hereditary thrombosis tendency. J Med 1972; 3: 349-358
• 5 Aoki N, Moroi M, Sakata Y, Yoshida N, Natsuda M. Abnormal plasminogen. A hereditary molecular abnormality found in a patient with recurrent thrombosis J Clin Invest 1978; 61: 1186-1195
• 6 Kazama M, Tahara C, Suzuki Z, Gohchi K, Abe T. Abnormal plasminogen, a case of recurrent thrombosis. Thromb Res 1981; 21: 517-522
• 7 Johansson L, Hedner U, Nilsson IM. A family with thromboembolic disease associated with deficient fibrinolytic activity in vessel wall. Acta Med Scand 1978; 203: 477-480
• 8 Nilsson IM, Ljungner H, Tengborn L. Two different mechanisms in patients with venous thrombosis and defective fibrinolysis: low concentration of plasminogen activator or increased concentration of plasminogen activator inhibitor. Br Med J 1985; 290: 1453-1456
• 9 Juhan-Vague I, Valadier J, Alessi MC, Aillaud MF, Ansaldi J, Philip-Joet C, Holvoet P, Serradimigni A, Collen D. Deficient t-PA release and elevated PA inhibitor levels in patients with spontaneous or recurrent deep venous thrombosis. Thromb Haemostas 1987; 57: 67-72
• 10 Isacson S, Nilsson IM. Defective fibrinolysis in blood and vein walls in recurrent “idiopathic” venous thrombosis. Acta Chir Scand 1972; 138: 313-319
• 11 Loskutoff DJ, Edgington TS. Synthesis of a fibrinolytic activator and inhibitor by endothelial cells. Proc Natl Acad Sci (USA) 1977; 74: 3903-3907
• 12 Wiman B, Mellbring C, Ranby M. Plasminogen activator release during venous stasis and exercise as determined by a specific assay. Clin Chim Acta 1983; 127: 279-288
• 13 Nathan IV, Han P, Pradhan MM. Protein C functional assay using snake venom activator. Thromb Res 1987; 47: 85-91
• 14 Aoki N, Saito H, Kamiya T, Koie K, Sakata Y, Kobakura M. Congenital deficiency of α₂-plasmin inhibitor associated with severe hemorrhagic tendency. J Clin Invest 1979; 63: 877-884