title: Lupus anticoagulant and history of thrombosis are not associated with persistent endothelial cell activation in systemic lupus erythematosus.
abstract: Antiphospholipid antibodies (aPL), especially lupus anticoagulant (LAC), characterize systemic lupus erythematosus (SLE) patients at increased risk for arterial and venous thromboembolic complications. It has been reported that purified human anti-phospholipid antibodies cause endothelial cell activation in in vitro experiments. In order to investigate whether increased endothelial cell activation is associated with thromboembolic events in SLE patients with LAC, we measured plasma levels of thrombomodulin (TM), von Willebrand factor (vWf), sP-selectin, vascular cell adhesion molecule-1 (sVCAM-1) and ED1-fibronectin in a study of 76 patients with SLE. Patients were subdivided on the basis of: no history of thrombosis and LAC-negative (n = 22) or LAC-positive (n = 17); positive history of thrombosis and LAC-negative (n = 16) or LAC-positive (n = 21). The median SLE disease activity index (SLEDAI) was 4. Although concentrations of sTM, vWf, sP-selectin and sVCAM-1 were significantly elevated in SLE compared with values in healthy controls, they did not differ between the four groups, between patients with or without history of thrombosis, and between patients with or without LAC. Presence of anticardiolipin antibodies could not explain these negative findings. Adjustment of the concentrations for significantly associated variables, such as age, hypertension, smoking, immunosuppressive treatment and concentrations of creatinine, cholesterol and homocysteine, did not change the main results of the study. Only sTM was significantly lower in patients with both LAC and thrombosis than in patients without both these features after adjustment for serum creatinine concentrations. In conclusion, we did not find an association between endothelial cell activation and presence of LAC or history of thrombosis in SLE.
authors.affiliation: Department of Neurology, University Medical Center Utrecht, Utrecht, The Netherlands. C.J.M.Frijns@neuro.azu.nl
authors.forename: C J
authors.initials: CJ
authors.lastname: Frijns
authors.forename: R H
authors.initials: RH
authors.lastname: Derksen
authors.forename: P G
authors.initials: PG
authors.lastname: De Groot
authors.forename: A
authors.initials: A
authors.lastname: Algra
authors.forename: R
authors.initials: R
authors.lastname: Fijnheer
mesh_terms: D000328:Adult; D015415:Biomarkers; D004730:Endothelium, Vascular / Q000166:cytology / Q000276:immunology*; D005260:Female; D006801:Humans; D016682:Lupus Coagulation Inhibitor / Q000097:blood*; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000276:immunology*; D008297:Male; D015999:Multivariate Analysis; D012044:Regression Analysis; D013927:Thrombosis / Q000097:blood / Q000276:immunology* / Q000473:pathology
chemical_list: D015415:Biomarkers; D016682:Lupus Coagulation Inhibitor