Strong association of autoantibodies to human nuclear lamin B1 with lupus anticoagulant antibodies in systemic lupus erythematosus

Objective. To determine the frequency and clinical significance of high tit ers of IgG autoantibodies to nuclear lamin B1 in a large number of unselect ed and well-characterized systemic Lupus erythematosus (SLE) patients, dise ase controls, and normal healthy controls. Methods, A cross-sectional study of anti-lamin B1 autoantibodies, as measur ed by enzyme-linked immunosorbent assay using human recombinant lamin B1 au toantigen, was performed on serum samples obtained at first evaluation of 2 38 consecutive French Canadian adults: 61 healthy control subjects, 20 pati ents,vith osteoarthritis, 22 with ankylosing spondylitis, 11 with autoimmun e hepatitis, 30 with rheumatoid arthritis, and 94 with SLE. SLE patients we re studied for 57 disease manifestations. A case-control study was performe d to analyze the relationship between anti-iamin B1 status and thrombotic m anifestations between SLE onset and last followup. Results. High titers of anti-lamin B1 were strikingly restricted to a subse t of 8 SLE patients (8.5%), The mean anti-lamin B1 titer was higher in this subset than in the other SLE patients or any control group (P < 0.001). By univariate analysis and stepwise multiple logistic regression, the most st riking association of anti-lamin B1 was with lupus anticoagulant (LAC) anti bodies (P = 0.00001). Although WC were significantly associated with thromb osis in our SLE patients, anti-lamin B1 was not. The frequency of thrombosi s in SLE patients expressing both LAC and anti-lamin B1 was similar to that in patients without LAC (P = 1.0), However, patients expressing LAC withou t anti-lamin B1 had a greater frequency of thrombosis (P = 0.018). Conclusion. High titers of IgG anti-lamin B1 autoantibodies are highly spec ific for a subset of SLE patients whose clinical characteristics include th e presence of LAC and other laboratory manifestations of the antiphospholip id syndrome. The presence of LAC without anti-lamin B1 may define a subset of SLE patients at greater risk for thrombosis.