OP0176 IDENTIFICATION OF INFLAMMATORY AND NON-INFLAMMATORY MECHANISMS TO IMPROVE TREATMENT STRATEGIES IN DIFFICULT-TO-TREAT PSA PATIENTS USING CLINICAL AND SONOGRAPHIC FINDINGS

Background: In psoriatic arthritis (PsA), patients with an inadequate response to ≥1 conventional DMARD and ≥2 b/tsDMARDs with different mechanisms of action are generally defined as "difficult-to-treat" (D2T) [1]. Recently, we proposed that subdividing these patients into persistent inflammatory PsA (PIPsA) and non-inflammatory PsA (NIPsA) (Figure 1a) could be useful to avoid unnecessary therapeutic switches in patients with persistent activity based on clinimetric scores but without evidence of inflammation on physical examination and/or imaging [2]. Objectives: 1To investigate the prevalence of D2T-PsA. 2To determine whether patients with PIPsA and NIPsA, distinguished by the presence or absence of clinical and ultrasound signs of inflammation, exhibit distinct clinical phenotypes. Methods: A multicenter cross-sectional study was conducted between May 2024 and December 2024, focusing on PsA patients treated with b/tsDMARDs. To be included in the analysis, patients had to meet the D2T criteria and have a Disease Activity Index for Psoriatic Arthritis (DAPSA) score >14, along with at least one of the following: a tender joint, a tender enthesis, or a swollen joint. Each patient underwent a thorough clinical assessment, which included a swollen joint count (SJC) across 66 joints, a tender joint count (TJC) across 68 joints, and Spondyloarthritis Research Consortium of Canada (SPARCC) scoring. PsA-related Patient-Reported Outcomes (PROs) were also collected. Detailed sonographic evaluations were performed, assessing 42 joints, 36 tendons, 12 entheses and 2 bursae. Patients were classified as PIPsA if ultrasound confirmed activity in at least one clinically active joint or enthesis (swollen and/or tender). Those without ultrasound-confirmed activity were classified as NIPsA. Ultrasound activity and damage scores were calculated according to UPsA score [3]. Clinical data (including adverse events and concomitant medications) were entered into the REDCap system. The study employed descriptive statistics (median, IQR, and percentages) to summarize patient characteristics. T-test or Mann-Whitney U tests were used to compare continuous variables as appropriate, while Chi-square or Fisher's exact tests assessed differences in categorical variables between PIPsA and NIPsA groups. Results: From a cohort of 517 PsA patients undergoing treatment with b/tsDMARDs, 53 patients (10.3%) met the criteria for D2T PsA (Figure 1b). The characteristics of this D2T population were as follows: median age of 59.0 years (IQR 49.0–65.0), 64% female, median BMI of 26.9 (IQR 24.2–30.5), disease duration of 11.0 years (IQR 7.0–23.0), and a median of 2.0 failed mechanisms of action (IQR 2.0–4.0). Among the D2T patients, 30 (57%) were classified as PIPsA, while 23 (43%) were classified as NIPsA. Distinguishing clinical features of the PIPsA phenotype included a higher median number of swollen joints (2.5 [IQR 1.0–7.0] vs. 0.0 [IQR 0.0–1.0], p < 0.001), the presence of at least one dactylitis (20% vs. 0%, p=0.03), and nail psoriasis as the predominant pattern (40% vs. 13%, p=0.027). In contrast, NIPsA patients exhibited a higher number of tender points (16.0 [IQR 0.0–18.0] vs. 0.0 [IQR 0.0–8.0], p=0.009) and a greater median number of painful entheses, as assessed by SPARCC (5.0 [IQR 2.0–8.0] vs. 2.0 [IQR 0.0–5.0], p=0.023). Notably, disease activity as measured by the DAPSA score, along with the number of tender joints, did not differ significantly between the two phenotypes (Table 1). Ultrasound examination revealed significant differences between PIPsA and NIPsA groups in both ultrasound activity (median score 3.22 [IQR 0.5–8.9] vs. 0.88 [IQR 0.3–2.7], p < 0.001) and structural damage (4.3 [IQR 0.0–7.1] vs. 2.0 [IQR 0.0–6.6], p < 0.001) (Figure 1c). Conclusion: D2T PsA patients account for just over 10% of cases, with 57% showing objective evidence of inflammation (PIPsA) and 43% presenting without objective inflammation (NIPsA) phenotypes (Figure 1d). This clear phenotypic distinction may help avoid unnecessary treatment escalations, optimize clinical management, and enhance the design of future clinical trials targeting D2T PsA patients. REFERENCES: [1] Singla S., Ribeiro A., Torgutalp M., Mease P. J., Proft F., RMD open, Jan 2024. [2] Zabotti A., Aydin S. Z., David P., Di Matteo A., McGonagle D., Nat Rev Rheumatol., under review. [3] Canzoni M., Piga M., Zabotti A., Scirè C. A., Carrara G., Olivieri I., Iagnocco A., BMJ open, Jul 2018. Table 1. Main demographic and clinical findings. D2T Psa, Difficult-to-treat Psoriatic Arthritis; BMI, Body Mass, Index; PASI, Psoriasis Area Severity Index; b/ts DMARDs, biologic/target synthetic Disease Modifying Anti-Rheumatic Drugs; CRP, C-reactive Protein; HAQ, Health Assessment Questionnaire; VAS Pain, Visual Analogue Scale Pain; DAPSA, Disease Activity Index for Psoriatic Arthritis; SPARCC, Spondyloarthritis Research Consortium of Canada. Figure 1Multi-panel. (A) Definitions. (B) Flow diagram of patients included in the study and proportions of PIPsA and NIPsA. (C) Main sonographic differences in activity and damage scores between PIPsA and NIPsA. (D) Main clinical differences between PIPsA and NIPsA. Acknowledgements: NIL . Disclosure of Interests: None declared . © The Authors 2025. This abstract is an open access article published in Annals of Rheumatic Diseases under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Neither EULAR nor the publisher make any representation as to the accuracy of the content. The authors are solely responsible for the content in their abstract including accuracy of the facts, statements, results, conclusion, citing resources etc.

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