Abstract Background/Aims Anti-CCP antibody positive individuals who present with new non-specific musculoskeletal symptoms in the absence of clinical synovitis (CCP+ at risk) are at risk of progression to RA. High-risk individuals should be identified and considered for preventive interventions. However, many CCP+ at risk have a low risk of developing arthritis and could be reassured, educated and receive long-term monitoring in a community setting. We aimed to identify baseline characteristics associated with a good prognosis (i.e. non-progression to RA) at 5- and 10-years after presentation. Methods CCP+ at risk recruited into the Leeds CCP study (a national, prospective observational cohort study in the UK) were included. Baseline demographic, clinical, serological and ultrasound (US) data were collated. Univariate and multivariate logistic regression analyses were undertaken to determine characteristics associated with non-progression (i.e. absence of arthritis) at 5- and 10-years follow up. Results CCP+ at risk who had at least 5- and 10-years of follow-up data available (450 and 157 individuals, respectively) were included. After 5 and 10 years, 317/450, and 73/157, did not progress to RA, respectively. Multivariable logistic regression analyses identified low anti-CCP level, rheumatoid factor negativity, normal ESR, ≤1 tender joint and absence of US tenosynovitis at baseline were all associated with non-progression at 5-years (R2 0.34), and 10-years (R2 0.60), respectively, with the exception of rheumatoid factor negativity for the latter (Table 1). No individuals with all good prognosis characteristics at baseline progressed to RA at 5- and 10-years, respectively. Conclusion In symptomatic CCP+ at risk individuals, we have identified good prognostic characteristics associated with remaining arthritis-free at 5- and 10-years. These data could be used to inform community-based management strategies for low-risk individuals and prevent unnecessary referrals to secondary care. Disclosure S. Sharrack: Grants/research support; I am a recipient of the NIHR Leeds BRC Doctoral Fellowship Scheme. L. Duquenne: None. A.B. Smith: None. J.L. Nam: None. A. Di Matteo: Grants/research support; ADM reports research grants from Alfasigma. Other; ADM has received speaking fees from Janssen and has received support for attending meetings by Galapagos outside the submitted work. K. Harnden: None. L. Thornton: Grants/research support; Lucy Thornton is a recipient of the NIHR Leeds BRC Clinical Doctoral Fellowship Scheme. H. Sugden: None. L.B. Garcia-Montoya: None. R.B. Chowdhury: None. E. Mumba: None. E. Obaro: None. N. Burnett: None. T. Hardy: None. K. Smith: None. K. Mbara: None. P. Emery: Member of speakers’ bureau; PE has provided expert advice to Abbvie, Activa, Anatptysbio, AstraZeneca, BMS, Boehringer Ingelheim, Galapagos, Gilead, Immunovant, Janssen, Lilly, Novartis. Other; PE clinical trials with Abbvie, BMS, Lilly, Novartis, Pfizer, Samsung. K. Mankia: Grants/research support; research grants from Gilead, Lilly, Serac Healthcare, Alfasigma, AstraZeneca and Deepcure. Other; KSM reports consulting fees from Abbvie, UCB, Lilly, Galapagos, Serac Healthcare, Zura Bio and Deepcure.
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