Increased soluble vascular cell adhesion molecule 1 concentrations in patients with primary or systemic lupus erythematosus-related antiphospholipid syndrome - Correlations with the severity of thrombosis

Objective. Recent studies have shown that in vitro endothelial cells are ac tivated by antiphospholipid antibodies and may support leukocyte adhesion. We studied levels of soluble intercellular adhesion molecule 1 (sICAM-1, sC D54), soluble vascular cell adhesion molecule I (sVCAM-1, sCD106), and solu ble E-selectin (soluble endothelial leukocyte adhesion molecule 1 [sELAM-1, sCD62E]) in sera from patients with primary antiphospholipid syndrome (pri mary APS), and compared them with those from patients with systemic lupus e rythematosus-associated APS (SLE-APS) or pure SLE, as well as with those fr om 2 control groups composed of healthy volunteers and patients with thromb osis unrelated to autoimmune diseases. Methods. Serum samples from 24 patients with primary APS, 15 patients with SLE-APS, 22 patients with pure SLE, 48 control patients with thrombosis, an d 18 healthy volunteers were examined using enzyme-linked immunosorbent ass ays specific for sICAM-1, sVCAM-1, and sELAM-1. Results. Serum levels of sVCAM-1, but not sICAM-1 or sELAM-1, were signific antly increased in all patient study groups compared with thrombosis contro l patients and healthy volunteers, but did not differ between the groups of patients with primary APS, SLE-APS, or pure SLE, Concentrations of sVCAM-1 were significantly higher in primary APS or SLE-APS patients with severe, recurrent thrombosis and were negatively correlated with platelet counts in primary APS patients. In patients with primary APS, sVCAM-1 levels were hi gher if there was thrombotic kidney involvement and correlated with creatin emia, Conclusion. Serum sVCAM-1 concentrations are increased in patients with pri mary APS, especially those with repeated thrombotic events or kidney involv ement. These findings suggest that endothelial/ monocyte interaction may be important in the pathogenesis of primary APS.