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Background: SARS-CoV-2, the virus responsible for acute respiratory distress syndrome (ARDS). It can cause chronic inflammatory changes known as post-COVID syndrome (PCS), which are associated with autoimmune diseases such as rheumatoid arthritis (RA), a chronic polyarticular inflammatory pathology generated by an overactivation of the inflammatory response, leading to the activation of different cytokine pathways that perpetuate the systemic inflammatory response. It is therefore important to understand the impact on the immune response generated in SARS-CoV-2 infected RA patients. Objectives: To assess the cytokine profile in patients with RA and COVID-19 infection and compare it with RA patients who have not been infected with COVID-19. Methods: A nested case-control study in a cohort of patients under a multidisciplinary model and strict follow-up; cases: patients with RA and confirmed COVID-19 infection in the last 2 years, and controls: RA patients without history of COVID-19. Long COVID (LC): Persistent symptoms ≥4 weeks, and PCS: persistent symptoms ≥12 weeks. Sociodemographic, clinical, and laboratory data were collected. Multiplex Cytometric Bead Array (CBA) to evaluate the levels of Interleukin IL-2, IL-4, IL-6, IL-10, IL-12p70, IFN-γ, and Tumor Necrosis Factor (TNF). Univariate and bivariate analyses were performed (STATA 17). Mann-Whitney U test was used to determine significant differences in cytokine levels between cases and controls. Results of pResults: A total of 300 patients were included (148 cases and 152 controls). Median age was 59 years (interquartile range - IQR 11). Disease activity was low in 71.86%. There were no significant differences in sociodemographic and clinical characteristics between cases and between cases and controls. For most cytokines, there were some losses due to insufficient sample for sample processing However, this loss was not greater than 20% in any of them apart from IL-6 (loss of 36%). No statistically significant differences were found in any cytokines between cases and controls, with P values > 0.05. Comparisons were made (No Covid vs. LC and No Covid vs. PCS) (Table 1) and among patients diagnosed with COVID-19 (LC vs. No LC) (Table 2), where no significant changes were found in any cytokine populations. Conclusion: The results provide a general perspective on a population of RA patients with low disease activity. In this group, no differences were identified in the cytokine profile, regardless of the presence of LC and PCS symptoms. This finding suggests that these patients tend to return to their baseline state. However, it is noteworthy that strict disease control treatment may also contribute to a rapid and effective regulation of cytokine levels. REFERENCES: NIL. Acknowledgements: NIL. Disclosure of Interests: Gabriel E. Acelas-Gonzalez: None declared, Julián Arias-Aponte: None declared, Rafael Parra-Medina: None declared, María Lorcy Monsalve-Córdoba: None declared, Adriana Rojas-Villarraga ARV reports fees for conferences in the last 5 year from AbbVie, Amgen and Pfizer, and fees for conferences and advisory board from Janssen outside the submitted work, Paula Daniela Nieto-Zambrano: None declared, Maria Camila Cortés-Osma: None declared, Hector Fabio Restrepo-Guerrero: None declared, Laura Villarreal: None declared, Arley Gómez-López: None declared, Pedro Santos-Moreno PSM has received fees for conferences, counseling, advisory boards, and travel to academic meetings expenses and research grants in the last 5 years from Janssen, AbbVie, Biopass-UCB, Bristol, Lilly, Pfizer, Roche, Tecnofarma, and Sanofi.
Acelas-Gonzalez et al. (Sat,) studied this question.