Prevalence of antibodies to beta(2)-glycoprotein I in systemic lupus erythematosus and their association with antiphospholipid antibody syndrome criteria: A single center study and literature review

Objective. To determine the prevalence of anti-beta (2)-glycoprotein I anti bodies (anti-beta (2)-GPI) in patients with systemic lupus erythematosus (S LE), and to assess their association with and predictive value for the clin ical classification criteria of the antiphospholipid antibody syndrome (APS ). Methods. One hundred thirty-three consecutive patients with SLE were rec ruited from 2 lupus clinics in the University of Toronto. Serum and plasma samples were tested for IgG anticardiolipin antibodies (aCL), prolonged par tial thromboplastin time (PTT), a panel of lupus anticoagulant (LAC) assays , and anti-beta (2)-GPI (IgG, IgM, IgA). Normal ranges for the assays were established using 129 healthy controls. A literature review from 1992 to 20 00 was performed using beta (2)-GPI, SLE, APS, thrombosis, and recurrent pr egnancy loss as key search words. Results. The distribution of anti-beta (2 )-GPI antibodies (of any isotype) in each group were as follows: all patien ts with SLE. 36.8%; SLE with clinical features of APS, 40.4%; SLE without c linical features of APS, 34.9%; and healthy controls, 3%. The positive pred ictive values of prolonged PTT, IgG aCL, and anti-beta (2)-GPI fur at least one clinical feature of APS in SLE were 59.3, 50.0, and 38.8%, respectivel y. There were 27 patients with SLE who had antibodies to beta (2)-GPI bur a normal PTT and negative aCL and LAG. Six (20.7%) of these had a history of thrombosis and/or recurrent pregnancy loss. Twelve studies (including ours ) were identified in which patient groups were similar and the same antibod y isotype was measured. No agreement was apparent after reviewing the liter ature regarding an association of anti-beta (2)- GPI IgG and clinical featu res of APS in patients with SLE. Conclusion. Antibodies to beta (2)-GPI wer e frequently seen (35%) in our SLE population. The prevalence of anti-beta (2)-GPI was similar in those with (19/47) and without (39/86) APS. Anti-bet a (2)-GPI did, however, identify 6 patients with clinical features of APS w ho were negative for aCL and prolonged PTT. Our results indicate that anti- beta (2)-GPI may provide additional information for the diagnosis of APS in SLE, but do not supercede other established assays. However, when we attem pted to place our results in the context of other reports, the literature r eview revealed that secondary diagnoses of patient groups and assay techniq ues are too variable among different investigators to allow useful comparis on. Thus, no conclusions could be drawn regarding anti-beta (2)-GPI and cli nical features of secondary APS in SLE.