Abstract
The pandemic of coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 has caused a large number of deaths, and there is still no effective treatment. COVID-19 can induce a systemic inflammatory response, and its clinical manifestations are diverse. Recently, it has been reported that COVID-19 patients may develop myositis and interstitial pulmonary disease similar to dermatomyositis (DM). This condition is similar to the rapidly progressive interstitial lung disease associated with MDA5+ DM that has a poor prognosis and high mortality, and this poses a challenge for an early identification. Suppression of the immune system can protect COVID-19 patients by preventing the production of inflammatory cytokines. This article attempts to explore the possibility of a relationship between COVID-19 and DM in terms of the potential pathogenesis and clinical features and to analyze the therapeutic effect of the immunosuppressive drugs that are commonly used for the treatment of both DM and COVID-19.
Highlights
In December 2019, a novel infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was reported [1]
Among the potential autoimmune diseases that may be related to COVID-19, the most intriguing is idiopathic inflammatory myopathy (IIM), a heterogeneous disease that primarily affects the skeletal muscles and can be divided into polymyositis, dermatomyositis (DM), immune-mediated necrotizing myopathy, anti-synthase syndrome, and inclusion body myositis [3]
The pathogenesis of DM is still unclear, it is likely associated with inappropriate complement activation and interferon (IFN) response [4, 5], which results in the production of myositis-specific autoantibodies that may be related to unique clinical features
Summary
In December 2019, a novel infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was reported [1]. Anti-MDA5+ DM is typically associated with rapidly progressive interstitial lung disease (RP-ILD), which has a high early mortality [18] It is still controversial whether the immune activation seen in DM is antibody-dependent or is triggered by a classical complement cascade [4]. SARS-CoV-2 enters human cells through the membranous angiotensin-converting enzyme 2 (ACE2) receptors, triggering an innate and adaptive immune response. This initiates the production of cytokines such as IL-1, IL-6, IL-10 and IFN-g, which can induce lung and muscle damage. Along with the increased understanding of COVID-19, several drugs commonly used to treat DM have potential therapeutic effects for COVID-19 patients
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