Background and aim: Mild hyperhomocysteinemia is recognised as a risk factor for venous thromboembolic disease, though its role in the thrombogenic processes is not understood. The aim was to establish possible associations between hyperhomocysteinemia and abnormal fibrinolysis in venous thromboembolism. Subjects and Methods: Fasting total plasma homocysteine (tHcys) was measured with high-performance liquid chromatography in 157 patients (61 females/96 males) below the age of 60 (mean 43) years, with history of objectively confirmed venous thromboembolic disease. Hyperhomocysteinemia was defined as tHcys above the 95 th percentile (>11.8 μmol/L) of 138 apparently healthy age matched subjects. Results: Patients had on average by 11 % higher tHcys than healthy controls (8.0, 6.6-9.9 vs 7.2, 5.9-8.6 umol/L. p <0.01). tHcys weakly correlated with t-PA antigen (r=0.19; p <0.05), PAI-1 antigen (r=0.16: p <0.05) and PA-1 activity (r=0.15; p=0.06). (Hey was associated also with age (r=0.27), total cholesterol (r=0.25) and triglycéride level (r=0.21, all p <0.01 ). In a multivariate analysis model age, total cholesterol and t-PA antigen explained 9 % of tHcy variability. A subgroup of 22 patients with mild hyperhomocysteinemia (tHcys: 17.1, 12.1 -18.8 jamol/L) was compared to 22 age, sex and serum lipids matched patients with normal tHcys levels (7.3,6.3-8.0 umol/L, all values medians with 1 .-3. quartiles). No significant differences between the two groups were observed neither in t-PA nor in PAI-1. Conclusions: In patients with history of venous thromboembolism no evidence was found for an independend association between iHcy and fibrinolytic factors. Therefore, this study does not support the hypothesis that hyperhomocystinemia contributes to development of venous thromboembolic disease by altering t-PA and PAI-1 levels.
|Number of pages||1|
|Journal||Fibrinolysis and Proteolysis|
|Issue number||SUPPL. 1|
|Publication status||Published - 1998|
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