Environment In Rheumatoid Arthritis Research Articles

P080 Self-management individualised learning environment in rheumatoid arthritis

Abstract Background/Aims An important but insufficient aspect of care in people with inflammatory arthritis (IA) is empowering them to acquire a good understanding of their disease and build their ability to deal effectively with the practical, physical and psychological impacts of it. This extends beyond drug therapy and emphasises the ability to self-manage, with the right support, as an essential component of care. Good self-efficacy and coping skills benefit and reduce health and financial burden to the individual as well as the health service, benefitting society overall. Provision of excellent supported self-management education is at the heart of what NRAS does and it was due to the difficulty of getting Commissioners to fund our group self-management that led to our deciding to build an e-learning programme to replace our 6- week face-to-face programme. Methods In 2019 with initial funding in place, we partnered with an e-learning platform provider who would help us realise our goal of developing a state-of-the art e-learning experience in a modular format for people with RA. We wanted the programme to be 1) simple to use; 2)interactive; 3)engaging; 4)able to measure impact through learning objectives and use of a validated patient reported outcome measure. The programme also had to be integrable with our Salesforce database within NRAS enabling us to target resources to individuals, driven by identified need. Results The pandemic delayed progress, however, we launched with 4 modules on 17th September, 2021. The four modules comprise: Foundation Module covering the importance of self-management which has the RA Impact of Disease PROM embedded; Newly Diagnosed; Meet the Team and Managing Pain and Flares. A fifth module on Medicines in RA will be launched by end 2021. SMILE meets NICE Quality Statement 3, against which teams are audited, and aligns with EULAR Recommendations for implementation of self-management strategies in IA. Since launch 3 weeks ago, nearly 300 people have registered. Well over 100 baseline RAID PROMs have been completed and we are starting to collect valuable data which will enable us to target more resources where they are needed. Conclusion SMILE-RA provides patients with a unique, engaging educational resource which they can watch and watch again with their family. It is also a useful resource for AHPs new to rheumatology. Further modules will be added in 2022 and beyond. Many modules on a wide range of topics are planned and so this is an on-going project which has input from health professionals and people with lived experience at its heart. Patients and HCPs have welcomed this new resource at a time when the rheumatology workforce is in crisis. We will be presenting more data in Q1 2022 which will be available for congress. Disclosure A.M. Bosworth: None.

Pro-inflammatory cytokines up-regulate and sensitize metabotropic and ionotropic cannabinoid receptors in rheumatoid arthritis and osteoarthritis synovial fibroblasts

In collagen-induced arthritis, elevation of endocannabinoid levels improves clinical parameters and decreases synovial inflammation. Joint pain and inflammation are driven by pro-inflammatory cytokines like TNF, which is also involved in sensitizing transient receptor potential channels (TRP). Besides activating cannabinoid receptors type I and II (CB1 and CB2), endocannabinoids also bind several TRPs e.g. TRPV1 and TRPA1. In this study we demonstrate the influence of TNF, IL-1beta and IFN-gamma on the expression and function of metabotropic (CB1 and CB2) and ionotropic (TRPs) cannabinoid receptors. Prolonged incubation with TNF significantly increased CB1, CB2, TRPV1, TRPA1 and FAAH protein (fatty acid amide hydrolase, important endocannabinoid metabolizing enzyme). Similar results were obtained with IL-1beta and IFN-gamma (1 ng/ml and 10 ng/ml, respectively). TNF-induced sensitization and up-regulation of TRPA1 was confirmed by an increase in intracellular calcium in response to TRPA1 agonist polygodial. While synovial fibroblasts only responded to high doses of TRPA1 agonist (50 μM) without TNF pretreatment, TNF incubation (72 h, 10 ng/ml) not only increased Emax, but also lowered the activation threshold of the receptor to 1 μ M. Furthermore, TNF sensitized synovial fibroblasts to the action of the endocannabinoid anandamide. The observed up-regulation of metabotropic and ionotropic cannabinoid receptors by TNF might explain lack of effects under healthy/basal conditions. Activation of the cannabinoid receptor system might be an adaptation to the pro-inflammatory environment in rheumatoid arthritis and might help to resolve inflammation.