Clinical significance of determining plasma homocysteine: case-control study on arterial and venous thrombotic patients.

AIM: To determine the differences in plasma homocysteine levels between three MTHFR 677 genotype subgroups in patients with thrombosis and in controls, as well as between patients with thrombosis and controls with the same MTHFR 677 genotype. METHODS: This case-control study was conducted in Clinical Center of Vojvodina, Novi Sad, from June to December 2011. We included 65 patients with either arterial or venous thrombosis (mean age, 40.97 ± 11.38 years) and 65 controls with no history or clinical evidence of any thrombotic event (mean age, 41.23 ± 11.12 years). Patients and controls were age- and sex-matched. RESULTS: In comparison with controls, thrombotic patients had significantly higher homocysteine levels (12.81 ± 4.94 µmol/L vs 9.82 ± 3.68 µmol/L; P<0.001) and significantly higher incidence of hyperhomocysteinemia (55% vs 22%; P<0.001; odds ratio [OR]=4.521). There were no significant differences in homocysteine levels between homozygous carriers, heterozygous carriers, and non-carriers of the MTHFR 677 mutation in either thrombotic patients (12.97 ± 5.40 µmol/L vs 12.55 ± 5.71 µmol/L vs 13.27 ± 1.71 µmol/L; P=0.100) or controls (10.07±2.50 µmol/L vs 10.25 ± 4.84 µmol/L vs 9.20 ± 2.44 µmol/L; P=0.651). However, in comparison with controls, homozygous carriers in thrombotic patient group did not have significantly higher levels of homocysteine (12.97 ± 5.40 µmol/L vs 10.07 ± 2.50 µmol/L; P=0.072), but heterozygous carriers (12.55 ± 5.71 µmol/L vs 10.25 ± 4.84 µmol/L; P=0.020) and non-carriers (13.27 ± 1.71 µmol/L vs 9.20 ± 2.44 µmol/L; P<0.001) did. There was no significant difference in homocysteine levels between patients with arterial and venous thrombosis (12.76 ± 3.60 µmol/L vs 12.86 ± 5.51 µmol/L; P=0.990) and between patients with one thrombotic event and those with recurrent thrombotic events (12.14 ± 3.20 µmol/L vs 15.25 ± 8.51 µmol/L; P=0.254). CONCLUSION: Plasma homocysteine levels have a greater clinical significance in the prevention of thrombosis and managing its complications than MTHFR 677 genotyping.

Fibrinolytic parameters, lipid status and lipoprotein(a) in ischemic stroke patients.

INTRODUCTION: Ischemic stroke is the third leading cause of mortality and morbidity in most countries in the world. Impaired fibrinolysis, as well as disordered lipid metabolism have been recognized as risk factors for this disease. OBJECTIVE: To study some of fibrinolytic parameters, lipid status and lipoprotein(a) - Lp(a) in ischemic stroke patients in Serbia and to examine associations between Lp(a) and fibrinolytic parameters. METHODS: Sixty ischemic stroke patients (case group, mean age 63.48 +/- 9.62 years) and 30 age and sex matched healthy controls (control group, mean age 60.2 +/- 7.96 years) were studied. RESULTS: A significantly longer euglobulin clot lysis time (219.7 +/- 78,8 min. vs 183.5 +/- 58,22 min; p = 0.005) and higher levels of plasminogen activator inhibitor-1 (PAI-1) (48.5 +/- 17.1 ng/ml vs 27.1 +/- 10.1 ng/ml; p = 6.2 x 10(-11)), tissue-type plasminogen activator antigen (t-PA) (11.1 +/- 7.14 ng/ml vs 6.0 +/- 3.66 ng/ml; p = 5.2 x 10(-5)) and D-dimer (382.27 +/- 504.22 ng/ml vs 116.12 +/- 88.81 ng/ml; p = 0.0002) were found in cases compared to controls. There were no significant differences in fibrinogen levels (4.30 +/- 0.84 g/l vs 4.09 +/- 0.64 g/l; p = 0.23) or plasminogen activity (92.67 +/- 11.37% vs 96.87 +/- 9.48%; p = 0.085). There was no significant difference in Lp(a) concentration between cases and controls (0.15 +/- 0.11 g/l vs 0.12 +/- 0.11 g/l; p = 0.261). However, in the cases, but not in the controls, multivariate analysis of associations between fibrinolytic parameters and Lp(a) showed the highest correlation between t-PA and PAI-1, and the latent effect of Lp(a) on t-PA and PAI-1. CONCLUSIONS: Our results show that there are important differences in the characteristics of the fibrinolytic mechanism in ischemic stroke patients compared to healthy population. The major differences are prolonged euglobulin clot lysis time and elevated PAI-1 and t-PA antigen in ischemic stroke patients. In addition, Lp(a) appears to be involved in the inhibition offibrinolysis in ischemic disease through a mechanism unrelated to its serum concentrations.