P183 Comparison of the cardiovascular protective effects between IL-17A monoclonal antibodies and TNF inhibitor medications: results from the outcomes of treatment in psoriatic arthritis study syndicate

Background/Aims Psoriatic arthritis (PsA) is a chronic inflammatory condition resulting in synovitis, enthesitis and joint erosion. It is associated with psoriasis and an increased risk of cardiovascular disease, partially due to inflammation-driven atherosclerosis. Due to their key role in this process, inhibitors of TNF-α and IL-17A are widely used in PsA management.The aim of this investigation is to evaluate the cardiovascular protective effects of IL-17A inhibitors (IL-17A-i) compared to TNF-α inhibitors (TNF-i). Methods Patients were recruited to The Outcomes of Treatment in Psoriatic Arthritis Study Syndicate (OUTPASS) study, a UK prospective observational cohort study of patients with PsA commencing a biologic or small molecule inhibitor. The lipid profiles of PsA patients were measured at baseline (pre-treatment) and 3 to 12 months after commencement of IL-17A inhibitor (n = 31). Patients were matched 1:1 with TNF-i treated patients (n = 31) using gmatch methods based on baseline height, weight, age, gender, smoking status, lipid-lowering therapy, systolic blood pressure and medical history of diabetes or major cardiovascular event. Lipid profiles were measured within the same timeframe. QRISK3 scores were calculated for each patient to assess cardiovascular risk. Paired and independent t-testing explored whether either biologic caused a significant reduction in cholesterol and if there was a significant difference between groups. Linear regression assessed the effect of baseline cholesterol, age, and gender on the degree of change. Results Patients prescribed IL-17A-i or TNF-i did not experience significant increases in all lipid measurements and QRISK3 score, with no significant difference in lipid profile change between either biologic. Only raised baseline cholesterol levels were associated with improved lipid reduction (p = 0.000 - 0.013). Despite a seemingly insignificant effect on cardiovascular health, as measured by traditional lipid profiling, by both TNF-i and IL-17A-i, their impact may have been masked by the “lipid paradox”. Inflammatory cytokine pathways suppress lipid levels in PsA patients. Biologics inhibit these pathways, causing a superficially worse lipid profile, despite improved cardiovascular risk by reduced vascular inflammation. Conclusion This investigation highlights the need to develop a cardiovascular outcome measure which more accurately represents the effect of biologics, such as vascular inflammation and endothelial function. Disclosure R. Connor: None. M. Rahman Khasru: None. N. Nair: None. P. Ho: None. A. Barton: None. J. Bluett: Grants/research support; JB has received a research grant award from Pfizer and travel/conference fees in the last 3 years from Fresenius Kabi and Novartis.