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SARS-CoV-2 infection in patients with systemic autoimmune diseases


1, 2, 3, 4, 5

 

  1. Laboratory of Autoimmune Diseases Josep Font, IDIBAPS-CELLEX, Barcelona, and Autoimmune Diseases Unit, Department of Internal Medicine, Hospital CIMA- Sanitas, Barcelona, Spain.
  2. Centre d’Atenció Primària Les Corts, Consorci d’Atenció Primària de Salut Barcelona Esquerre (CAPSBE), Barcelona; Grup Tranversal de Recerca en Atenció Primària, Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona; and Department of Medicine, Universitat de Barcelona, Barcelona, Spain. asiso@clinic.cat
  3. Laboratory of Autoimmune Diseases Josep Font, IDIBAPS-CELLEX, Barcelona, Spain.
  4. Rheumatology Department, Hospital Universitari Parc Taulí, Sabadell, Barcelona; Instituto Modelo de Cardiología Privado SRL, Córdoba, and Instituto Universitario de Ciencias Biomédicas de Córdoba (IUCBC), Argentina.
  5. Laboratory of Autoimmune Diseases Josep Font, IDIBAPS-CELLEX, Barcelona; Department of Medicine, Universitat de Barcelona, and Department of Autoimmune Diseases, ICMiD, Hospital Clínic, Barcelona, Spain.

CER14406
2021 Vol.39, N°3
PI 0676, PF 0687
Review

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PMID: 34001305 [PubMed]

Received: 11/01/2021
Accepted : 23/02/2021
In Press: 05/05/2021
Published: 21/05/2021

Abstract

Systemic autoimmune diseases (SAD) are a heterogeneous group of diseases with a common aetiopathogenic basis affecting all ages characterised by a systemic phenotypic expression with a wide range of severity and outcomes that often require immunosuppressive therapies, leaving patients at high risk of infection. Knowledge of the impact of COVID-19 in patients with SAD is limited because most are included in studies carried out in patients with autoimmune and rheumatic diseases (mainly inflammatory arthritis). Most studies supported an increased risk of SARS-Cov-2 infection in patients with AD and SAD. Although case-control studies reported no significant differences in the rate of poor outcomes between patients with and without AD, large population-based studies analysing baseline risk factors reported a 2-3 times higher rate of poor outcomes in patients with AD, especially in those with SAD. Individual risk factors associated with poor outcomes included gender male, older age, and underlying comorbidities and therapies (glucocorticoids, sulfasalazine, immunosuppressants and rituximab). Patients with SAD had less favourable COVID-19 outcomes than those with inflammatory arthritis, possibly due to a differentiated underlying therapeutic approach (glucocorticoids, immunosuppressants and B-cell depleting agents for most SAD, anti-cytokine therapies and JAK inhibitors for inflammatory arthritis). Despite the limited evidence, most studies suggest that patients with SAD have an increased risk of a worse evolution of SARS-CoV-2 infection, including a greater risk of hospitalisation/ICU admission and worse survival rates and, therefore, should be considered a high-risk group for COVID-19.

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