Anti-Phospholipid Antibodies and COVID-19 Thrombosis: A Co-Star, Not a Supporting Actor.

COVID-19 antiphospholipid antibodies antiphospholipid syndrome autoimmunity thrombosis

Journal

Biomedicines
ISSN: 2227-9059
Titre abrégé: Biomedicines
Pays: Switzerland
ID NLM: 101691304

Informations de publication

Date de publication:
27 Jul 2021
Historique:
received: 08 06 2021
revised: 19 07 2021
accepted: 23 07 2021
entrez: 27 8 2021
pubmed: 28 8 2021
medline: 28 8 2021
Statut: epublish

Résumé

COVID-19 clinical features include a hypercoagulable state that resembles the antiphospholipid syndrome (APS), a disease characterized by thrombosis and presence of antiphospholipid 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. 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. 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. 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-mediated thrombosis, with SARS-CoV-2 behaving as a second hit.

Sections du résumé

BACKGROUND BACKGROUND
COVID-19 clinical features include a hypercoagulable state that resembles the antiphospholipid syndrome (APS), a disease characterized by thrombosis and presence of antiphospholipid 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 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 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 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-mediated thrombosis, with SARS-CoV-2 behaving as a second hit.

Identifiants

pubmed: 34440103
pii: biomedicines9080899
doi: 10.3390/biomedicines9080899
pmc: PMC8389622
pii:
doi:

Types de publication

Journal Article

Langues

eng

Subventions

Organisme : Fondo de Investigaciones Sanitarias, Instituto de Salud Carlos III
ID : PI17-00147 and PI20-01361

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Auteurs

Francisco Javier Gil-Etayo (FJ)

Department of Immunology, Hospital Universitario 12 de Octubre, 28041 Madrid, Spain.

Sara Garcinuño (S)

Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), 28041 Madrid, Spain.

Antonio Lalueza (A)

Department of Internal Medicine, Hospital Universitario 12 de Octubre, 28041 Madrid, Spain.

Raquel Díaz-Simón (R)

Department of Internal Medicine, Hospital Universitario 12 de Octubre, 28041 Madrid, Spain.

Ana García-Reyne (A)

Department of Internal Medicine, Hospital Universitario 12 de Octubre, 28041 Madrid, Spain.

Daniel Enrique Pleguezuelo (DE)

Department of Immunology, Hospital Universitario 12 de Octubre, 28041 Madrid, Spain.

Oscar Cabrera-Marante (O)

Department of Immunology, Hospital Universitario 12 de Octubre, 28041 Madrid, Spain.

Edgard Alfonso Rodriguez-Frias (EA)

Department of Immunology, Hospital Universitario 12 de Octubre, 28041 Madrid, Spain.

Alfredo Perez-Rivilla (A)

Department of Microbiology, Hospital Universitario 12 de Octubre, 28041 Madrid, Spain.

Manuel Serrano (M)

Department of Immunology, Hospital Universitario Clínico San Carlos, 28041 Madrid, Spain.

Antonio Serrano (A)

Department of Immunology, Hospital Universitario 12 de Octubre, 28041 Madrid, Spain.
Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), 28041 Madrid, Spain.
Department of Epidemiology, Biomedical Research Centre Network for Epidemiology and Public Health (CIBERESP), 28029 Madrid, Spain.

Classifications MeSH