title: Serum anti-beta2-glycoprotein-I and anticardiolipin antibodies during thrombosis in systemic lupus erythematosus patients.
abstract: OBJECTIVE
  Antibodies to beta2-glycoprotein-I are more strongly associated with clinical antiphospholipid syndrome than are anticardiolipin antibodies. We previously found a decrease in anticardiolipin antibodies at the time of thrombosis in 6 patients with systemic lupus erythematosus (SLE). We therefore sought to determine the prevalence and levels of antibodies to beta2-glycoprotein-I and to cardiolipin before, during, and after thrombosis in patients with SLE, and to compare them with patients who did not have thrombosis.
  
  
  METHODS
  We studied 24 patients with SLE who had at least one episode of thrombosis and 102 patients with SLE without thrombosis. Serum anticardiolipin antibodies were measured by conventional enzyme-linked immunosorbent assay (ELISA) using newborn calf serum as the blocking agent. Serum anti-beta2-glycoprotein-I antibodies were measured by ELISA on nonirradiated plates, using purified human beta2-glycoprotein-I without phospholipid.
  
  
  RESULTS
  All patients with thrombosis had anti-beta2-glycoprotein-I antibodies, compared with only 17% of controls (P <0.0001). We observed a significant decrease in serum anti-beta2-glycoprotein-I levels at the time of thrombosis, as compared with previous and subsequent samples. The prevalence and levels of IgG and IgM anticardiolipin antibodies were similar in patients with and without thrombosis. A decrease in IgG or IgM anticardiolipin titers occurred during thrombosis in 6 patients. Anticoagulant, corticosteroid, and immunosuppressive treatments did not appear to affect anti-beta2-glycoprotein-I levels at the time of thrombosis.
  
  
  CONCLUSIONS
  Anti-beta2-glycoprotein-I antibodies are strongly associated with thrombosis in patients with SLE. The decrease of anti-beta2-glycoprotein-I levels at the time of thrombosis may indicate a pathogenic role. This antibody may also be a marker of predisposition for thrombosis in these patients.
authors.affiliation: Department of Immunology and Rheumatology, Instituto Nacional de la Nutrición Salvador Zubirán, Mexico City, Mexico.
authors.forename: L
authors.initials: L
authors.lastname: Gómez-Pacheco
authors.forename: A R
authors.initials: AR
authors.lastname: Villa
authors.forename: C
authors.initials: C
authors.lastname: Drenkard
authors.forename: J
authors.initials: J
authors.lastname: Cabiedes
authors.forename: A R
authors.initials: AR
authors.lastname: Cabral
authors.forename: D
authors.initials: D
authors.lastname: Alarcón-Segovia
mesh_terms: D000293:Adolescent; D000328:Adult; D017153:Antibodies, Anticardiolipin / Q000097:blood*; D001323:Autoantibodies / Q000097:blood*; D016022:Case-Control Studies; D002648:Child; D005260:Female; D006023:Glycoproteins / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D013927:Thrombosis / Q000276:immunology*; D053482:beta 2-Glycoprotein I
chemical_list: D017153:Antibodies, Anticardiolipin; D001323:Autoantibodies; D006023:Glycoproteins; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D053482:beta 2-Glycoprotein I