New Onset of Autoimmune Diseases Following COVID-19 Diagnosis

Abstract

There is growing evidence that coronavirus disease 2019 (COVID-19) can lead to a dysregulation of the immune system with the development of autoimmune phenomena. The consequence of this immune dysregulation ranges from the production of autoantibodies to the onset of rheumatic autoimmune disease. In this context, we conducted a systematic review to analyze the current data regarding the new-onset systemic and rheumatic autoimmune diseases in COVID-19 patients. A literature search in PubMed and Scopus databases from December 2019 to September 2021 identified 99 patients that fulfilled the specific diagnostic/classification criteria and/or nomenclature for each rheumatic autoimmune disease. The main diseases reported were vasculitis and arthritis. Idiopathic inflammatory myopathies, systemic lupus erythematosus, and sarcoidosis were also reported in a limited number of patients, as well as isolated cases of systemic sclerosis and adult-onset Still’s disease. These findings highlight the potential spectrum of systemic and rheumatic autoimmune diseases that could be precipitated by SARS-CoV-2 infection. Complementary studies are needed to discern the link between the SARS-CoV-2 and new onset-rheumatic diseases so that this knowledge can be used in early diagnosis and the most suitable management.

COVID-19 in an Adult with Down Syndrome: Impact on Autoimmune Response

“…Moreover, Gracia-Ramos et al describe the characteristics of patients of new-onset systemic lupus erythematosus during or after SARS-CoV-2 infection. Serosal involvement was seen in 4 cases, (pleural effusion 3, pericardial effusion 2, ascites 1), as was observed in our case [ 16 ]. As pleuritis is the most common pulmonary complication in patients with SLE but uncommon in COVID-19, its presence is considered to be associated with activity of SLE [ 17 ].…”

Dysregulated Immune Responses in SARS-CoV-2-Infected Patients: A Comprehensive Overview

“…The long-term consequences of COVID-19 may involve different cardiac pathophysiological mechanisms, including severe hypoxia-mediated injury, thromboembolic disease, systemic inflammatory response, and direct myocardial inflammation [ 161 ]. Hyperactivation of Th17 and Tfh cells, changes in their subsets, the imbalance between ‘regulatory’ and ‘pro-inflammatory’ T cell subsets in general, and uncontrolled B cell activation and antibody production increase the risk of autoimmune inflammation and autoimmune-related manifestations [ 6 , 162 ].…”

Overview of infections as an etiologic factor and complication in patients with vasculitides

“…Evidence of central nervous system vasculitis following COVID-19 was confirmed via biopsy despite a mild form of SARS-CoV-2 infection [52]. Gracia-Ramos et al reviewed the available evidence on the incidence of autoimmune diseases in COVID-19 patients [53]. In incidence vasculitis patients, they noted a male sex predisposition, with the majority of patients exhibiting a mild-to-moderate COVID-19 disease course [53].…”

“…Gracia-Ramos et al reviewed the available evidence on the incidence of autoimmune diseases in COVID-19 patients [53]. In incidence vasculitis patients, they noted a male sex predisposition, with the majority of patients exhibiting a mild-to-moderate COVID-19 disease course [53]. Vasculitis onset was reported approximately one month after SARS-CoV-2 infection and completely resolved in the vast majority of cases [53].…”

“…In incidence vasculitis patients, they noted a male sex predisposition, with the majority of patients exhibiting a mild-to-moderate COVID-19 disease course [53]. Vasculitis onset was reported approximately one month after SARS-CoV-2 infection and completely resolved in the vast majority of cases [53]. In a recently reported positron emission tomography/computed tomography study of recovered adult COVID-19 patients with residual symptoms, a higher target-to-blood pool ratio was observed in the thoracic aorta, right iliac artery, and femoral artery of COVID-19 patients compared to control, indicating a persistent vascular inflammation which could be responsible for vasculitic manifestations in the long-term recovery period [54].…”