An increase in the incidence of inflammatory arthritis after COVID-19 has been reported. Since many diseases exhibit population-specific causal effect sizes, we aimed to evaluate the incidence trends of inflammatory arthritis, including rheumatoid arthritis (RA), after COVID-19 in a large admixed Colombian population. Data analysis for this retrospective, population-based cohort study was carried out using the COOSALUD EPS registry. The following codes were selected for analyses: M059, seropositive RA, M069, unspecified RA, M060 seronegative RA, and other RA-related diagnoses: M064, M139, M068, M058, M130 and M053. The study period was limited to January 01, 2018, through December 31, 2022. Incidence rates (IRs) and incidence rate ratios (IRRs) were assessed. A Cox survival model was built to evaluate the influence of age, gender, and COVID-19 vaccination status on the development of inflammatory arthritis. A bioinformatic analysis was performed to evaluate the homology between SARS-CoV-2 and autoantigen peptides related to RA. The entire population study comprised 3,335,084 individuals. During the pandemic period (2020ampersand-flag-changeminus;2022) the total IIR for seropositive and unspecified RA were 1.60 (95percent-flag-change CI, 1.16-2.22) and 2.93 (95percent-flag-change CI, 2.04-4.19), respectively, and the IIR for overall RA-related diagnosis was 2.01 (95percent-flag-change CI 1.59-2.53). The age groups hazard ratios (HRs) were increased until the age group of 51-60 years (HR: 9.16; 95percent-flag-change CI, 7.24-11.59) and then decreased slightly in the age group 61 years or older (HR: 5.364; 95percent-flag-change CI, 4.24-6.78) compared to those within 18-30 years. Men were less at risk than women to develop inflammatory arthritis (HR: 0.21; 95percent-flag-change CI, 0.18-0.24). The greater time since COVID-19 diagnosis was associated with a lower likelihood of developing inflammatory arthritis (HR: 0.99; 95percent-flag-change CI:0.998-0.999). Vaccination (all types of COVID-19 vaccines included) did not prevent the development of inflammatory arthritis after COVID-19. Low identity was found between the SARS-CoV-2 ORF1ab antigen and the human antigens Poly ADP-ribose polymerase 14 and Protein mono-ADP-ribosyltransferase PARP9 isoform D (39percent-flag-change and 29percent-flag-change, respectively). In conclusion, our study confirms increased incidence of inflammatory arthritis, including RA, after COVID-19, with the greatest increase occurring before the first year post-covid. Women in their fifties were more susceptible. Further research is required to examine the effectiveness of vaccination in preventing post-COVID inflammatory arthritis and the mechanisms implicated in the development of RA after COVID-19.
