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ObjectiveSystemic Lupus Erythematosus (SLE) is characterized by arthritis, rash, glomerulonephritis, and hematologic manifestations, including secondary immune mediated thrombocytopenia (ITP). Presence of ITP type, platelet specific glycoprotein antibodies have been detected in SLE, but their exact role and frequency is not known although thrombocytopenia can be of prognostic importance. The objective of this study was to determine the frequency of platelet specific antibodies in patients with SLE and if the presence of these antibodies is associated with disease activity.MethodsWe collected serum samples from 74 patients with SLE (≥ 4 American College of Rheumatology 1982 criteria) during high (H) and lower (L) SLE Disease activity index 2000 (SLEDAI-2K) score (median SLEDAI-2K, H = 8.5 and L = 0.5). Mean age at the first sampling was 43,6 and the second 48,6 years. Antibodies towards platelet glycoproteins (GP) IIb/IIIa, GP V and GP Ib/IX were detected in H and L serum samples, using the direct monoclonal antibody immobilization of platelet antigens assay (MAIPA). We also analyzed the presence of antiphospholipid criteria and non-criteria antibodies: Anti-CL (IgG and IgM) Anti-B2GP1 (IgG and IgM) Anti-PS/PT (IgG and IgM) Anti-AnnexinV (IgG and IgM), using ELISA.ResultsDuring H and L SLEDAI-2K we detected anti-GP IIb/IIIa antibodies in 29.7% vs 28.4%; anti-GP V antibodies in 48.6% vs 27.0% and anti-GP Ib/X antibodies in 58.1% vs 31.1%. The anti-GP V and anti-GP Ib/X levels were significantly higher in SLEDAI-2K H vs L and positively correlated with SLEDAI-2K score (r=0,322, p<0,0001 and r=0,265, p=0,001) using spearman correlation. During active disease, 66% had at least one positive GP-antibody, compared to 44% in the less active disease. All antiphospholipid antibodies of IgG type had significantly higher levels during SLEDAI-2K H. In total, 45% of patients had at least one positive antiphospholipid antibody during SLEDAI-2K H and 26% during L.ConclusionThis study shows that platelet autoantibodies are prevalent in SLE and their increased presence may be modulated by treatment and/or mechanisms regulating disease activity. Future studies will assess the functional contribution from these antibodies on platelet activation, thrombocytopenia and other aspects of SLE pathophysiology.