Background A disturbance in the fibrinolytic system may cause thrombosis in patients with antiphospholipid syndrome (APS).
Objectives To determine the levels of plasminogen (Pg) and plasminogen activator inhibitor type 1 (PAI-1) in patients with APS and evaluation of a relationship between theirecontent and clinical-laboratory manifestations of APS.
Methods The level of Pg has been identified 78 patients with APS: 35 of them were with systemic lupus erythematosus (SLE) and APS, 43 - with primary antiphospholipid syndrome (PAPS) and 19 patients were with idiopathic thrombosis (IT). PAI-1 was determined in 63 patients with APS, 26 of them with SLE and APS, 37 with PAPS, and 18 patients with IT. The control group consisted of 10 men without autoimmune diseases and thrombosis in the study period or in history. Patients were matched by age. Antiphospholipid antibodies (aPL) were measure in all studied patients: lupus anticoagulant (LA) in a phospholipid-dependent coagulation tests, antibodies to cardiolipin (aCL), antibodies to β2-glycoprotein-1 (antiβ2-GP-1) - by ELISA. The content of Pg and PAI-1 was determined by the kinetic method. The level of Pg was stratified: the normal level was from 1.5 to 2.0mM, high level - more than 2.0mM –and low level - less than 1.5mM. In history thromboses were recorded in 67 patients, 32 - arterial, 53 - venous, while 14 of these patients had co-localization of thrombosis.
Results The normal level of Pg detected in 34 out of 78 APS patients (44%), high - in 20 (25%), low - in 24 (31%). Low levels of Pg were detected in 8 (19%) of 43 of patients with PAPS and in 16 (46%) of 35 patients with SLE and APS. Pg concentration in APS patients who had thrombosis was (1.59 [1,4-1,98] microM), and it was significantly lower than in patients with IT (2,4 [1,74-2,99] mkM (p=0,0001)). It was a trend of lower Pg content in APS patients in comparison with the control group, 1.95 [1,63-2,26] microM (p=0.07). The levels of PAI-1 varied: in patients with PAPS from 0.45 to >1 nM (upper limit of the kinetic method), in patients with SLE and APS from 0.44 to >1 nM, and patients with IT - from 0.65 to 0.81 nM. In all patients with APS and IT the levels of active PAI-1 were higher than in healthy donors and varied in the range 0.44 - ≥1 nM. The majority of patients with APS (52 (83%)) had moderately high levels of PAI-1 (PAI-1 from 0.1 to 1), of whom 22 (85%) patients with SLE and APS, 30 (73%) with PAPS. The level of PAI-1 were stratified as high (PAI-1 >1) in 11 (17%) patients with APS, 4 (15%) of them with SLE and APS, and 7 (27%) patients with PAPS. All patients with the IT had the moderately high level of PAI-1.
Conclusions In patients with APS low levels of Pg occurred significantly more frequently than in patients with IT (p=0.04) and controls group (p=0.05) and was associated with thrombosis, predominantly arterial localization. Moderately high levels of PAI-1 were detected in 83% of 63 patients with APS, 17% of them had high levels of PAI-1. Patients with IT had only moderately high levels of PAI-1. High levels of PAI-1 in APS patients associated with thrombosis, mainly with arterial localization (p<0.05).
Disclosure of Interest None Declared