SARS-CoV-2 outbreak in immune-mediated inflammatory diseases: the Euro-COVIMID multicentre cross-sectional study.
Journal
The Lancet. Rheumatology
ISSN: 2665-9913
Titre abrégé: Lancet Rheumatol
Pays: England
ID NLM: 101765308
Informations de publication
Date de publication:
Jul 2021
Jul 2021
Historique:
pubmed:
5
5
2021
medline:
5
5
2021
entrez:
4
5
2021
Statut:
ppublish
Résumé
The COVID-19 pandemic has raised numerous questions among patients with immune-mediated inflammatory diseases regarding potential reciprocal effects of COVID-19 and their underlying disease, and potential effects of immunomodulatory therapy on outcomes related to COVID-19. The seroprevalence of SARS-CoV-2 and factors associated with symptomatic COVID-19 in patients with immune-mediated inflammatory diseases are still unclear. The Euro-COVIMID study aimed to determine the serological and clinical prevalence of COVID-19 among patients with immune-mediated inflammatory diseases, as well as factors associated with COVID-19 occurrence and the impact of the pandemic in its management. In this multicentre cross-sectional study, patients aged 18 years or older with a clinical diagnosis of rheumatoid arthritis, axial spondyloarthritis, systemic lupus erythematosus, Sjögren's syndrome, or giant cell arteritis were recruited from six tertiary referral centres in France, Germany, Italy, Portugal, Spain, and the UK. Demographics, comorbidities, treatments, and recent disease flares, as well as information on COVID-19 symptoms, were collected through a questionnaire completed by participants. SARS-CoV-2 serology was systematically tested. The main outcome was the serological and clinical prevalence of COVID-19. Factors associated with symptomatic COVID-19 were assessed by multivariable logistic regression, and incidence of recent disease flares, changes in treatments for underlying disease, and the reasons for treatment changes were also assessed. This study is registered with ClinicalTrials.gov, NCT04397237. Between June 7 and Dec 8, 2020, 3136 patients with an immune-mediated inflammatory disease answered the questionnaire. 3028 patients (median age 58 years [IQR 46-67]; 2239 [73·9%] women and 789 [26·1%] men) with symptomatic COVID-19, serological data, or both were included in analyses. SARS-CoV-2 antibodies were detected in 166 (5·5% [95% CI 4·7-6·4]) of 3018 patients who had serology tests. Symptomatic COVID-19 occurred in 122 (4·0% [95% CI 3·4-4·8]) of 3028 patients, of whom 24 (19·7%) were admitted to hospital and four (3·3%) died. Factors associated with symptomatic COVID-19 were higher concentrations of C-reactive protein (odds ratio 1·18, 95% CI 1·05-1·33; p=0·0063), and higher numbers of recent disease flares (1·27, 1·02-1·58; p=0·030), whereas use of biological therapy was associated with reduced risk (0·51, 0·32-0·82; p=0·0057). At least one disease flare occurred in 654 (21·6%) of 3028 patients. Over the study period, 519 (20·6%) of 2514 patients had treatment changes, of which 125 (24·1%) were due to the pandemic. This study provides key insights into the epidemiology and risk factors of COVID-19 among patients with immune-mediated inflammatory diseases. Overall, immunosuppressants do not seem to be deleterious in this scenario, and the control of inflammatory activity seems to be key when facing the pandemic. Pfizer, Sanofi, Amgen, Galapagos, and Lilly.
Sections du résumé
BACKGROUND
BACKGROUND
The COVID-19 pandemic has raised numerous questions among patients with immune-mediated inflammatory diseases regarding potential reciprocal effects of COVID-19 and their underlying disease, and potential effects of immunomodulatory therapy on outcomes related to COVID-19. The seroprevalence of SARS-CoV-2 and factors associated with symptomatic COVID-19 in patients with immune-mediated inflammatory diseases are still unclear. The Euro-COVIMID study aimed to determine the serological and clinical prevalence of COVID-19 among patients with immune-mediated inflammatory diseases, as well as factors associated with COVID-19 occurrence and the impact of the pandemic in its management.
METHODS
METHODS
In this multicentre cross-sectional study, patients aged 18 years or older with a clinical diagnosis of rheumatoid arthritis, axial spondyloarthritis, systemic lupus erythematosus, Sjögren's syndrome, or giant cell arteritis were recruited from six tertiary referral centres in France, Germany, Italy, Portugal, Spain, and the UK. Demographics, comorbidities, treatments, and recent disease flares, as well as information on COVID-19 symptoms, were collected through a questionnaire completed by participants. SARS-CoV-2 serology was systematically tested. The main outcome was the serological and clinical prevalence of COVID-19. Factors associated with symptomatic COVID-19 were assessed by multivariable logistic regression, and incidence of recent disease flares, changes in treatments for underlying disease, and the reasons for treatment changes were also assessed. This study is registered with ClinicalTrials.gov, NCT04397237.
FINDINGS
RESULTS
Between June 7 and Dec 8, 2020, 3136 patients with an immune-mediated inflammatory disease answered the questionnaire. 3028 patients (median age 58 years [IQR 46-67]; 2239 [73·9%] women and 789 [26·1%] men) with symptomatic COVID-19, serological data, or both were included in analyses. SARS-CoV-2 antibodies were detected in 166 (5·5% [95% CI 4·7-6·4]) of 3018 patients who had serology tests. Symptomatic COVID-19 occurred in 122 (4·0% [95% CI 3·4-4·8]) of 3028 patients, of whom 24 (19·7%) were admitted to hospital and four (3·3%) died. Factors associated with symptomatic COVID-19 were higher concentrations of C-reactive protein (odds ratio 1·18, 95% CI 1·05-1·33; p=0·0063), and higher numbers of recent disease flares (1·27, 1·02-1·58; p=0·030), whereas use of biological therapy was associated with reduced risk (0·51, 0·32-0·82; p=0·0057). At least one disease flare occurred in 654 (21·6%) of 3028 patients. Over the study period, 519 (20·6%) of 2514 patients had treatment changes, of which 125 (24·1%) were due to the pandemic.
INTERPRETATION
CONCLUSIONS
This study provides key insights into the epidemiology and risk factors of COVID-19 among patients with immune-mediated inflammatory diseases. Overall, immunosuppressants do not seem to be deleterious in this scenario, and the control of inflammatory activity seems to be key when facing the pandemic.
FUNDING
BACKGROUND
Pfizer, Sanofi, Amgen, Galapagos, and Lilly.
Identifiants
pubmed: 33942031
doi: 10.1016/S2665-9913(21)00112-0
pii: S2665-9913(21)00112-0
pmc: PMC8081401
doi:
Banques de données
ClinicalTrials.gov
['NCT04397237']
Types de publication
Journal Article
Langues
eng
Pagination
e481-e488Informations de copyright
© 2021 Elsevier Ltd. All rights reserved.
Déclaration de conflit d'intérêts
DS has received grant or research support from Amgen, Galapagos, Sanofi, Janssen, Lilly, Pfizer, Roche Chugai, Mylan, GlaxoSmithKline, and Hifibio, and consulting fees from AbbVie, Amgen, Janssen, Celgene, Sanofi, and UCB outside the submitted work. ES has received research support from AbbVie outside the submitted work. LG has received grant or research support from Amgen, Lilly, Janssen, Pfizer, Sandoz, Sanofi, and Galapagos, and consulting fees from AbbVie, Amgen, Bristol Myers Squibb, Biogen, Celgene, Gilead, Janssen, Lilly, Novartis, Pfizer, Samsung Bioepis, Sanofi-Aventis, and UCB outside the submitted work. PMM has received consulting or speaker's fees from AbbVie, Bristol Myers Squibb, Celgene, Eli Lilly, Janssen, Merck Sharp & Dohme, Novartis, Orphazyme, Pfizer, Roche, and UCB outside the submitted work, and is supported by the UK National Institute for Health Research and University College London Hospitals Biomedical Research Centre. XB has received grant or research support from AbbVie and Novartis, and consulting fees from AbbVie, Amgen, Bristol Myers Squibb, Celgene, Celltrion, Galapagos, Gilead, Janssen, Lilly, Novartis, Pfizer, and UCB outside the submitted work. JMAG is partially supported by the Instituto de Salud Carlos III. All other authors declare no competing interests.
Références
Arthritis Rheumatol. 2021 Feb;73(2):e1-e12
pubmed: 33277981
Lancet Rheumatol. 2020 Sep;2(9):e557-e564
pubmed: 32838309
Arthritis Rheum. 2012 Aug;64(8):2677-86
pubmed: 22553077
Ann Rheum Dis. 2020 Jul;79(7):851-858
pubmed: 32503854
Ann Rheum Dis. 2021 Mar;80(3):384-391
pubmed: 33051220
Ann Rheum Dis. 2020 Sep;79(9):1170-1173
pubmed: 32532753
Arthritis Rheum. 1990 Aug;33(8):1122-8
pubmed: 2202311
Lancet. 2020 Oct 24;396(10259):1335-1344
pubmed: 32987007
Autoimmun Rev. 2012 Aug;11(10):754-65
pubmed: 22387972
Arthritis Rheum. 2010 Sep;62(9):2569-81
pubmed: 20872595
JAMA. 2020 Apr 7;323(13):1239-1242
pubmed: 32091533
Ann Rheum Dis. 2009 Jun;68 Suppl 2:ii1-44
pubmed: 19433414
JAMA. 2020 Jun 16;323(23):2425-2427
pubmed: 32421144
J Autoimmun. 2021 Jan;116:102545
pubmed: 32972804
Lancet. 2020 Mar 28;395(10229):1054-1062
pubmed: 32171076
Nat Med. 2020 Aug;26(8):1193-1195
pubmed: 32504052
JAMA Intern Med. 2021 Apr 1;181(4):450-460
pubmed: 33231628
Ann Rheum Dis. 2021 Feb;80(2):238-241
pubmed: 32963052
J Rheumatol. 2016 Jan;43(1):187-93
pubmed: 25877496
Lancet Infect Dis. 2020 Jun;20(6):669-677
pubmed: 32240634
Ann Rheum Dis. 2017 Jan;76(1):9-16
pubmed: 27789466
Ann Rheum Dis. 2020 Jul;79(7):859-866
pubmed: 32471903
Ann Rheum Dis. 2011 May;70(5):722-6
pubmed: 21257615
Nat Rev Immunol. 2020 Jun;20(6):363-374
pubmed: 32346093
Lancet. 2020 Aug 22;396(10250):535-544
pubmed: 32645347
Ann Rheum Dis. 2021 Apr;80(4):518-526
pubmed: 33158877
Ann Rheum Dis. 2021 Jul;80(7):930-942
pubmed: 33504483