In:
Clinical Infectious Diseases, Oxford University Press (OUP), Vol. 73, No. 9 ( 2021-11-02), p. e2869-e2874
Kurzfassung:
Severe coronavirus disease 2019 (COVID-19) frequently entails complications that bear similarities to autoimmune diseases. To date, there are little data on possible immunoglobulin (Ig) A–mediated autoimmune responses. Here, we aim to determine whether COVID-19 is associated with a vigorous total IgA response and whether IgA antibodies are associated with complications of severe illness. Since thrombotic events are frequent in severe COVID-19 and resemble hypercoagulation of antiphospholipid syndrome, our approach focused on antiphospholipid antibodies (aPL). Methods In this retrospective cohort study, clinical data and aPL from 64 patients with COVID-19 were compared from 3 independent tertiary hospitals (1 in Liechtenstein, 2 in Switzerland). Samples were collected from 9 April to 1 May 2020. Results Clinical records of 64 patients with COVID-19 were reviewed and divided into a cohort with mild illness (mCOVID; 41%), a discovery cohort with severe illness (sdCOVID; 22%) and a confirmation cohort with severe illness (scCOVID; 38%). Total IgA, IgG, and aPL were measured with clinical diagnostic kits. Severe illness was significantly associated with increased total IgA (sdCOVID, P = .01; scCOVID, P & lt; .001), but not total IgG. Among aPL, both cohorts with severe illness significantly correlated with elevated anticardiolipin IgA (sdCOVID and scCOVID, P & lt; .001), anticardiolipin IgM (sdCOVID, P = .003; scCOVID, P & lt; .001), and anti–beta 2 glycoprotein-1 IgA (sdCOVID and scCOVID, P & lt; .001). Systemic lupus erythematosus was excluded from all patients as a potential confounder. Conclusions Higher total IgA and IgA-aPL were consistently associated with severe illness. These novel data strongly suggest that a vigorous antiviral IgA response, possibly triggered in the bronchial mucosa, induces systemic autoimmunity.
Materialart:
Online-Ressource
ISSN:
1058-4838
,
1537-6591
DOI:
10.1093/cid/ciaa1496
Sprache:
Englisch
Verlag:
Oxford University Press (OUP)
Publikationsdatum:
2021
ZDB Id:
2002229-3
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