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).