Triple aPL positivity was seen in 2/11 (18

Triple aPL positivity was seen in 2/11 (18.2%) versus none (0/93) of the patients with and without thrombotic events (p?=?0.01). [159C282]231 [153C368]0.355?CRP, mg/L69 A939572 [30C107]64.2 [28.3C104.1]124 [64.7C253]0.021?Fibrinogen, g/L6.0 [4.83C6.98]5.95 [4.88C6.93]6.5 [4.5C8.15]0.861?D-Dimer, g/L950 [480C1920]890 [450C1615]5860 [2555C17,750] 0.001?Ferritin, g/L876 [364C1463]867 [356C1526]979 [368C1413]1.0?IL-6, pg/mL60 [34C83]61.5 [34.8C91.8]54 [31.8C123]0.980Anti-phospholipid Ab markers?IgG anticardiolipin Ab8 (7.7)5 (5.4)3 (27.3)0.037? em IgG titer (fold UNL) /em 1.5 [1.3C2]1.6 [1.2C2]1.3/1.5/2.3?0.786?IgM anticardiolipin Ab8 Efna1 (7.7)3 (3.2)5 (45.5) 0.001? em IgM titer(fold UNL) /em 1.6 [1.4C2.2]1.2/1.5/1.6?1.7 [1.5C2.5]0.143?IgA anticardiolipin Ab31 (28)26 (28)5 (45.5)0.297? em IgA titer (fold UNL) /em 1.5 [1.4C1.7]1.4 [1.3C1.7]1.7 [1.6C2.6]0.081?IgG anti-2-GPI Ab5 (4.8)4 (4.3)1 (9.1)0.435? em IgG titer (fold UNL) /em 4.5 [1.8C14]6.9 [1.6C15.1]4.5?C?IgM anti-2-GPI Ab3 (2.9)2 (2.2)1 (9.1)0.287? em IgM titer(fold UNL) /em 1/4/26?4/26?1?C?IgA anti-2-GPI Ab6 (5.8)3 (3.2)3 (27.3)0.015? em IgA titer (fold UNL) /em 10 [3.1C13]2.6/3.3/15.210/10/120.7?Lupus anticoagulant, yes/nb tested21/53 (39.6)18/48 (37.5)3/5 (60)0.374?Anti-phospholipid markers positivity#?Single positivity35 (33.7)31 (33.3)4 (36.4)0.740?Double positivity12 (11.5)11 (11.8)1 (9.1)1?Triple positivity2 (1.9)0 (0)2 (18.2)0.01 Open in a separate window IQR: InterQuartil Range; BMI: Body Mass Index; CRP: C reactive protein; Ab: antibody. #Positivity of anti-phospholipid marker among anticardiolipin Ab, anti-2-GPI Ab and lupus anticoagulant. ?When n??3, singles values are given. Eleven (10.6%) patients presented a thrombotic event on admission or during follow up, i.e., 9 acute pulmonary embolisms, 1 deep vein thrombosis and 1 aortic thrombus. The main differences in patient characteristics according to the presence of a thrombotic event are detailed in Table 1. Patients with a thrombotic event had more frequently a past medical history of venous thrombosis (36.4% vs. 13.9%) and higher levels of neutrophil count (6460 vs. 4420/mm3, em p /em ?=?0.019), CRP (124 vs. 64.2?mg/L, em p /em ?=?0.021), and D-Dimer (5860 vs. 890?g/L, em p /em ? ?0.001). Most previous studies evaluating the prevalence of thrombotic events in COVID-19 have been conducted in critically ill patients. Helms et al. reported up to 43% of clinically relevant thrombotic events3. In a series of 184 A939572 critically ill COVID-19 patients, pulmonary embolism and deep vein thrombosis were found in 13.6% and 0.5%, respectively [2]. Venous thrombotic events have been associated with higher D-Dimer levels and prolonged aPPT [4]. Other studies reported pulmonary embolism in 6.6 to 10% in non-ICU patients [6,7,9,10]. In the present study, the presence of aCL was noted in 35/104 (33.7%) patients, mostly IgA aCL. Anti-2-GPI were found in 9/104 (8.7%) patients. IgG, IgM and IgA a2-GPI were positive in 8.7%, 2.9% and 5.8%, respectively. Lupus anticoagulant was found positive in 21 out of 53 (39.6%) patients. Overall, 49/104 (47.1%) patients had a least one positive aPL marker while double or triple antiphospholipid seropositivity was found in 11.1% and 1.9%, respectively. Then, we analyzed the results of aPL positivity according to the presence of thrombotic events. Anticardiolipin antibodies were more frequently found in patients with thrombotic events. The only aCL isotypes significantly associated with thrombotic events were IgG and IgM aCL ( em p /em ?=?0.037 and em p /em ? ?0.001, respectively). IgA a2-GPI were more frequently found in patients with thrombotic events [3/11 (27.3%) vs. 3/93 (3.2%), em p /em ?=?0.015)]. Lupus anticoagulant was found to be positive in 60% (3/5) of patients with thrombotic event vs. 37.5% (18/48, em p /em ?=?0.374) of those without. Triple aPL positivity was seen in 2/11 (18.2%) versus none (0/93) of the patients with and without thrombotic events (p?=?0.01). In the first patient, a 80-year-old man with a thrombus of the ascendant aorta, LA, aCL (IgG and IgA), and a2-GPI (IgG, IgM, IgA) were found positive. The other patient was an 83-year-old man with a history of multiple deep venous thromboses A939572 and a factor V deficiency who experienced a recent deep venous thrombosis. Lupus anticoagulant, IgM and IgA aCL and IgA a2-GPI were positive. If we consider only highly positive aPL (cut off 40?U/mL), 26/103 (25.2%) non-ICU A939572 individuals had at least one positive aPL [4/11 (36%) vs 22/91 (24%) individuals with or without thrombosis, em p /em ?=?0.461]. The presence of at least two positive aPL ( 40?U/ml) was associated with thrombosis [3/11 (27.3%) vs 1/93 (1.1%), em p /em ?=?0.004]. Overall, almost half of non-ICU COVID-19 individuals experienced at least one aPL, primarily aCL whereas a2-GPI were more rarely found ( 10%). Viral-induced aCL are hardly ever associated with a2-GPI, often transient and are not correlated with thrombosis A939572 risk [12]. One limitation of this study is definitely that we could not assess if these aPL were prolonged are not. Inside a COVID-19 case series of 216 individuals, lupus anticoagulant was found in 31 out of 35 of those with a prolonged aPPT, from which only two experienced suspected or confirmed.