OBJECTIVES: To investigate whether plasma levels of Lp(a) lipoprotein (Lp(a)) are predictors of defective fibrinolytic activity, leading to thrombosis, in patients with Behçet's disease. METHODS: Plasma Lp(a) was measured by enzyme linked immunosorbent assay, lipids and lipoproteins by enzymatic methods, and apolipoproteins A-I and B, fibrinogen (turbidimetric method), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), and D-dimer levels by enzyme immunoassay. Their levels and interactions were evaluated in 33 patients with Behçet's disease (including five with thrombotic complications) and 30 healthy control subjects. RESULTS: Plasma Lp(a) concentration was significantly greater in the patients than in controls. Nine patients (27%) had levels > 0.30 microgram. There was no correlation between Lp(a) and other lipids and lipoproteins apart from apolipoprotein B. Lp(a) showed inverse correlation with t-PA (r = -0.34, p < 0.05) and D-dimer (r = 0.35, p < 0.05). Patients with thrombotic complications had significantly greater Lp(a) and PAI-1, and lower D-dimer concentrations than control subjects. CONCLUSIONS: Measurement of plasma Lp(a) levels in patients with Behçet's disease may provide useful information regarding the potential development of thrombotic events, because of its possible role in defective fibrinolysis.
OBJECTIVES: To investigate whether plasma levels of Lp(a) lipoprotein (Lp(a)) are predictors of defective fibrinolytic activity, leading to thrombosis, in patients with Behçet's disease. METHODS: Plasma Lp(a) was measured by enzyme linked immunosorbent assay, lipids and lipoproteins by enzymatic methods, and apolipoproteins A-I and B, fibrinogen (turbidimetric method), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), and D-dimer levels by enzyme immunoassay. Their levels and interactions were evaluated in 33 patients with Behçet's disease (including five with thrombotic complications) and 30 healthy control subjects. RESULTS: Plasma Lp(a) concentration was significantly greater in the patients than in controls. Nine patients (27%) had levels > 0.30 microgram. There was no correlation between Lp(a) and other lipids and lipoproteins apart from apolipoprotein B. Lp(a) showed inverse correlation with t-PA (r = -0.34, p < 0.05) and D-dimer (r = 0.35, p < 0.05). Patients with thrombotic complications had significantly greater Lp(a) and PAI-1, and lower D-dimer concentrations than control subjects. CONCLUSIONS: Measurement of plasma Lp(a) levels in patients with Behçet's disease may provide useful information regarding the potential development of thrombotic events, because of its possible role in defective fibrinolysis.