Study of fibrinolytic parameters in Indian patients with venous thrombosis

A. Prabhudesai1, S. Shetty1, K. Ghosh2, B. Kulkarni1 (1Mumbai, India, 2Surat, India)

Venous thrombosis
Date: 17.02.2017,
Time: 17:15 - 18:15

Objective: To establish a co-relation between impaired or defective fibrinolytic system and venous thrombosis in Indian patients by comprehensively studying the fibrinolytic pathway factors and detect any possible defects which may be causative for venous thrombosis in Indian patients.

Methods: 224 venous thrombosis patients were studied for conventional thrombophilia markers along with Fibrinolytic markers Plasminogen (PLG), Tissue Plasminogen Activator (TPA), Plasminogen Activator Inhibitor (PAI-1), Thrombin activatable fibrinolysis inhibitor (TAFI), Alpha-2-Antiplasmin (A2-AP) along with Thrombomodulin (TM) and Tissue factor pathway inhibitor (TFPI). PAI-1 4G/5G promoter polymorphism was also studied.

Results: 17.9% (40 cases) of venous thrombosis were accounted by conventional thrombophilia screening alone. 7.6% (17 cases) of them had Factor V Leiden mutation, 5.8% (13 cases) had Protein C deficiency, 3.1% (7 cases) had Protein S deficiency and 1.3% (3 cases) had Antithrombin III deficiency. However, a comprehensive study including fibrinolytic parameters could explain 35.3% (79 cases) of venous thrombosis. These include 13 cases (5.8%) wherein there was a combined defect i.e. positive for a conventional thrombophilia marker and a defective fibrinolytic parameter. There were also 4 cases (1.8%) wherein at least two fibrinolytic proteins were abnormal. High PAI-1 levels were seen in 16.5% (37 cases) (170.67± 89.89 ng/ml). 17 of these cases also had high CRP level. PAI-1 4G/5G promoter polymorphism is associated with circulating levels of PAI-1. Cases with a 4G/4G genotype had significantly high mean of 96.25 ± 71.19 ng/ml PAI-1 level in comparison with those with 4G/5G genotype (60.84 ± 43.82 ng/ml) and 5G/5G genotype (54.11 ± 41.54 ng/ml). 21.9 % of venous thrombosis cases had a 4G/4G genotype as compared to 13 % in healthy controls. 4.5% (10 cases) had reduced TPA level (0.66 ± 0.08 ng/ml). 2.7% (6 cases) had high A2-AP level (292.52 ± 23.23 ng/ml). 1.3% (3 cases) had reduced PLG level (228.71 ± 40.60 µg/ml). 0.9% (2 cases) had high TAFI level (1120 ± 42.42 ng/ml). 0.9% (2 cases) had low TM level (0.22 ± 0.3 ng/ml). 0.4% (1 case) had low TFPI (7 ng/ml) level.

Conclusion: Data shows that testing for markers both in the anti- coagulant system and in the fibrinolytic pathway will facilitate in a comprehensive explanation of the cause of venous thrombosis.