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ß2 glycoprotein I containing immune-complexes in lupus patients: association with thrombocytopenia and lipoprotein (a) levels
Department of Medicine B', Tel Aviv University, Israel
The Rheumatology Unit, Tel Aviv University, Israel
Department of Medicine B', Tel Aviv University, Israel
Department of Immunology, Weizmann Institute of Science, Rehovot, Israel
Institute of Lipid and Atherosclerosis Research, Sheba Medical Center, Tel Hashomer, Sackler Faculty of Medicine, Tel Aviv University, Israel
Department of Medicine B', Tel Aviv University, Israel; Department of Medicine B', Sheba Medical Center, Tel-Hashomer 52621, Israel In this study we determined the prevalence and clinical associations of immune-complexescontaining beta-2-glycoprotein I (b2GPI) in randomly selected SLE patients. We studied 38 consecutive SLE patients attending the Rheumatology Unit. Previous arterial or venous-thrombosis were documented by the appropriate diagnostic test. Lipid profile including total cholesterol, LDL, VLDL, HDL and Lp(a) levels were determined from the sera of the fasting patients. Antibodies to cardiolipin, oxidized LDL and b2GPI were detected employing ELISA. b2GPI containing IgG immune-complexes were assayed by using a dot-blot assay. Fourteen SLE patients (36.8%) were found to be positive for the presence of IgG anti-b2GPI antibodies. Ten of the SLE patients (26.3%) were found to have high levels of b2GPI containing immune-complexes. There was a positive correlation between b2GPI-IC levels and the occurrence of thrombocytopenia in the patients (P < 0.05). Furthermore, patients with SLE and venous thrombosis had higher levels of b2GPI-IC when compared with thrombosis-free patients or with healthy controls (P < 0.05). Patients with higher Lp(a) levels (> 50 mg/dl) possessed higher levels of b2GPI-IC as compared with patients with lower Lp(a) concentration (< 20 mg/dl) (P < 0.05). These results suggest that IC-containing b2GPI can help in defining a subpopulation of SLE patients with increased risk of thrombocytopenia and further aid in resolving mechanisms of immune-mediated tissue damage.
Key Words: APS ß2GPI autoimunity Lp(a) immune-complex SLE
Lupus, Vol. 8, No. 2,
116-120 (1999) This article has been cited by other articles:
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