COVID-19 and RA share similar immune-inflammatory features of disease pathogenesis executed by analogous mechanistic pathways. However, the treatment of RA patients in the COVID-19 setting itself stands as a challenging task. Implementation of individualized clinical surveillance of RA patients considering the disease severity and appropriate risk-benefit study referring to the recommendations of using anti-rheumatic drugs in the COVID-19 setting by different professional rheumatology associations would stand as the optimal therapeutic strategy for effective disease control during the COVID-19 pandemic.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection that caused coronavirus disease 2019 (COVID-19) usually produces a mild to moderate respiratory disease . However, it occasionally leads to severe alveolar disease resulting in shortening of breath, reduced oxygen saturation in blood, and pulmonary infiltration in the lung that can substantially contribute to pulmonary failure . Age, the severity of infection, and the existence of comorbidities are potential risk factors in COVID-19 patients [1,3]. Emerging evidence revealed that SARS-CoV-2 develops a specific type of alveolar disease that is clinically different from other acute respiratory syndromes . Immune hyperactivation and cytokine involvement in alveolar structures have been identified as the key contributors to produce severe lung disease in COVID-19 patients. Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation and hyperactivation of T cells. Several pro-inflammatory cytokines act as contributing factors in developing synovial inflammation in RA. The patterns of cytokine and immune activation in COVID-19 patients seem to resemble the RA case. Interestingly, some common therapeutic strategies including cytokine inhibition have been found to be fruitful against both COVID-19 and RA . Thus, a possibility of pathological crosstalk is inevitable between COVID-19 and RA.
In general, there is a close association between viral infection and arthritis with a wide spectrum of symptoms ranging from arthralgia to arthritis. Earlier reports revealed that individuals infected with hepatitis C and several alphaviruses frequently develop prolonged arthritis; however, Parvovirus B19, Hepatitis B, and Rubella viruses frequently cause self-limited arthritis. In contrast, respiratory viruses, such as corona and influenza viruses more frequently can cause arthralgia and/or myalgia. Approximately 15 and 44% of COVID-19 patients present arthralgia and/or myalgia, respectively, during the infective stage . Emerging evidence hypothesized that SARS-CoV-2 infection can attack musculoskeletal systems through immune-inflammation-dependent mechanisms, which may develop inflammatory arthritis during the infective or post-infective stage [3,4,5]. However, little is known about the manifestations or worsening of RA by this infection. Since musculoskeletal manifestations phenotypically resemble RA, it has been attempted to find out the association between COVID-19 and RA. In this article, we reviewed the pathological crosstalk between COVID-19 and RA. In addition, our understanding of the risk of RA patients in acquiring SARS-CoV-2 infection and worsening COVID-19 outcomes was critically discussed on the basis of available clinical readouts. The therapeutic strategies and guidelines were conferred referring to recently published literature. Moreover, critical arguments on therapeutic challenges raised in different case studies were discussed in this review.