CO:07:3 | Does articular and entheseal structural damage drive pain and patient-driven reported outcomes in difficult-to-treat psoriatic arthrtis patients? Results from a cross-sectional study

Fabio Massimo Perrotta¹, Alen Zabotti², Mauro Fatica¹, Nicola Cabas², Andrea Guiotto², Nicoletta Franzolini³, Giovanni Striani², Maria De Martino⁴, Cristina De Nicola⁵, Miriam Isola⁴, Andrea Di Matteo⁶, Gabriele De Marco⁶, Denis McGonagle⁶, Ennio Lubrano¹, Luca Quartuccio⁴. | ¹Università degli studi del Molise, Campobasso; ²University Hospital Santa Maria della Misericordia, Udine; ³Presidio Ospedaliero S. Antonio, San Daniele del Friuli (UD); ⁴University of Udine; ⁵Epidemiology Unit, Italian Society for Rheumatology, Milano, Italy; ⁶University of Leeds, Leeds, UK

Background. To assess difficult-to-treat psoriatic arthritis (D2T-PsA) and determine whether articular and entheseal structural damage, assessed by ultrasound (US), may drive pain and patient-driven outcomes in D2T-PsA.

Methods. A multicenter cross-sectional study was conducted on PsA patients treated with b/tsDMARDs. For each patient, complete demographic data were recorded. Eligible participants were required to meet the following inclusion criteria: age >=18 years; diagnosis of PsA fulfilling the CASPAR criteria; classification as D2T-PsA, defined by failure of >=2 classes of b/tsDMARDs (with different mechanisms of action) following the failure or contraindication of >=1 csDMARD, and persistently active disease (DAPSA >14); Presence of at least one clinically significant site, defined as a tender and/or swollen joint or a tender enthesis for peripheral disease. Sonographic evaluations were performed by expert sonographers, blinded to clinical data, using the US damage score from the UPSTREAM study calculated as follow: [number of (entheseal calcifications count + entheseal bone irregularity count)*2.98 + number (tendon lesion count)* 1.1 + number (entheseal erosion count)*0.9 + number (joint erosion count*0.7 + number (joint osteoproliferation count + enthesophytes count)*0.54]. Moreover, we use Spearman rho correlation coefficient to evaluate possible correlations between US damage score and clinical features including pain on NRS, HAQ, DAPSA, PsAID, physician global assessment of disease activity on NRS (PhGA), patient global assessment of disease activity (PtGA) on NRS and deltaPtGA-PhGA.

Results: A total of 517 patients with PsA identified, 191/517 (36.9%) patients were on their second mechanism of action b/tsDMARDs. Of whom, 53 out of 191 patients (27.7%) met the criteria for D2T-PsA and were included in the analysis. Table 1 shows the clinical and US characteristics of the 53 D2T patients. Of these, 34 (64.1%) showed at least one site of active inflammation at US evaluation, while 19 showed no signs of active inflammation. The median (IQR) US damage score of the 53 D2T patients was 9.88 (4.76-23.56). Notably, the US damage score negatively correlates with tender joint count (rho -0.27, p=0.04) but positively correlates with swollen joint count (rho +0.27, p=0.05). Moreover, considering each item of the total US score, both the number of joint erosions and the number of joint osteopythes/osteoproliferation correlates positively with PhGA (rho +0.41, p=0.002) (rho +0.27, p=0.04) and correlates negatively with deltaPtGA-PhGA (rho -0.30, p=0.02) (rho -0.31, p=0.02) (table 2). No significant correlation was detected between pain and PtGA with US damage score. In patients without US signs of inflammation, no significant correlation was found between each comparison.

Conclusions. Preliminary results of our study in D2T PsA patients showed that articular damage is associated with PhGA and swollen joints, but not with pain, suggesting that patient-driven outcomes are potentially driven by inflammation rather than damage itself.