Beta-2-Glycoprotein-I Deficiency Could Precipitate an Antiphospholipid Syndrome-like Prothrombotic Situation in Patients With Coronavirus Disease 2019

Abstract

Objective. Patients with coronavirus disease 2019 (COVID-19) present coagulation abnormalities and thromboembolicevents that resemble antiphospholipid syndrome (APS). This work has aimed to study the prevalence of APS-relatedantigens, antibodies, and immune complexes in patients with COVID-19 and their association with clinical events.Methods. A prospective study was conducted on 474 adults with severe acute respiratory syndrome coronavirus2 infection hospitalized in two Spanish university hospitals. Patients were evaluated for classic and extra-criteriaantiphospholipid antibodies (aPLs), immunoglobulin G (IgG)/immunoglobulin M (IgM) anticardiolipin, IgG/IgM/immunoglobulin A (IgA) anti-β2- glicoprotein- I (aβ2GPI), IgG/IgM antiphosphatidylserine/prothrombin (aPS/PT), theimmune complex of IgA aβ2GPI (IgA- aβ2GPI), bounded to β2- glicoprotein- 1 (β2GPI) and β2GPI levels soon afterCOVID-19 diagnosis and were followed-up until medical discharge or death.Results. Prevalence of aPLs in patients with COVID-19 was as follows: classic aPLs, 5.8%; aPS/PT, 4.6%; IgA-aβ2GPI, 15%; and any aPL, 21%. When patients were compared with individuals of a control group of a similar age,the only significant difference found was the higher prevalence of IgA-aβ2GPI (odds ratio: 2.31; 95% confidenceinterval: 1.16-4.09). No significant differences were observed in survival, thrombosis, or ventilatory failure in aPL-positive versus aPL-negative patients. β2GPI median levels were much lower in patients with COVID-19 (15.9 mg/l)than in blood donors (168.8 mg/l; P < 0.001). Only 3.5% of patients with COVID-19 had normal levels of β2GPI (>85mg/l). Low levels of β2GPI were significantly associated with ventilatory failure (P = 0.026).Conclusion. β2GPI levels were much lower in patients with COVID-19 than in healthy people. Low β2GPI- levelswere associated with ventilatory failure. No differences were observed in the COVID-19 evolution between aPL-positive and aPL-negative patients. Functional β2GPI deficiency could trigger a clinical process similar to that seenin APS but in the absence of aPLs.