Abstract
Autoimmune diseases and infections are often closely intertwined. Patients with autoimmune diseases are more susceptible to infections due to either active autoimmune disease or the medications used to treat them. Based on infections as environmental triggers of autoimmunity, an autoimmune response would also be expected in COVID-19. Although some studies have shown the occurance of autoantibodies and the possible development of autoimmune diseases after SARS-CoV-2 infection, current data suggest that the levels of autoantibodies following SARS-CoV-2 infection is comparable to that of some other known infections and that the autoantibodies might only be transient. The risk of SARS-CoV-2 infection in patients with a systemic autoimmune rheumatic disease (SARD) appears slightly higher compared to the general population and the course of COVID-19 disease does not seem to be very different, however, specific therapies such as glucocorticoids and anti-TNF might modulate the risk of hospitalization/death. Cytokine release syndrome is a severe complication in COVID-19. Many drugs used for the treatment of SARD are directly or indirectly targeting cytokines involved in the cytokine release syndrome, therefore it has been suggested that they could also be effective in COVID-19, but more evidence on the use of these medications for the treatment of COVID-19 is currently being collected.
Highlights
Coronavirus disease 2019 (COVID-19) is a pandemic respiratory infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
This review found that the majority of children with COVID-19 were generally less affected or asymptomatic, but infants might be seriously ill and older children may develop multisystem inflammatory syndrome in children (MIS-C) with severe systemic impairment
Each study is described by month of paper publication; diagnoses in study cohort are reported (ANCA, anti-neutrophil cytoplasmic antibodies; APS, antiphospholipid syndrome; AS, ankylosing spondylitis; CTD, connective tissue disease; b/tsDMARDs, biological/targeted synthetic disease-modifying antirheumatic drugs; JIA, juvenile idiopathic arthritis; PsA, psoriatic arthritis; Pts., patients; RA, rheumatoid arthritis; SjS, Sjögren syndrome; SLE, systemic lupus erythematosus; PM/DM, polymyositis/dermatomyositis; SpA, spondyloarthritis; SSc, systemic sclerosis; TNFi, TNF inhibitor) and most prevalent therapy taken in study population are described
Summary
Coronavirus disease 2019 (COVID-19) is a pandemic respiratory infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The shared pathogenic mechanisms and clinical aspects between the hyper-inflammatory diseases and COVID-19 may suggest SARS-CoV-2 as a triggering factor for the development of a rapid autoimmune and/or autoinflammatory dysregulation, leading to severe interstitial pneumonia, in susceptible individuals [7]. Large vessel thrombosis Pulmonary intravascular coagulopathy Deposition of complement components C5b-9, C4d, and MASP2 in the lung and skin microvasculature Increased release of inflammatory cytokines characteristic of a cytokine storm Transiently elevated aPL values (LA 64%, aCL 9%, anti-b2-GPI 13%) during the acute phase of the disease. An Italian study from the province of Bergamo, reported a 30-fold increase in the incidence of KD (0.3 per month before the epidemic, 10 per month at the time of the epidemic), with children diagnosed after the COVID-19 outbreak being older, had a higher rate of cardiac involvement, features of macrophage activation syndrome, and more patients more often required additional glucocorticoid treatment [29]. Patients with autoimmune diseases may have been tested earlier and more frequently compared to the general population, but it should be noted that SARD patients suspected of having an increased risk may have followed the recommendations for social distancing more carefully than the general population
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