POS1050 UPADACITINIB VERSUS ADALIMUMAB ON ROUTINE ASSESSMENT OF PATIENT INDEX DATA 3 (RAPID3) IN PATIENTS WITH PSORIATIC ARTHRITIS

Abstract

BackgroundRAPID3 (Routine Assessment of Patient Index Data 3) is a disease activity index that is calculated from 3 patient-reported measures: physical function, pain, and patient global assessment. A fast and convenient tool, RAPID3 can be easily used in clinical practice and is applicable to multiple rheumatic diseases, including psoriatic arthritis (PsA), and was shown to correlate with other clinical composite measures of disease activity1. Here, we assessed the long-term effect of upadacitinib (UPA), an oral JAK inhibitor, and adalimumab (ADA) on RAPID3 scores in patients with PsA via a post hoc analysis from the SELECT-PsA 1 phase 3 trial2,3.ObjectivesTo evaluate the impact of treatment with UPA vs ADA on RAPID3 through 56 weeks in SELECT-PsA 1, as well as the association of RAPID3 with other disease measures used in PsA.MethodsData are from the double-blind SELECT-PsA 1 trial, in which patients with PsA and an inadequate response or intolerance to ≥1 non-biologic DMARD received UPA 15 mg or 30 mg once daily, ADA 40 mg every other week (wk), or placebo (PBO; switched at wk 24 to either UPA 15 mg or 30 mg). This analysis included data from the UPA 15 mg, ADA, and PBO treatment arms. RAPID3 endpoints were calculated using pain scores, patient’s global assessment of disease activity, and HAQ-DI (each rescaled to 0–10 in this analysis); summed together, RAPID3 scores range from 0 (no disease activity) to 30 (severe activity). Mean change from baseline (BL) in RAPID3 as well as the proportions of patients reporting minimal clinically important differences (MCID) in RAPID3 and RAPID3 remission (≤3), low (LDA, >3 to ≤6), moderate (MDA, >6 to ≤12), and high disease activity (HDA, >12) were assessed through wk 56. Associations between RAPID3 scores and disease activity in psoriatic arthritis (DAPSA) and Minimal Disease Activity (MDA)/Very Low Disease Activity (VLDA) were determined by Mantel-Haenszel chi-square test. All data are as observed.ResultsA total of 1,274 patients (PBO: n=421; UPA 15 mg: n=425; ADA: n=428) were included from SELECT-PsA 1. RAPID3 scores at BL were comparable across all treatment arms, and most patients were in HDA. Patients receiving UPA showed a greater improvement from BL in RAPID3 vs ADA at all visits from wk 16 to wk 56 as well as better responses compared with PBO at all assessments (Figure 1). Similarly, a higher proportion of patients treated with UPA achieved MCID in RAPID3 scores than those on ADA from wk 24 to wk 56. By wk 56, approximately half of patients on either therapy were in RAPID3 remission or LDA, with UPA showing a slight numerical improvement relative to ADA (30/21/31/18% of patients were in remission/LDA/MDA/HDA on UPA vs 28/17/30/25% on ADA). RAPID3 disease categories were strongly associated with DAPSA and MDA/VLDA status at wk 56 across all treatment arms pooled together (Table 1) and for the UPA 15 mg arm alone (nominal P <0.0001 for all associations).Table 1.Association of RAPID3 With DAPSA and MDA/VLDA Across All Treatment Arms at Week 56aRAPID3n (%)Moderate-High [>6]Low [3 - ≤6]Remission [≤3]DAPSA (n=879) Moderate-High [>14]292 (33)33 (4)14 (2) Low [4 - ≤14]154 (18)122 (14)87 (10) Remission [≤4]6 (1)21 (2)150 (17)MDA/VLDA (n=907) Not in MDA410 (45)39 (4)5 (1) MDA but not VLDA63 (7)129 (14)80 (9) VLDA013 (1)168 (19)aDAPSA vs RAPID3 and MDA/VLDA vs RAPID3 were nominally significant at P <0.0001. Data were pooled across UPA 15 mg, ADA, and PBO to UPA 15 mg groups.ConclusionUPA 15 mg treatment led to greater improvements over PBO in RAPID3 scores over 56 wks in patients with PsA, and greater improvements over ADA from wk 16 to 56. The majority of patients achieved MCID in RAPID3 after 12 wks of UPA or ADA, with higher proportions achieving MCID on UPA vs ADA by wk 24. RAPID3 was strongly associated with other joint-focused (DAPSA) or multiple manifestation (MDA/VLDA) composite measures, further supporting the utility of RAPID3 in assessing disease activity in PsA.