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O005 - ASSOCIATION OF THE PRESENCE OF IMMUNE-COMPLEXES OF IGG/IGM BOUND TO B2-GLYCOPROTEIN-I WITH COMPLEMENT CONSUMPTION AND THROMBOCYTOPENIA IN A MULTICENTRIC COHORT OF PATIENTS WITH ANTIPHOSPHOLIPID SYNDROME (ID 725)
Abstract
Background and Aims
Antiphospholipid syndrome (APS) is a multisystemic autoimmune disorder characterized by thrombotic events and/or gestational morbidity in antiphospholipid antibodies (aPL) carriers. By a single-center study, the presence of circulating immune-complexes (CIC) formed by beta-2-glycoprotein-I (B2GP1) and IgG/IgM anti-B2GPI antibodies (B2-CIC) was associated with clinical manifestations related to APS but not included in the classification criteria (livedo reticularis, thrombocytopenia, low levels of complement factors). The aims of this multicentric study were to evaluate the prevalence and association of B2-CIC with APS-related characteristics.
Methods
A multicentric, cross-sectional, retrospective, and observational study was performed with 303 patients who met the APS classification criteria, recruited from 6 European Union hospitals. The presence of B2-CIC (IgG/IgM isotypes) and their association with clinical manifestations and biomarkers related to the disease activity were assessed.
Results
The prevalence of B2-CIC in APS patients was 39.3%. B2-CIC-positive patients with thrombotic APS had a higher incidence of heart valve thickening and dysfunction (OR: 9.6, p=0.015), triple aPL positivity (OR: 1.83; p=0.027), and thrombocytopenia (OR: 2.32; p=0.007), as well as lower levels of blood platelets, C3 and C4 (p=0.001, p<0.001 and p<0.001) compared to those B2-CIC negative. These differences were not observed in B2-CIC-positive patients with isolated gestational APS or in patients negative for B2-CIC.
Conclusions
Patients with thrombotic events and positive for B2-CIC had higher platelets and complement consumption than those negative, suggesting a greater degree of platelet activation associated with an increase of thrombocytopenia. B2-CIC could act as a possible biomarker of disease activity in APS patients.