Anti‐phospholipid antibodies and covid‐19 thrombosis: A co‐star, not a supporting actor

Abstract

Background: COVID‐19 clinical features include a hypercoagulable state that resembles the antiphospholipid syndrome (APS), a disease characterized by thrombosis and presence of an-tiphospholipid antibodies (aPL). The relationship between aPL‐presence and the appearance of thrombi as well as the transience or permanence of aPL in COVID‐19 patients is not sufficiently clear. Methods: A group of 360 COVID‐19 patients were followed‐up for 6 months. Classic aPL, anti‐B2GPI IgA, anti‐phosphatidylserine/prothrombin IgG/M and anti‐SARS‐CoV‐2 antibodies were determined at acute phase and >12 weeks later. The reference group included 143 healthy volunteers of the same age‐range distribution. Results: aPL prevalence was similar in COVID‐19 patients and the reference population. aPL presence in both determinations was significantly associated with thrombosis (OR: 2.33 and 3.71), strong agreement being found for classic aPL and anti‐ B2GPI IgA (Weighted kappa: 0.85–0.91). Thrombosis‐associated aPL occurred a median of 17 days after hospital admission (IQR: 6–28) vs. 4 days for the rest (IQR: 3–7). Although anti‐SARS‐CoV‐2 antibodies levels increased during convalescence, aPL hardly changed. Conclusions: Most COVID‐ 19 patients would carry these aPL before the infection. At least two mechanisms could be behind thrombosis, early immune‐dysregulation‐mediated thrombosis after infection and belated‐aPL‐me-diated thrombosis, with SARS‐CoV‐2 behaving as a second hit.