AB0188 PERSISTENT ARTHRITIS DEVELOPS IN JOINTS PREVIOUSLY AFFECTED BY PALINDROMIC FLARES: A LONGITUDINAL STUDY INVESTIGATING PALINDROMIC RHEUMATISM PATIENTS WHO PROGRESS TO RHEUMATOID ARTHRITIS
Authors: D. Sahin Eroglu, R. Chowdhury, L. Duquenne, A. Di Matteo, K. Harnden, J. Nam, L. Thornton, P. Emery, K. Mankia
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> Rheumatoid arthritis (RA) is preceded by different Pre-RA phenotypes. These include palindromic rheumatism (PR) and musculoskeletal symptoms in the presence of autoantibodies (CCP+ at risk). The hallmark of PR is recurrent, episodic articular flares. In those who progress to RA, the relationship between these flares and the subsequent RA phenotype is unclear. <h3>Objectives:</h3> To investigate, in PR patients who develop RA (PR progressors), whether i) arthritis develops in those joints previously affected by flares of PR ii) PR progressors and CCP+ at risk progressors have a different clinical phenotype at the time of RA development. <h3>Methods:</h3> PR patients and CCP+ at risk individuals were recruited and followed between July 2008 and October 2023 in the Leeds PR and CCP cohorts respectively. Clinical and serological markers were collected three monthly for one year and then annually. PR patients were asked to keep a flare diary and flare details were recorded at each visit. In the absence of consensus criteria, PR was diagnosed in patients who had 'a documented history or physical examination consistent with joint pain and swelling, which subsequently resolved to normal between episodes, in the absence of an alternative diagnosis'. A flare of PR was defined as 'two or more features of pain, swelling and erythema in or around at least one joint region that later normalized'. In shoulders and hips, swelling/erythema was not mandatory. Data on the joints affected by PR flares prior to progression were compared with the joints involved at the time of progression. In both PR and CCP+ at risk progressors, demographic, clinical and serological data at the time of progression were analysed. Categorical variables were compared using Chi-Square or Fisher Exact tests. Continuous variables were compared using either Student's t-test or Mann-Whitney test. <h3>Results:</h3> 63 PR (60 CCP+) and 171 CCP+ at risk individuals progressed to persistent inflammatory arthritis (PIA) of whom 56 (88.9%) and 151 (88.3%) met the 2010 ACR/EULAR classification criteria for RA, respectively. In 44 PR patients with complete dataset, the most frequently affected joints at the initial flare were the shoulders (left and right 25.0% and 22.7%, respectively), whereas the small joints of the hands were the most frequently affected in all flares, with 95.5% and 79.5% experiencing inflammation in the right and left hand small joints, respectively. 15/44 (34.1%) patients developed PIA (i.e. progressed) in ≥1 of the joints affected in their initial flare and 34/44 (77.3%) progressed in ≥1 of the joints that had been previously affected in a PR flare. At joint level, 45 of the progressed joints (19.2%) had been affected during the initial flare, while 143 (60.9%) had been affected in at least one flare prior to progression (Table 1). Comparing PR and CCP+ at-risk progressors, there were no differences in demographic characteristics or PROs (Table 2). PR progressors had a higher number of swollen joints at progression compared with CCP+ at risk (4.3 vs 3.2, p= 0.016). However, mean DAS28-CRP and -ESR scores were not different. <h3>Conclusion:</h3> These data suggest patients with PR develop PIA in joints that they have previously experienced flares of PR in. Despite the phenotypic differences between PR and CCP+ at risk, in progressors the phenotype of RA appears similar. The high frequency of PR flares in joints that later progressed to RA might reflect the potential influence of local joint-centric factors. In patients with PR, joints that have previously flared should be closely monitored for progression to PIA. <h3>REFERENCES:</h3> <b>NIL.</b> <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> Didem Sahin Eroglu: None declared, Rahaymin Chowdhury: None declared, Laurence Duquenne: None declared, Andrea Di Matteo Janssen, Kate Harnden: None declared, Jacqueline Nam: None declared, Lucy Thornton: None declared, Paul Emery Abbvie, Astra-Zeneca, BMS, Boehringer Ingelheim, Galapagos, Gilead, Janssen, MSD, Lilly, Novartis, Pfizer, Roche, Samsung, Abbvie, BMS, Lilly, Novartis, Pfizer, Roche, Samsung, Kulveer Mankia Abbvie, Galapagos, UCB, Serac Healthcare, Deepcure, Zura Bio, AZ, Gilead, Lilly, Serac.