Discussion
To our knowledge, this the first case of RA triggered by COVID-19 infection. RA is an immune-mediated disease which etiopathogenesis involves genetic predisposition, environmental and hormonal factors. Ambient respiratory viral infections are suggested to be associated with an increased incidence rate of RA after a moderate time interval (3). In an ecological study, Coronavirus was among the viruses most associated with the number of incident RA (3).
Since the emergence of COVID-19, only few cases of reactive arthritis post SARS-CoV-2 infection have been reported. This low frequency can be explained by the use of corticosteroids in the treatment of this viral infection (4). All cases reported were man and joint inflammation affected lower extremities and occurred approximately 12 to 32 days after COVID-19 diagnosis (4). However, reactive arthritis remains a diagnosis of exclusion in all these cases.
The development of rheumatological diseases such as systemic lupus erythematosus (SLE), following the infection with SARS-CoV-2 has been described (2). Most cases reported were women with a median age of 43 years (range 18–85) (2). SLE was suspected when severe complications occurred such as severe thrombocytopenia, serositis and kidney damage which were not related to the severity of the respiratory disease. Glucocorticoids alone or in association with hydroxychloroquine were used as the first line of treatment (2).
Infections can activate the innate immune system leading to the production of autoantibodies, either through an aberrant response or lack of immune control. This mechanism is implicated in the pathogenesis of SLE (5). In a meta-analysis, patients (n=120) hospitalized for COVID-19 underwent immunological workup, the prevalence of ANA and RF were 32.1% and 19.9%, respectively (6). Other autoantibodies have also been reported but at lower frequencies; 5.46% for anti-CCP antibodies (6–8).
This highlights the ability of SARS-CoV-2 to trigger autoimmunity phenomena. This effect is caused by the ability of this virus to induce hyper-stimulation of the immune system and its molecular similarity to humans (9).