Beta-2-Glycoprotein-I Deficiency Could Precipitate an Antiphospholipid Syndrome-like Prothrombotic Situation in Patients With Coronavirus Disease 2019
© 2021 The Authors. ACR Open Rheumatology published by Wiley Periodicals LLC on behalf of American College of Rheumatology..
OBJECTIVE: Patients with coronavirus disease 2019 (COVID-19) present coagulation abnormalities and thromboembolic events that resemble antiphospholipid syndrome (APS). This work has aimed to study the prevalence of APS-related antigens, 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 coronavirus 2 infection hospitalized in two Spanish university hospitals. Patients were evaluated for classic and extra-criteria antiphospholipid 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), the immune complex of IgA aβ2GPI (IgA-aβ2GPI), bounded to β2-glicoprotein-1 (β2GPI) and β2GPI levels soon after COVID-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% confidence interval: 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 (>85 mg/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-levels were 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 seen in APS but in the absence of aPLs.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2021 |
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Erschienen: |
2021 |
Enthalten in: |
Zur Gesamtaufnahme - volume:3 |
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Enthalten in: |
ACR open rheumatology - 3(2021), 4 vom: 19. Apr., Seite 267-276 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Serrano, Manuel [VerfasserIn] |
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Date Revised 24.04.2021 published: Print-Electronic Citation Status PubMed-not-MEDLINE |
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doi: |
10.1002/acr2.11245 |
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funding: |
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PPN (Katalog-ID): |
NLM322954789 |
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520 | |a © 2021 The Authors. ACR Open Rheumatology published by Wiley Periodicals LLC on behalf of American College of Rheumatology. | ||
520 | |a OBJECTIVE: Patients with coronavirus disease 2019 (COVID-19) present coagulation abnormalities and thromboembolic events that resemble antiphospholipid syndrome (APS). This work has aimed to study the prevalence of APS-related antigens, antibodies, and immune complexes in patients with COVID-19 and their association with clinical events | ||
520 | |a METHODS: A prospective study was conducted on 474 adults with severe acute respiratory syndrome coronavirus 2 infection hospitalized in two Spanish university hospitals. Patients were evaluated for classic and extra-criteria antiphospholipid 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), the immune complex of IgA aβ2GPI (IgA-aβ2GPI), bounded to β2-glicoprotein-1 (β2GPI) and β2GPI levels soon after COVID-19 diagnosis and were followed-up until medical discharge or death | ||
520 | |a 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% confidence interval: 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 (>85 mg/l). Low levels of β2GPI were significantly associated with ventilatory failure (P = 0.026) | ||
520 | |a CONCLUSION: β2GPI levels were much lower in patients with COVID-19 than in healthy people. Low β2GPI-levels were 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 seen in APS but in the absence of aPLs | ||
650 | 4 | |a Journal Article | |
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700 | 1 | |a Lalueza, Antonio |e verfasserin |4 aut | |
700 | 1 | |a Bravo-Gallego, Luz Yadira |e verfasserin |4 aut | |
700 | 1 | |a Diaz-Simón, Raquel |e verfasserin |4 aut | |
700 | 1 | |a Garcinuño, Sara |e verfasserin |4 aut | |
700 | 1 | |a Gil-Etayo, Javier |e verfasserin |4 aut | |
700 | 1 | |a Moises, Jorge |e verfasserin |4 aut | |
700 | 1 | |a Naranjo, Laura |e verfasserin |4 aut | |
700 | 1 | |a Prieto-González, Sergio |e verfasserin |4 aut | |
700 | 1 | |a Ruiz-Ortiz, Estibaliz |e verfasserin |4 aut | |
700 | 1 | |a Sánchez, Beatriz |e verfasserin |4 aut | |
700 | 1 | |a Moreno-Castaño, Ana Belen |e verfasserin |4 aut | |
700 | 1 | |a Díaz-Pedroche, Carmen |e verfasserin |4 aut | |
700 | 1 | |a Viñas-Gomis, Odette |e verfasserin |4 aut | |
700 | 1 | |a Cervera, Ricard |e verfasserin |4 aut | |
700 | 1 | |a Serrano, Antonio |e verfasserin |4 aut | |
700 | 0 | |a APS-COVID 19 Study Group/European Forum on Antiphospholipid Antibodies |e verfasserin |4 aut | |
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700 | 1 | |a Bravo-Gallego, Luz |e investigator |4 oth | |
700 | 1 | |a Camprubí, Daniel |e investigator |4 oth | |
700 | 1 | |a Calvo, Júlia |e investigator |4 oth | |
700 | 1 | |a Capdevila-Reniu, Aina |e investigator |4 oth | |
700 | 1 | |a Carbonell, Irene |e investigator |4 oth | |
700 | 1 | |a Espígol-Frigolé, Georgina |e investigator |4 oth | |
700 | 1 | |a Fuertes, Irene |e investigator |4 oth | |
700 | 1 | |a Gabara, Cristina |e investigator |4 oth | |
700 | 1 | |a Giavedoni, Priscila |e investigator |4 oth | |
700 | 1 | |a Grafia, Ignacio |e investigator |4 oth | |
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700 | 1 | |a Matas-García, Ana |e investigator |4 oth | |
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700 | 1 | |a Pellicé, Martina |e investigator |4 oth | |
700 | 1 | |a Pinazo, María Jesús |e investigator |4 oth | |
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700 | 1 | |a Rodríguez, Natalia |e investigator |4 oth | |
700 | 1 | |a Rodríguez-Núñez, Olga |e investigator |4 oth | |
700 | 1 | |a Sotil, Ruth |e investigator |4 oth | |
700 | 1 | |a Tomé, Adrià |e investigator |4 oth | |
700 | 1 | |a Ventosa, Helena |e investigator |4 oth | |
700 | 1 | |a Zamora-Martínez, Carles |e investigator |4 oth | |
700 | 1 | |a Allende, Luis |e investigator |4 oth | |
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700 | 1 | |a Cabrera-Marante, Oscar |e investigator |4 oth | |
700 | 1 | |a de la Calle, Cristina |e investigator |4 oth | |
700 | 1 | |a Castro, María José |e investigator |4 oth | |
700 | 1 | |a Folgueira, Dolores |e investigator |4 oth | |
700 | 1 | |a García-Reyne, Ana |e investigator |4 oth | |
700 | 1 | |a Laguna, Rocío |e investigator |4 oth | |
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700 | 1 | |a Talayero, Paloma |e investigator |4 oth | |
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