Dear Editor
There is now growing evidence of COVID-19-triggered rheumatic and skin disorders [1]. Some of them, like psoriatic arthritis(PsA), have combined cutaneous and joint lesions [2].
The co-occurrence of PsA and COVID-19 can complicate diagnosis and treatment. Therefore, exploration of the shared molecular mechanisms between COVID-19 and PsA may explain some causes of cutaneous and rheumatologic symptoms that occur in COVID-19 patients.
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Both COVID-19 and PsA pose a challenge to the body’s immune system. Thus, an important question is how common molecular mechanisms may link the immune system with PsA and COVID-19. Evidence suggests that angiotensin-converting enzyme 2(ACE2) is a key molecule connecting these two conditions because there is a correlation between tissue-specific expression of ACE2(a primary receptor for virus entry) and COVID-19 susceptibility. Therefore, ACE2 expression in human tissues that can be affected during PsA may increase the risk of PsA in infected patients.
The ACE2 expression in human synovial tissues, the basal epidermal layer, or keratinocytes, indicates a new potential skin and joint injury mechanism among patients. The binding of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2) spike protein to ACE2 may initiate the pathogenic cascade of skin and rheumatic diseases in infected patients.
An association of higher ACE2 expression with COVID-19 adverse effects and elevated expression of ACE2 in psoriatic lesional skin or active rheumatoid synovium may also increase tissue susceptibility to disease progression. Virus presence in the skin or synovial fluid of patients raises the possibility that SARS-CoV‐2 can be a pathologic stimulus for synovial or skin inflammation [3].
Transmission of SARS-CoV-2 to skin and joints may also occur indirectly, through interaction with ACE2 that is expressed on the surface of lymphatic endothelial cells or the cutaneous vasculature. Virus-endothelial interaction can result in the recruitment of inflammatory cells and initiation of the inflammation cascade.
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An overactive immune system and dysregulated inflammatory responses, after COVID-19 seem to play a role in skin and joint damage. This process can result from different mechanisms, including molecular mimicry, epitope spreading, or bystander activation [4].
Drug side effects are another important aspect because certain medications which were initially believed promising agents for COVID-19 treatments are the known causes of drug-induced psoriasis. This is supported by findings including the exacerbation of PsA in COVID-19 patients who were treated with hydroxychloroquine [5].
Overall, a possible relationship may exist between COVID-19 and PsA. So, clarification of the disease mechanisms is necessary to get an accurate diagnosis and effective treatment.
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