The relationship between risk factors for premature vascular disease in systemic lupus erythematosis (SLE) with secondary anti-phospholipid syndrome (APS)

Abstract number: P1510

Hampton^* K., Brookfield† C., Sheli† N., Akil† M., Snaith† M.

†UK ^*University of Sheffield, UK;

SLE is a multisystem collagen vascular disease that can cause premature morbidity and mortality by many mechanisms. However, the primary cause of premature death in SLE is vascular disease, especially premature arterial thrombosis. A proportion of patients with SLE have laboratory evidence of APS, manifested by lupus anticoagulant activity (LA), or raised IgG or IgM anti-cardiolipin antibodies (ACA). These patients are especially prone to arterial and venous thrombosis, similar to that seen in primary APS, i.e. in the absence of SLE. Aim this study was to investigate risk factors for premature vascular disease in patients with SLE and secondary APS. We have studied 51 patients. All fulfilled the American Rheumatological Association criteria for SLE and had laboratory evidence of secondary APS, either LA activity in a Dilute Russel Viper Venom assay, with phospholipid correction, or IgG or IgM ACA of moderate or high titre, or both. We assayed IgG antib2 Glycoprotein 1 (antib2GP1) by ELISA. Antib2GP1 has been associated with vascular events in primary APS and secondary APS previously. Plasma homocysteine was assayed by Fluorescent P immunoassay. Elevated homocysteine is associated with increased arterial and venous vascular events in normal subjects and both primary APS and secondary APS. IgG antioxidised Low Density Lipoprotein (antioxoLDL) were measured by ELISA and have previously been proposed as a marker of thrombotic potential and vascular pathology in APS. Patients were predominantly Caucasian (92%) and female (80%) age 28–54 years. Mean antib2GP1 was 7.1 U mL^-1 (SD 3.3 U mL^-1), homocysteine 10.05 µmol mL^-1 (SD 1.64) and antioxoLDL 8.7 U mL^-1 (SD 5.6 U mL^-1. Linear regression analysis revealed a significant correlation between antib2GP1 and plasma homocysteine, P = 0.029, but no association between antib2GP1 and antioxoLDL or antioxoLDL and homocysteine. Further studies are necessary to determine the mechanism of this association but it may explain why elevated antib2GP1 is associated with vascular events, and as homocysteine may be lowered by folate supplementation, may suggest patients with SLE and secondary APS may benefit from assay of homocysteine and folate therapy if elevated.