OP0260 RESPONSIVENESS OF A COMBINED POWER DOPPLER AND GREYSCALE ULTRASOUND SCORE FOR ASSESSING SYNOVITIS AT JOINT LEVEL IN PSORIATIC ARTHRITIS PATIENTS WITH INADEQUATE RESPONSE TO csDMARDs: DATA FROM THE ULTIMATE TRIAL

Author:

D’Agostino M. A.,Boers M.,Gaillez C.,Gamez C.,Ventura L.,Rosa J.,Padovano I.,Mandl P.,Kleyer A.,Bakewell C.,Bao W.,Goyanka P.,Conaghan P. G.,Schett G.

Abstract

BackgroundPower Doppler ultrasound (PDUS) is a sensitive non-invasive imaging tool that allows the visualisation of articular and periarticular inflammation in patients with psoriatic arthritis (PsA).1 ULTIMATE (NCT02662985) was the first large randomised clinical trial that showed the responsiveness of the Global OMERACT-EULAR ultrasound synovitis score (GLOESS) in PsA and confirmed the rapid and continued benefits of secukinumab through 52 weeks.2,3ObjectivesTo report the distribution of ultrasound-detected synovitis at joint level, by degree of severity at baseline and over time, and the contribution of each core component of GLOESS, synovial hypertrophy (SH) by greyscale (GS; B-mode) and power Doppler (PD) signal, to responsiveness.3MethodsThis was a 52-week study with a 12-week double-blind, placebo-controlled treatment period followed by a 12-week open-label period and a 6-month open-label extension secukinumab treatment period.3 The number of joints with synovitis measured by GLOESS2 was assessed up to Week 52. The assessments included distribution of synovitis based on composite PDUS score across 24 pairs of joints (with worse score of the pair of the joints used) by grade of severity (0-3) and change from baseline to Week 52 in each core component of GLOESS.3-5 Data are presented as observed.ResultsA total of 166 patients (mean age, 46.7 years; males, 45.2%) were enrolled, of which 90% (75/83) of secukinumab and 83% (69/83) of placebo-secukinumab participants completed 52 weeks. The mean (SD) number of PDUS detected synovitis at baseline was 9.2 (4.9) and 10.2 (5.2) in the secukinumab and placebo group, respectively. The most frequent locations with synovitis at baseline were: wrist, metatarsophalangeal (MTP), knees and metacarpophalangeal (MCP) joints (Table 1). An early and continued improvement in GLOESS was observed in both secukinumab and placebo-secukinumab groups after switching to active therapy, as previously reported at Week 12 and through Week 52.2,3 Among the two core components of GLOESS, SH was mainly responsible for the change in GLOESS from baseline to Week 52, in contrast with PD signal in this dataset. The distribution of synovitis by grade of severity showed that MTP joints, wrist, knee, MCP1/2 and tibiotalar joints mostly contributed to the composite PDUS at Week 12 (Figure 1). Similar patterns were observed through 52 weeks.Table 1.Proportion of patients with PDUS detected synovitis at baseline*Synovitis joint, data presented as n (%)Secukinumab (N=83)Placebo (N=83)Wrist66 (80)66 (80)MTP256 (68)65 (78)MTP158 (70)60 (72)MTP352 (63)60 (72)MTP446 (55)59 (71)Knee50 (60)47 (57.)MCP136 (43)52 (63)MCP235 (42)41 (49)MTP530 (36)41 (49)*Data for top nine pairs of joints with most frequently detected power Doppler ultrasound (PDUS) synovitis are presented here. Synovitis was scored by a OMERACT-EULAR synovitis composite score >0 for each paired joint (irrespective of right or left side). The OMERACT-EULAR composite PDUS score (for individual joints) ranged from 0 to 3 and was composed of the two core components synovial hypertrophy and power Doppler.N, total number of randomised patients; n, number of evaluable patientsConclusionThe distribution of synovitis at baseline reflected a predominance of small joints (feet and hands) and large joints (wrist and knee) and were mostly responsive to secukinumab over time in the ULTIMATE trial. Synovial hypertrophy was the most responsive core component of GLOESS driving an early and continued reduction of synovitis with secukinumab through Week 52. This finding could be useful to select a restricted number of joints in future ultrasound trials in PsA.References[1]D’Agostino MA and Coates LC. J Rheumatol. 2019;46:337–9.[2]D’Agostino MA et al. Arthritis Rheumatol. 2021;73(10).[3]D’Agostino MA, et al. Rheumatology (Oxford) 2021;keab628.[4]D’Agostino MA and Coates LC. RMD Open 2017;3:e000428.[5]Uson J, et al. Rheumatol Clin. 2018;14:27–35.Disclosure of InterestsMaria-Antonietta D’Agostino Speakers bureau: Sanofi, Novartis, BMS, Janssen, Celgene, Roche, AbbVie, UCB, and Eli Lilly, Consultant of: Sanofi, Novartis, BMS, Janssen, Celgene, Roche, AbbVie, UCB, and Eli Lilly, Maarten Boers Consultant of: Novartis, Corine Gaillez Shareholder of: Novartis and BMS, Employee of: Novartis, Carlos Gamez: None declared, LUCIO VENTURA: None declared, Javier Rosa Speakers bureau: Abbvie, Pfizer, Lilly, Janssen, Novartis and BMS, Ilaria Padovano: None declared, Peter Mandl Speakers bureau: AbbVie, BMS, Celgene, Janssen, Lilly, MSD, Novartis, Roche and UCB, Grant/research support from: AbbVie, BMS, Celgene, Janssen, Lilly, MSD, Novartis, Roche and UCB, Arnd Kleyer Speakers bureau: Abbvie, Lilly, Novartis, MEDAC; Janssen, Consultant of: Abbvie, Lilly, UCB, Novartis, BMS, Sanofi, Galapagos, Catherine Bakewell Speakers bureau: AbbVie, Novartis, Pfizer, Janssen, UCB, and Sanofi Genzyme/Regeneron, Consultant of: AbbVie, Novartis, Pfizer, Janssen, UCB, and Sanofi Genzyme/Regeneron, Weibin Bao Shareholder of: Novartis, Employee of: Novartis, Punit Goyanka Employee of: Novartis, Philip G Conaghan Speakers bureau: AbbVie, Amgen, AstraZeneca, Eli Lilly, Galapagos, Gilead, Novartis, Pfizer and UCB, Consultant of: AbbVie, Amgen, AstraZeneca, Eli Lilly, Galapagos, Gilead, Novartis, Pfizer and UCB, Georg Schett Speakers bureau: AbbVie, BMS, Celgene, Janssen, Lilly, Novartis, Roche and UCB

Publisher

BMJ

Subject

General Biochemistry, Genetics and Molecular Biology,Immunology,Immunology and Allergy,Rheumatology

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