| Popis: |
Excessive immune activation and cytokine release in alveoli/lung structures is a prominent sign of coronavirus disease 2019 (COVID-19) pathology caused by infectious severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The progressive sign of pro-inflammatory cytokines elicited in COVID-19 clinically resembles hyper immune-reactive features often seen in rheumatoid arthritis (RA), an autoimmune disorder. Recent clinical data from the ongoing COVID-19 pandemic conferred the severity and risk of COVID-19 to RA patients. Amid the evidence of musculoskeletal manifestations involving immune-inflammation-dependent mechanisms and cases of arthralgia and/or myalgia in COVID-19, crosstalk between COVID-19 and RA is debated. The present review sheds light on the overlapping COVID-19 and RA clinical features, aspects of SARS-CoV-2 infection in RA development, and associated risks. It also confers whether RA can worsen COVID-19 outcomes based on available clinical readouts. To gain mechanistic insights into the overlapping immune-inflammatory features in SARS-CoV-2 infection and RA, we reviewed the emerging links of angiotensin-converting enzyme (ACE)-dependent and macrophage-mediated pathways. Moreover, a detailed review of immediate challenges and key recommendations for anti-rheumatic drugs in the COVID-19 setting was presented for better clinical monitoring and management of RA patients. Taken together, present review summarizes available knowledge on the emerging COVID-19 and RA crosstalk and their mechanistic overlaps, challenges, and therapeutic options. |
