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O001 - ANTI-PHOSPHOLIPID ANTIBODIES AND COVID-19 THROMBOSIS: A REAL AND OVERLAPPING RELATIONSHIP (ID 19)
Abstract
Background and Aims
COVID-19 thrombosis resembles the antiphospholipid syndrome, characterized by vascular or gestational thrombosis and presence of antiphospholipid antibodies (aPL). The appearance of aPL in infections, the permanence or transience of these autoantibodies and their clinical repercussion has been widely studied. However, this situation has not yet been clarified in COVID-19.
Methods
A prospective study with 360 COVID-19 patients enrolled from the onset of the disease and followed-up for 6 months was performed. Criteria aPL included in Sidney classification aPL, extra-criteria aPL, including anti-B2GPI IgA and anti-phosphatidylserine/prothrombin IgG/M and anti-SARS-CoV-2 antibodies were determined at acute phase and >12 weeks later. A cohort of 143 healthy volunteers of the same age-range distribution was used as a reference group.
Results
The study of the prevalence of aPL in COVID-19 patients and the reference population did not show significant differences. The presence of aPL in both determinations was associated with thrombosis (OR: 2.33 and 3.71). Strong agreement for presence of classic aPL and anti-B2GPI IgA in first and second serum samples (Weighted kappa: 0.92) was observed. aPL-associated thrombosis appeared significantly later than non-apl related thrombosis with a median of 17 days after hospital admission (IQR: 6–28) vs. 4 days for the rest of thrombosis (IQR: 3–7). COVID-19 did not seem to induce aPL de novo, since anti-SARS-CoV-2 antibodies levels increased, aPL hardly changed.
Conclusions
In COVID-19 thrombosis at least two overlapping mechanism could co-exist, an early cytokine-storm related and a later-aPL-mediated thrombosis, with SARS-CoV2 infection as a second hit.