The role of hyperhomocysteinemia in systemic lupus erythematosus and antiphospholipid syndrome

Aim. To assess the role of hyperhomocysteinemia (HHC) in development of vascular complications in systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). Material and methods. A total of 125 participants (24 males and 101 females aged 38 +/- 3 years) were divided into three groups: group 1 - SLE patients (n = 51); group 2 - SLE +/- APS patients (n = 49); group 3 - primary APS patients (n = 25). The patients had the disease for 14 +/- 11 years. Lupus anticoagulant (LA) and anticardiolipin antibodies (aCL) marked APS serologically. Homocystein (HC) was assayed by high performance liquid chromatography. HHC (HC > 15 mcg/l) was diagnosed in 82 of 125 (66%) patients: in 59% patients of group 1, 67% - of group 2 and 76% - of group 3. There was a relationship between HHC and digital necrosis (DN): 80% of DN patients had HHC while HHC was diagnosed in 57% patients free of DN (chi-square = 4.76, p = 0. 03). Development of occlusions in APS was associated with HHC. Elevated levels of HC in blood was registered in 43 of 55 (78%) APS patients with thromboses vs 9 of 19 (47%) patients with APSfree of thromboses (p = 0. 03). HHC occurred significantly more frequently in patients with arterial thromboses (in all 14 patients) than in patients with venous thromboses (in 16 of 23 -69.6%, p = 0.03) and in the absence of thromboses (in 9 of 19, 474%, p = 0.04). HHC was associated with thromboses of cerebral, peripheral arteries (90 vs 47% in patients without thrombosis, p = 0. 005; 84 vs 47%, p = 0. 04, respectively), coronary vessels (79 vs 47%, p = 0. 04). In APS patients having arterial thromboses with duration of postthrombocytic period (PTP), estimated as time from thrombosis to entering the trial, less than 2 months, HC concentration was significantly higher (22.9 +/- 7.0 mcg/l) compared to patients with PTP more than 2 years (16.6 +/- 3.7 mcg/l (p = 0.04). Conclusion. More than 50% patients with SLE and APS, irrespective of APS variants, had an elevated HC level in the blood. Correlation between HHC and development of thromboses, primarily arterial, in APS gives grounds for the role of HHC in development of vascular complications in SLE and APS.