Anti-phospholipid antibodies in the setting of thromboembolic events associated with severe COVID-19 pneumonia

BACKGROUND: Thrombotic consequences have been reported in COVID-19-infected patients, especially those who are critically ill. Multiple studies have tested antiphospholipid antibodies (aPLs) among COVID-19 patients, but to date, the actual frequency of aPLs is still uncharted. In this cohort study, we analyzed the outcomes of 173 consecutive patients with confirmed COVID-19 infection. Anti-phospholipid antibodies, which include anti-cardiolipin antibodies [aCL (IgM), aCL (IgG)], and B2-glycoprotein I antibodies [aβ2GPI (IgM), aβ2GPI (IgG)] were detected by using immunoassays. In contrast, lupus anti-coagulant (LAC) antibodies are identified through a coagulation-based assay. RESULTS: The study demonstrated a high incidence of thrombotic consequences in severe COVID pneumonia cases and supported an increased risk of developing aPLs following COVID-19 infection. Pulmonary embolism had the most common prevalence of all thrombotic events. Among the various aPLs tested in thrombotic patients, lupus anti-coagulant (LAC) had the highest positivity (46.2%). Most patients with arterial thromboembolism (stroke, myocardial infarction, limb ischemia, bowel ischemia, and renal artery thrombosis) had triple positivity of anti-phospholipid antibodies. Testing aPLs antibodies after 12 weeks of recovery for survived patients only 2 out of 23 patients had aPLs positivity compared to 35 out of 65 tested during hospital admission. Furthermore, we found no significant changes in aPLs positivity between survived and non-survived patients with thrombotic event. CONCLUSIONS: aPLs increased transiently as an inflammatory-mediated condition. Individuals with aPLs triple positivity (positive LAC, aCL, and aB2GPI) had a considerable risk of arterial thromboembolism (ATE).