Serum tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) and leptin as biomarkers of accelerated atherosclerosis in patients with systemic lupus erythematosus and antiphospholipid syndrome

Abstract

BackgroundPatients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) are at increased risk of atherosclerosis, and occurs much earlier compared to the general population even after accounting for traditional risk factors. Aim of the workTo examine the association between serum TWEAK, leptin and subclinical atherosclerosis in SLE and APS patients. Patients and methodsSerum tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) and leptin were measured in 30SLE patients, 26SLE patients with secondary APS (SLE–APS), 14 with primary APS (pAPS) and 20age and sex matched control. The SLE disease activity index (SLEDAI) was assessed in SLE patients. The intima media thickness (IMT) was measured by carotid ultrasound. ResultsSerum TWEAK was significantly higher in patients with pAPS (945.1±16.2pg/ml) than in SLE–APS (755.3±59.9pg/ml), SLE patients (499.2±47.1pg/ml) and control (129.6±18.6pg/ml) (p<0.001). Also, serum leptin was significantly higher in pAPS patients (14.0±2.8ng/ml) compared to that in SLE–APS (6.5±0.9ng/ml), SLE patients (3.8±1.2ng/ml) and control (1.6±0.6ng/ml) (p<0.001). The IMT was significantly increased in the pAPS patients compared to SLE–APS group (p<0.001), SLE patients (p=0.006) and to the control (p<0.001). A significant correlation was found between TWEAK with the body mass index and high density lipoprotein in SLE–APS and inversely with the random blood sugar and the diastolic blood pressure in SLE patients. Serum leptin only significantly correlated with the total leucocytic count in SLE patients. ConclusionPatients with pAPS are more liable to develop premature atherosclerosis even in the absence of the traditional risk factors.