Psoriatic Arthritis Pts Research Articles

Prognostic factors associated with non-remission and low disease activity status af ter one year of psoriatic arthritis patients treatment in real practice

Background. Remission/low disease activity (LDA) are acceptable goal of psoriatic arthritis (PsA) treatment. Prognostic factors for non-remission/LDA hasn’t been fully studied yet and data is limited. The aim – to determine the prognostic factors associated with non-remission/LDA status within 1 year of treatment in PsA pts in real practice. Methods. 292 pts (M/F=122/170) with active PsA fulfilling the CASPAR criteria were included. Mean age 46.1±12.5 years (yrs), PsA duration 10.4±7.1 months (mos), psoriasis (Ps) duration 19.32±12.08 mos, body mass index (BMI) 27.7±5.6 kg/m2 , median (Me) of DAPSA – 23.8 [14.7; 37.4]. 182 pts was given therapy with synthetic (s) DMARDs predominantly methotrexate (MTX), 110 pts – bDMARDs as monotherapy or with combination with MTX or other sDMARDs. At baseline (BL) and at 1 year of therapy PsA activity by tender/swelling joint count (TJC)/68, (SJC)/66, pain (VAS), Patient global assessment disease activity (PtGA, VAS), CRP (mg/l), dactylitis, enthesitis by LEI and plantar fascia, BSA (%), HAQ, DAPSA were evaluated. DAPSA>28 indicate high disease activity (HDA), DAPSA=15–28 – moderate activity (MoDA), DAPSA=5–14 – LDA, DAPSA≤4 – remission. By 1 year of therapy the proportion of pts who had not reached remission or LDA were calculated. The one-factor model of logistic regression was used to identify a group of features that are associated with remission or LDA nonachievement. M±SD, Me [Q25; Q75], Min–Max, %, t-test, Peаrson χ2 , Mann – Whitney tests, ORs with 95% CI were performed. All p<0.05, were considered to indicate statistical significance. Results. At 1 year of therapy 116 pts of 292 (40%) have HDA/MoDA by DAPSA. Remission/LDA was reached in 176 (60%) pts, 110 of them (62.5%) were treated with bDMARDs. Comparative analysis in both groups and one-factor model of logistic regression showed the following features at BL were associated with non-remission/LDA status: TJC>5 (p<0.001), SJC>3 (p<0.001), CRP>10 mg/l (p<0.001), HAQ>0.5 (p<0.001), presence of enthesitis (p<0.001), dactylitis (p<0.001), BMI>30 (p<0.002) and had to be treated with sDMARDs. PsA pts with combination of these clinical features at first visit have a higher risk of not achieving remission/LDA status in comparison to PsA pts without them, OR with 95% CI. Conclusion. In real practice remission/LDA cannot achieve 40% PsA pts despite going through therapy. It is a combination of clinical fea tures at BL – TJC>3, SJC>5, CRP>10 mg/l, HAQ>0.5, presence of enthesitis, dactylitis, BMI>30 kg/m2 and sDMARDs monotherapy – that constitutesa prognostic factor with negative impact on achievement remission/LDA after 1 year of treatment.

P553 Active tuberculosis and opportunistic infections: Pooled safety analysis of ustekinumab through up to 5 years across all approved indications

Abstract Background Ustekinumab (UST) is an approved treatment for adults with inflammatory bowel disease (IBD: Crohn’s disease [CD] and ulcerative colitis [UC]), psoriasis (PsO), and psoriatic arthritis (PsA). Here, we present pooled safety analyses in these approved indications of patients (pts) with active tuberculosis (TB) and opportunistic infections (OIs) through 5 years (yrs) of UST treatment. Methods Pooled data included 13 Phase 2/3 UST studies through 5 yrs of CD and PsO, 2 yrs of UC, and 1 yr of PsA. OIs were identified by clinician review. Herpes zoster (HZ) was evaluated separately. Event rates per 100 pt yrs (PYs) are presented. Concomitant immunomodulators/corticosteroids were permitted in IBD and PsA pts. All pts who received ≥1 UST dose were included. In IBD, placebo (PBO) pts included data up to the first UST dose for pts initially treated with PBO, or >16 weeks after the last UST dose for UST pts who switched to PBO. Results Across all approved indications, 19 OIs including TB were reported, with rates in PBO of 0.40 and UST of 0.10 through 5 yrs in 13807 PYs of follow-up (Table 1); rates of HZ were 1.21 and 0.63, respectively. Of 19 OIs, 18 were in IBD pts and 1 in a PsO pt. Overall, 14/16 pts (12/13 UST) with OIs excluding TB were also receiving confounding concomitant medications. A total of 3 active TB cases (2 pts with CD and 1 pt with UC) were reported in PBO (n=2; 1 in a Hungarian CD pt 10 months after receiving last UST dose) and UST (n=1) pts (Table 1). One active TB case was reported in an asymptomatic South African CD pt treated with UST who had a positive QuantiFERON®-TB Gold test on routine screening and bronchial brushings positive for M. tuberculosis. Both CD pts completed TB treatment with disease resolution. The most common OIs were esophageal candidiasis (UST n=3; PBO n=2) and cytomegalovirus colitis (UST n=3; PBO n=1). Conclusion Rates of OIs, including active TB, in UST-treated pts were low across approved indications through up to 5 yrs with 13807 PYs of follow-up and not higher in UST pts vs PBO pts, suggesting no increased risk of OI with long-term UST treatment.

Prognostic factors associated with achieving minimal disease activity in early psoriatic arthritis patients treated according to “treat-to-target” st rategy within 12 months

Background. The goal of “treat-to-target” strategy (T2T) in psoriatic arthritis (PsA) is attaining remission or minimal disease activity (MDA). The benefits of T2T are shown recently in the study TICOPA and REMARCA. But prognostic factors for achievement MDA in PsA patients (pts) at the early-stage hasn’t been studied yet.Objective – to determine the prognostic factors associated with achievement of minimal disease activity within 12 months (mo) of treatment according to T2T strategy in early psoriatic arthritis patients.Methods. 77 pts (M/F=36/41) with early PsA fulfilling the CASPAR criteria were included. Mean age 36.9±10.45 years, PsA duration 11.1±10.0 mo, psoriasis duration 82.8±92.1 mo. At baseline (BL) and at 12 mo of therapy PsA activity by tender joins count (TJC) out of 68; swelling joints count (SJC) out of 66; pain; patient global assessment disease activity (PGA) using visual analogue scale; CRP; dactylitis, enthesitis by LEI and plantar fascia; BSA; HAQ and fatigue by FACIT 4 scale were evaluated. A score FACIT <30 indicates severe fatigue, the higher the score – the better the quality of life. All pts were given therapy with Methotrexate (MTX) s/c, 29 pts with ineffectiveness of MTX after 3–9 mo of treatment were added biologic DMARDs. The one-factor model of logistic regression was used to identify a group of features that are associated with achievement MDA.Results. By 12 mo of therapy, the proportion of pts who have reached MDA (5/7) were calculated. Pts were split into 2 groups: MDA+ (n=45) and MDA– (n=32).Comparative analysis of BL features in both groups and one-factor model of logistic regression showed the following features were associated with achievement MDA: TJC and SJC<3 (p<0.001); PGA≤20 mm (p<0.001); pain≤15 mm (p<0.001); CRP≤5 mg/l (p<0.03); HAQ≤0.5 (p<0.001); FACIT>30 points (p<0.021); absent of entesitis (p<0.003), dactylitis (p<0.029) and nail damage (p<0.012). Early PsA pts with combination of these features on first visit have more chance to achieve MDA in comparison to PsA pts without them (OR=9.684 [95% CI: 4.6–20.4]).Conclusion. It is a combination of features on first visit – oligoarthritis, moderate activity, absent of entesitis, dactylitis, nail psoriasis, significant impact on function and fatigue – that constitutes a clinical prognostic factors for achievement MDA after 12 mo of treatment in pts with early PsA according T2T.

S932 Active Tuberculosis and Opportunistic Infections: Pooled Safety Analysis of Ustekinumab Through up to 5 Years Across All Approved Indications

Introduction: Ustekinumab (UST) is an approved treatment for adults with inflammatory bowel disease (IBD: Crohn’s disease [CD] and ulcerative colitis [UC]), psoriasis (PsO), and psoriatic arthritis (PsA). Here, we present pooled safety analyses in these approved indications of patients (pts) with active tuberculosis (TB) and opportunistic infections (OIs) through 5 years (yrs) of UST treatment. Methods: Pooled data included 13 Phase 2/3 UST studies through 5 yrs of CD and PsO, 2 yrs of UC, and 1 yr of PsA. OIs were identified by clinician review. Herpes zoster (HZ) was evaluated separately. Event rates per 100 pt yrs (PYs) are presented. Concomitant immunomodulators/corticosteroids were permitted in IBD and PsA pts. All pts who received ≥1 UST dose were included. In IBD, placebo (PBO) pts included data up to the first UST dose for pts initially treated with PBO, or >16 weeks after the last UST dose for UST pts who switched to PBO. Results: Across all approved indications, 19 OIs including TB were reported, with rates in PBO of 0.40 and UST of 0.10 through 5 yrs in 13807 PYs of follow-up (Table); rates of HZ were 1.21 and 0.63, respectively. Of 19 OIs, 18 were in IBD pts and 1 in a PsO pt. Overall, 14/16 pts (12/13 UST) with OIs excluding TB were also receiving confounding concomitant medications. A total of 3 active TB cases (2 pts with CD and 1 pt with UC) were reported in PBO (n=2; 1 in a CD pt 10 months after receiving UST 130 mg IV) and UST pts (n=1) (Table). One active TB case was reported in an asymptomatic South African CD pt treated with UST who had a positive QuantiFERON®-TB Gold test on routine screening and bronchial brushings positive for M. tuberculosis. Both CD pts completed TB treatment with disease resolution. The most common OIs were esophageal candidiasis (UST n=3; PBO n=2) and cytomegalovirus colitis (UST n=3; PBO n=1). Conclusion: Rates of OIs, including active TB, in UST-treated pts were low across approved indications through up to 5 years with 13807 PYs of follow-up and not higher in UST pts vs PBO, suggesting no increased risk of OI with long-term UST treatment. Table 1. - Opportunistic infections (OIs) and active tuberculosis (TB) in Inflammatory Bowel Disease (CD, UC) and Psoriatic studies (PsO, PsA) through up to 5 yrs; numbers of events per 100 patient-years (PYs) of follow-up Inflammatory Bowel Disease Indications a Psoriatic Indications a All Approved Indications Pooled Placebo b (n=1389) Ustekinumab c (n=2575) Placebo d (n=1112) Ustekinumab e (n=4135) Placebo b,d (n=2501) Ustekinumab c.e (n=6710) Total PYs of follow-up 916 3960 327 9847 1244 13807 Average duration of follow-up (weeks) 34.31 79.97 15.30 123.83 25.86 107.00 All OIs, event rates per 100 PYs [n] 0.55 [5] 0.33 [13] 0.00 [0] 0.01[1] 0.40 [5] 0.10 [14] OIs excluding TB 0.33 [3] 0.30 [12] 0.00 [0] 0.01 [1] 0.24 [3] 0.09 [13] TB 0.22 [2] 0.03 [1] 0.00 [0] 0.00 [0] 0.16 [2] 0.01 [1] aPsoriatic (PsO and PsA) trials evaluated subcutaneous ustekinumab (UST) 45/90 mg or placebo (PBO), generally at week 0 and 4, then every 12 weeks (q12w). IBD (CD and UC) trials generally evaluated a single intravenous UST dose (130 mg or weight range-based dosing of ∼6 mg/kg) or PBO induction dose at week 0, followed by subcutaneous UST 90 mg at week 8, then q8w or q12w.bCD and UC: includes data up to the first UST dose for patients who were initially treated with PBO; includes data at or after 16 weeks from the first UST dose onward, up to the dose adjustment if patients had a dose adjustment, for patients who crossed-over or re-randomized to PBO maintenancecCD and UC: includes data up to 16 weeks from the first UST dose for patients who crossed-over or re-randomized to PBO maintenance, and from the dose adjustment onward if patients had a dose adjustment from subcutaneous PBO to subcutaneous UST 90 mg q8wdPsoriatic diseases: includes data up to the time of early escape or crossoverePsoriatic diseases: includes data from the first UST dose onward for patients who early escaped or crossed-over from PBO

нigh prevalence of atherosclerosis comorbidity and his risk factors in patients with psoriatic arthritis compared to psoriasis without arthritis: A retrospective dermatological clinic-based study

Background and Aims : An association between atherosclerosis and psoriasis (PsO) has still limited data. Objectives: to evaluate the prevalence of atherosclerosis comorbidity and his risk factors in patients (pts) with psoriatic arthritis (PsA) compared to PsO without arthritis in a dermatological hospital cohort.Methods: 765 pts (Male-439/Female-326) with moderate-to-severy plaque PsO, age PSO pts 52.4±15,6 years were included. 274 out of 765 pts (35.8%) had PsA and 491 out of 765 pts (64.2%) had PsO alone. PsA pts were older then PsO pts – 55.3±13.7 and 50.4±17,6 (p<0.001).Results: Atherosclerosis coding as I 70 were registered often in PsA pts compared to PsO pts – in 40 out of 274 pts (14.6%) and in 35 out of 491 pts (7.3%) accordingly (p<0.001). Smoking patients was found often in PsO pts compare to PsA pts – in 230 out of 491 pts (46.9%) and in 101 out of 274 pts (36.9%) accordingly (p<0.05). In PsA pts AH coding as I 10 - I 15 was found in more cases than in PsO pts - in 260 out of 491 PsO pts (52.8%) and in 187 out of 274 PsA pts (68.2%) accordingly (p<0.001). Obesity coding as Е65-Е68 was identify in 102 out of 765 pts (13.3%). Obesity were found in more cases in PsA pts - in 53 out of 491 PsO pts (10.9%) and in 49 out of 274 PsA pts (17.9%) accordingly (p<0.001).Conclusions: Atherosclerosis found increased frequency in PsA than PsO due to share inflammation pathways between atherosclerosis and PsA. Background and Aims : An association between atherosclerosis and psoriasis (PsO) has still limited data. Objectives: to evaluate the prevalence of atherosclerosis comorbidity and his risk factors in patients (pts) with psoriatic arthritis (PsA) compared to PsO without arthritis in a dermatological hospital cohort. Methods: 765 pts (Male-439/Female-326) with moderate-to-severy plaque PsO, age PSO pts 52.4±15,6 years were included. 274 out of 765 pts (35.8%) had PsA and 491 out of 765 pts (64.2%) had PsO alone. PsA pts were older then PsO pts – 55.3±13.7 and 50.4±17,6 (p<0.001). Results: Atherosclerosis coding as I 70 were registered often in PsA pts compared to PsO pts – in 40 out of 274 pts (14.6%) and in 35 out of 491 pts (7.3%) accordingly (p<0.001). Smoking patients was found often in PsO pts compare to PsA pts – in 230 out of 491 pts (46.9%) and in 101 out of 274 pts (36.9%) accordingly (p<0.05). In PsA pts AH coding as I 10 - I 15 was found in more cases than in PsO pts - in 260 out of 491 PsO pts (52.8%) and in 187 out of 274 PsA pts (68.2%) accordingly (p<0.001). Obesity coding as Е65-Е68 was identify in 102 out of 765 pts (13.3%). Obesity were found in more cases in PsA pts - in 53 out of 491 PsO pts (10.9%) and in 49 out of 274 PsA pts (17.9%) accordingly (p<0.001). Conclusions: Atherosclerosis found increased frequency in PsA than PsO due to share inflammation pathways between atherosclerosis and PsA.

OA38 Efficacy and safety of upadacitinib in patients with psoriatic arthritis and axial involvement

Abstract Background/Aims Patients (pts) with psoriatic arthritis (PsA) and axial involvement exhibit greater disease activity and quality of life impairments compared with those without axial involvement. Here the aim was to characterize PsA pts with and without axial involvement and compare efficacy of UPA vs placebo (PBO) in PsA pts with axial involvement. Methods In SELECT-PsA 1 (NCT03104400; N = 1705, non-biologic DMARD IR) and SELECT-PsA 2 (NCT03104374; N = 642, biologic DMARD IR), pts with active PsA (≥3 swollen and ≥3 tender joints), active or historical psoriasis, and on ≤ 2 non-biologic DMARDs were randomized to once daily UPA 15 mg, UPA 30 mg, adalimumab 40 mg every other week (SELECT-PsA 1 only), or PBO. Efficacy was assessed in pts with axial involvement (diagnosed by investigators based on totality of information) pooled from the two studies. Assessments included change from BL in BASDAI, BASDAI Q2 (neck/back/hip pain) and Q3 (joint swelling/pain), and the AS Disease Activity Score (ASDAS-CRP), and percentage with BASDAI 50 response, ASDAS inactive disease (ID), ASDAS low disease activity (LDA), ASDAS major improvement (MI), and ASDAS clinically important improvement (CII). Uveitis and inflammatory bowel disease (IBD) adverse events were reviewed. Data on 24-week PBO-controlled period are presented. Results Prevalence of axial involvement was 31.3% in SELECT-PsA 1 and 34.2% in SELECT-PsA 2 (Table). Treatment with UPA 15 mg and 30 mg resulted in significantly greater improvements from BL in the BASDAI, BASDAI Q2 (neck/back/hip pain) and Q3 (joint swelling/pain) and ASDAS-CRP at weeks 12 and 24 vs PBO. Similarly, significantly higher percentages of pts on UPA 15 mg and 30 mg achieved BASDAI 50, ASDAS ID, LDA, MI, and CII at weeks 12 and 24 vs PBO. One pt on UPA 30 mg had incident uveitis, and no IBD was reported on UPA. Conclusion PsA pts with axial involvement had higher BL disease burden compared with those without axial involvement. UPA was efficacious in treating axial symptoms in pts with psoriatic spondylitis. Disclosure A. Deodhar: Consultancies; A.D. has received consultancy fees from Novartis, Pfizer, AbbVie, Eli-Lilly, UBC Pharma, GlaxoSmithKline, Galapagos, Janssen, Boehringer Ingelheim, Celgene. Member of speakers’ bureau; A.D. is a member of the speakers' bureau of Novartis and Pfizer. Grants/research support; A.D. has received research grants from Novartis, Pfizer, AbbVie, Eli-Lilly, UBC Pharma, GlaxoSmithKline. R. Ranza: Consultancies; R.R. has acted as a consultant to AbbVie, Janssen, Lilly, Novartis, Pfizer. Member of speakers’ bureau; R.R. is a member of the speakers' bureau of AbbVie, Janssen, Lilly, Novartis, Pfizer. Grants/research support; R.R. has received grant/research support from AbbVie, Janssen. F. Ganz: Shareholder/stock ownership; F.G. is an employee of AbbVie and may hold stock or options. T. Gao: Shareholder/stock ownership; T.G. is an employee of AbbVie and may hold stock and options. J. Anderson: Shareholder/stock ownership; J.A. is an employee of AbbVie and may hold stock and options. A. Ostor: Consultancies; A.O. has acted as a consultant for AbbVie, BMS, Roche, Janssen, Lilly, Novartis, UBC, Pfizer, Gilead, Paradigm.

POS0234 SECUKINUMAB RETENTION AND SAFETY IN PATIENTS WITH ACTIVE PSORIATIC ARTHRITIS OR ANKYLOSING SPONDYLITIS: 2 YEAR INTERIM RESULTS OF THE OBSERVATIONAL SERENA STUDY

Background:SERENA is an ongoing, prospective, non-interventional study evaluating retention, effectiveness, safety/tolerability and quality of life in more than 2900 patients (pts) with moderate to severe plaque psoriasis, active psoriatic arthritis (PsA) or active ankylosing spondylitis (AS) treated with secukinumab (SEC) at 438 sites across Europe for a period of up to 5 years1.Objectives:We present interim results reporting SEC treatment retention and safety data through 2 years in the PsA and AS pts enrolled in the study.Methods:This interim analysis presents data from 534 PsA and 470 AS pts who were enrolled (target population fulfilling all eligibility criteria) in the study and were followed up for at least 2 years. Pts (aged ≥18 years) with active PsA or AS should have received at least 16 weeks SEC treatment before enrolment in the study1. Retention rate was defined as the percentage of pts who have not discontinued SEC treatment. A treatment break was defined as interruption of therapy for at least 3 months after last injection.Results:The mean treatment duration prior to enrolment in the study was 1.0 year and 0.91 year for PsA and AS, respectively. The retention rates for SEC after 1 year since enrolment and since initiation of treatment were: PsA, 85.2% [n=519, CI: 82.01–88.32] and 96.8% [n=528, CI: 95.18–98.38]; AS, 85.8% [n=452, CI: 82.52–89.17] and 94.2% [n=464, CI: 91.94–96.42], respectively. After 2 years since enrolment and since initiation of treatment, the retention rates were: PsA, 74.9% [n=498, CI: 70.99–78.81] and 87.0% [n=515, CI: 83.99–89.99]; AS, 78.9% [n=437, CI: 75.01–82.88] and 84.8% [n=454, CI: 81.39–88.21], respectively. Survival probabilities for individual indications are presented in Figure 1. At baseline, the majority of PsA (79.5%; n/N=423/532) pts were receiving SEC 300 mg, while 97.0% (n/N=456/470) of AS pts were receiving SEC 150 mg. The majority of pts continued their initial SEC dose; “no dose change” in SEC treatment was reported after 1 and 2 years in the study (Year 1: PsA, 93.4% [n=499] and AS, 92.6% [n=435]; Year 2: PsA, 89.7% [n=479] and AS, 87.9% [n=413]). SEC treatment break was recorded for 31 PsA pts [median (min, max) treatment break duration in days: 125.0 (61, 461)] and for 42 AS [118.0 (61, 813)] pts mainly due to adverse events reported in 58.1% (n=18) and 45.2% (n=19) of pts, respectively. The retreatment started with monthly dosing in most of the cases: PsA, 80.6% (n/N=25/31) and AS, 76.2% (n/N=32/42). No new or unexpected safety signals were reported (Table 1).Table 1.Safety profile of treatment-emergent adverse events within the study periodAE summary, n (%)PsA N=575AS N=499Year 1Year 2Year 1Year 2Subject with any AE239 (41.6)289 (50.3)203 (40.7)247 (49.5)Subject with any serious AE29 (5.0)45 (7.8)29 (5.8)44 (8.8)Subject with AE leading to discontinuation55 (9.6)84 (14.6)47 (9.4)62 (12.4)Death0 (0.0)0 (0.0)0 (0.0)1 (0.2)AEs of special interest, n (IR per 100 subject-years)Serious infections and infestations5 (0.96)9 (0.95)8 (1.78)11 (1.33)Candida infections1 (0.19)2 (0.21)2 (0.44)2 (0.24)Malignancy5 (0.96)7 (0.74)N/R3 (0.36)Major adverse cardiovascular eventsN/R1 (0.11)2 (0.44)3 (0.36)Inflammatory bowel diseaseN/RN/R1 (0.22)1 (0.12)N, total number of patients in the safety set; n, number of patients with event; AE, adverse events; IR, incidence rate; N/R, not reported.Conclusion:Secukinumab retention rates in a real world setting after more than 2 years since initiation of treatment and after 2 years since enrolment in the study indicate high persistence rates. Safety data collected prospectively for up to 2 years confirm the favorable safety profile of secukinumab.

AB0546 5 YEARS FOLLOW-UP OF PSORIATIC ARTHRITIS PATIENTS TREATED ACCORDING TREAT-TO-TARGET STRATEGY. PRELIMINARY RESULTS

Background:The concept of treat to target (T2T) in psoriatic arthritis (PsA) has been established recently and already shown its benefits [1]. But the long-term outcomes of the T2T have not been studied yet.Objectives:To study 5 years (yrs) follow-up of PsA patients (pts) treated according to T2T strategy at the early stage.Methods:35 (M/F–17/18) PsA pts fulfilling CASPAR criteria, who were treated according to T2T strategy at the early stage (PsA duration≤2 yrs) within 24 months (mos) were analyzed. At the time of evaluation mean age is 42.7±11.2 yrs, median (Me) PsA duration 72 [60;95] mos, psoriasis duration 120 [88;180] mos. All pts underwent standard clinical examinations of PsA before started T2T therapy and at follow-up. Within 24 mos of T2T strategy all pts were taking Methotrexate (MTX) monotherapy in increasing dose up to 25 mg/wk and 18 out of 35 (51%) pts received MTX in combination with iTNF. When T2T study was stopped all pts were treated according to standard care with NSAIDs, bDMARDs, MTX, tsDMARDs based on PsA activity and physician decision. The number of pts achieved minimal disease activity (MDA, 5 of 7) and remission by DAPSA (≤4)/low disease activity (LDA)≤14) at the 24 mos of T2T strategy and at 5 yrs follow-up were calculated. The results are presented in the form of mean values, median, upper and lower quartiles.Results:Me duration of follow-up is 68 [53.5;81.5] mos. At 24 mos Me DAPSA 3.48 [0.45;21.76], remission by DAPSA (REM-DAPSA) were seen in 20 out of 35 (57%) pts, LDA-DAPSA in 4 (12%) pts, moderate activity (MoA) by DAPSA in 6 (17%) pts and high disease activity by DAPSA (HDA-DAPSA) in 5 (14%) pts. MDA was noted in 21 out of 35 (60%) pts. At 5 yrs Me DAPSA 7.4 [2.22;13.87], REM-DAPSA was noted in 12 (34%) pts, LDA-DAPSA in 14 (40%), MoA-DAPSA in 5 (14%), HDA-DAPSA in 4 (12%) pts. MDA was observed in 17 of 35 pts (49%). Among 20 pts who had REM-DAPSA at 24 mos only 6 pts (30%) remained in remission at 5 yrs follow-up and 12 out of 21 pts (57.14%) remained in MDA status.Conclusion:In early PsA pts remission and MDA are achievable goal of T2T strategy. But most pts lost remission/MDA after this strategy was changed to a standard care, despite being in remission/MDA status before change of therapy. Further investigations of the long-term outcomes of T2T strategy in PsA, including radiographic outcomes are needed.

POS0976 ANALYSIS OF BIOLOGIC THERAPY RETENTION RATE IN PSORIATIC ARTHRITIS PATIENTS WITH AND WITHOUTV AXIAL INVOLVEMENT. DATA FROM CLINICAL PRACTICE

Background:Limited data are available on retention rates of biologic therapy in psoriatic arthritis (PsA) patients (pts) with axial involvement. It has been shown that in the subset of pts with prevalent axial involvement (AS versus PsA and AxSpA versus PsA) a longer duration of anti-TNF-α-therapy was observed as compared to peripheral arthritis [1].Objectives:To compare retention rates of biologic therapy in PsA pts with and without axial involvement in routine clinical practice.Methods:731 pts with PsA according to CASPAR criteria were included in the study. Data were collected from 43 rheumatology clinics over various regions of the Russian Federation. Among the pts, 243 (33.0%) (M/F 132/111) were given biologic therapy. Pts’ age 45.9±12.8 years (yrs), disease duration 8.6±6.5 yrs. Pts underwent standard clinical examination of PsA activity and were split into two groups (gr.), with and without axial PsA (axPsA): axPsA(+) and axPsA(-). Pts in the axPsA(+) gr. had inflammatory back pain by ASAS criteria and/or radiographic sacroiliitis (SI) (unilateral grade≥3 or bilateral grade≥2) and/or active MRI SI and/or typical of axPsA changes of the cervical and/or lumbar spine (marginal/paramarginal syndesmophytes, ankylosis of the facet joints). Pts in the axPsA(-) gr. had only peripheral arthritis. The axPsA(+) gr. included 143 (58.8%) pts, the axPsA(-) gr. 100 (41.2%) pts. 163 (67.1%) pts were treated with TNF inhibitors (TNF-i), 80 (32.9%) pts with interleukin inhibitors (IL-i): 55 pts with Ustekinumab, 25 pts with Secukinumab. During the TNF-i treatment courses Infliximab was given to 34 pts, Adalimumab to 53 pts, Etanercept to 36 pts, Golimumab to 27 pts and Certolizumab Pegol to 8 pts. The observation period lasted 12 months. Treatment retention rates were analyzed using Kaplan-Meier curves and the log-rank test.Results:Analysis of the treatment retention rates revealed statistically significant differences between the axPsA(+) and the axPsA(-) grs. After 12 months of observation, 72.9% of pts in the axPsA(-) gr. continued receiving biologic therapy, while in the axPsA(+) gr. only 53.1% of pts (р=0.0027) received it. The same kind of differences in anti-TNF therapy were found between the axPsA(-) gr. and the axPsA(+) gr.: 82.2% and 62.3% pts respectively (р=0.011) continued receiving TNF-i after 12 months. However no statistically significant differences were found between the two grs. in the treatment retention rates of IL-i therapy: after 12 months of observation 55.5% of axPsA(-) pts and 37% of axPsA(+) pts (р=0.086) continued receiving IL-i.Conclusion:In routine clinical practice, retention rates of biologic therapy were found to be worse in PsA pts with axial involvement. In clinical practice, TNF-i are prescribed twice as often than IL-i. However, considering the need of personalized therapy, in case of axPsA the use of IL-i is preferable because their treatment retention rates don’t depend on axial involvement.

OP0233 EFFICACY AND SAFETY OF UPADACITINIB IN PATIENTS WITH PSORIATIC ARTHRITIS AND AXIAL INVOLVEMENT

Background:Patients (pts) with psoriatic arthritis (PsA) and axial involvment exhibit greater disease activity and quality of life impairments compared with those without axial involvment.Objectives:To characterize PsA pts with and without axial involvement and compare efficacy of UPA vs placebo (PBO) in PsA pts with axial involvement.Methods:In SELECT-PsA 1 (NCT03104400; N=1705, non-biologic DMARD IR) and SELECT-PsA 2 (NCT03104374; N=642, biologic DMARD IR), pts with active PsA (≥3 swollen and ≥3 tender joints), active or historical psoriasis, and on ≤2 non-biologic DMARDs were randomized to once daily UPA 15 mg, UPA 30 mg, adalimumab 40 mg every other week (SELECT-PsA 1 only), or PBO. Efficacy was assessed in pts with axial involvement (diagnosed by investigators based on totality of information) pooled from the 2 studies. Assessments included change from BL in BASDAI, BASDAI Q2 (neck/back/hip pain) and Q3 (joint swelling/pain), and the AS Disease Activity Score (ASDAS-CRP), and percentage with BASDAI 50 response, ASDAS inactive disease (ID), ASDAS low disease activity (LDA), ASDAS major improvement (MI), and ASDAS clinically important improvement (CII). Uveitis and inflammatory bowel disease (IBD) adverse events were reviewed. Data on 24-week PBO-controlled period are presented.Results:Prevalence of axial involvment was 31.3% in SELECT-PsA 1 and 34.2% in SELECT-PsA 2 (Table). Treatment with UPA 15 mg and 30 mg resulted in significantly greater improvements from BL in the BASDAI, BASDAI Q2 (neck/back/hip pain) and Q3 (joint swelling/pain) and ASDAS-CRP at weeks 12 and 24 vs PBO (Figure). Similarly, significantly higher percentages of pts on UPA 15 mg and 30 mg achieved BASDAI 50, ASDAS ID, LDA, MI, and CII at weeks 12 and 24 vs PBO (Figure). One pt on UPA 30 mg had incident uveitis, and no IBD was reported on UPA.Table 1.Demographics and Baseline CharacteristicsSELECT-PsA 1SELECT-PsA 2Parameter, mean (SD)With Psoriatic Spondylitis(n=534)Without Psoriatic Spondylitis(n=1170)Pvalue*With Psoriatic Spondylitis(n=219)Without Psoriatic Spondylitis(n=421)Pvalue*BMI (kg/m2)29.9 (6.5)30.5 (6.9).081031.6 (8.0)31.3 (6.9).6226TJC6821.6 (15.1)19.2 (13.5).002227.5 (18.0)23.3 (16.2).0027SJC6611.7 (9.4)11.0 (7.9).118412.9 (9.2)11.7 (8.7).0804Physician’s Global Assessment (NRS 0–10)6.7 (1.6)6.5 (1.7).04376.6 (1.8)6.5 (1.7).1897HAQ-DI1.2 (0.6)1.1 (0.6).01701.2 (0.6)1.2 (0.7).2049n=531n=1164n=218n=416Presence of dactylitis, n (%)†188 (35.2)328 (28.0).002869 (31.5)100 (23.8).0348Presence of enthesitis, n(%)‡432 (80.9)884 (75.6).0147189 (86.3)337 (80.0).0125ASDAS–CRP3.4 (0.9)3.1 (1.0)&lt;.00013.3 (1.0)3.2 (1.1).1032n=530n=1161n=217n=416BASDAI5.8 (2.0)5.3 (2.2)&lt;.00016.2 (2.2)5.8 (2.2).0673n=530n=1161n=217n=416Morning Stiffness Duration (NRS 0–10; BASDAI Q6)5.0 (3.0)4.7 (3.0).03685.6 (3.2)5.1 (3.0).0454n=530n=1161n=217n=416Patient’s Assessment of Inflammatory Neck, Back, or Hip Pain (NRS 0–10; BASDAI Q2)5.8 (2.7)4.6 (3.2)&lt;.00016.4 (2.8)5.4 (3.1).0001n=530n=1161n=217n=416*Calculated by t-test for continuous variables and chi-square test for categorical values. Bolded if &lt;0.05.Defined as †LDI&gt;0 and ‡total enthesitis count &gt;0Conclusion:PsA pts with axial involvement had higher BL disease burden compared with those without axial involvement. UPA was efficacious in treating axial symptoms in pts with psoriatic spondylits.

AB0522 SAFETY PROFILE OF UPADACITINIB UP TO 3 YEARS IN PATIENTS WITH PSORIATIC ARTHRITIS: AN INTEGRATED ANALYSIS FROM THE PHASE 3 PROGRAM

Background:The efficacy and safety of upadacitinib (UPA), an oral Janus kinase inhibitor, in patients (pts) with active psoriatic arthritis (PsA) were demonstrated through 24 weeks in the phase 3 SELECT-PsA 1 and SELECT-PsA 2 placebo-controlled clinical trials.1,2Objectives:To describe the long-term integrated safety profile of UPA relative to adalimumab (ADA) in pts with PsA treated in the SELECT program.Methods:The SELECT-PsA program enrolled pts with prior inadequate response or intolerance to ≥1 non-biologic DMARD (SELECT-PsA 1) or ≥1 biologic DMARD (SELECT-PsA 2). Both trials include UPA 15 mg and 30 mg, and only SELECT-PsA 1 includes long-term comparison with ADA 40 mg every other week. Treatment-emergent adverse events (TEAEs: AE onset ≥first dose and ≤30 days after last dose for UPA and ≤70 days for ADA) were summarized for the following: pooled UPA 15; pooled UPA 30; and ADA. TEAEs are reported as exposure-adjusted event rates (EAERs; events/100 pts years [E/100 PY]) up to a cut-off date of 20 June 2020.Results:2257 pts received ≥1 dose of UPA 15 (N=907; 1247.2 PYs), UPA 30 (N=921; 1257.4 PYs), or ADA (N=429; 549.7 PYs), with median (max) exposures of 69 (155), 69 (154), and 68 (152) weeks, respectively. EAERs of TEAEs and serious AEs were generally similar between UPA 15 and ADA and higher with UPA 30; rates of AEs leading to study drug discontinuation were generally similar across all groups (Table 1). Similarly, rates of serious infection were comparable between UPA 15 and ADA and higher with UPA 30 (Figure 1 next page). The most common serious infection was pneumonia. Rates of herpes zoster were lower with UPA 15 than UPA 30 but higher than ADA. Most herpes zoster events involved a single dermatome; no events involved the central nervous system or other internal organs. Lower rates of opportunistic infections (OI) excluding tuberculosis were observed with UPA 15 vs UPA 30; the most common OI was mucosal candida infection. Malignancies were reported at similar rates across all treatment groups; no events of lymphoma were reported. Age-gender-adjusted standardized incidence ratios for malignancies excluding NMSC indicated no increased risk with UPA compared to the general population. Rates of adjudicated major adverse cardiovascular events and venous thromboembolic events were ≤0.3 E/100 PY for both UPA arms; all pts had ≥1 risk factor. One adjudicated gastrointestinal perforation was reported with UPA 15.Table 1.Overall Treatment-emergent AEs for Upadacitinib and Adalimumab (E/100 PY [95% CI])UPA 15 mg QDN=907(1247.2 PY)UPA 30 mg QDN=921(1257.4 PY)ADA 40 mg EOWN=429(549.7 PY)AEs263.9 (254.9, 272.9)321.5 (311.6, 331.5)286.5 (272.4, 300.7)Serious AEs10.3 (8.6, 12.1)13.2 (11.2, 15.2)9.6 (7.0, 12.2)AE leading to discontinuation6.7 (5.2, 8.1)7.8 (6.2, 9.3)7.8 (5.5, 10.2)Deathsa0.2 (-0.1, 0.4)0.2 (-0.0, 0.5)0.2 (-0.2, 0.5)aDeaths included non-treatment emergent deaths: UPA 15, 1; UPA 30, 1.ADA, adalimumab; AE, adverse event; CI, confidence interval; E, event; EOW, every other week; PY, patient years; QD, once daily; UPA, upadacitinib.Hepatic disorders were mostly transient, non-serious transaminase increases. Creatine phosphokinase elevations were reported more frequently with UPA 30 vs UPA 15; most were asymptomatic with no rhabdomyolysis reported. AEs of anemia, neutropenia, and lymphopenia were generally mild or moderate, non-serious. Except for rates of lymphopenia (higher with UPA 15), hepatic disorders, and neutropenia (both higher with ADA), lab-related TEAEs occurred at generally consistent rates between UPA 15 and ADA. Study drug discontinuation due to lab-related TEAEs was uncommon.Conclusion:The safety profiles of UPA 15 and ADA were generally similar; the rates of most AEs were higher with UPA 30 compared with ADA. Through the cut-off date, the safety profile of UPA 15 and UPA 30 in PsA pts demonstrated consistent results compared to what has been observed with UPA in rheumatoid arthritis.3

AB0524 EFFICACY OF GUSELKUMAB ACROSS BASDAI COMPONENTS IN TREATING AXIAL-RELATED SYMPTOMS OF PSORIATIC ARTHRITIS: RESULTS FROM TWO PHASE 3, RANDOMIZED, PLACEBO-CONTROLLED STUDIES

Background:The monoclonal antibody guselkumab (GUS; anti- IL-23p19-subunit) is approved to treat psoriatic arthritis (PsA). Post hoc analyses of DISCOVER-1&amp;2 suggested that GUS may be effective in improving symptoms of axial manifestation of PsA.Objectives:Evaluate the efficacy of GUS across components of the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) in improving symptoms of axial manifestations of active PsA patients (pts) using data from Phase 3, randomized, placebo (PBO)-controlled studies.Methods:DISCOVER-1&amp;2 enrolled pts with active PsA; pts were randomized to subcutaneous injections of guselkumab 100 mg every 4 weeks (Q4W) or at Wk0, 4, and Q8W, or PBO. These post hoc analyses included pts who were identified by the investigator as having axial symptoms and sacroiliitis (prior X-ray or MRI or screening X-ray). BASDAI scores were assessed at Wks 0, 8, 16, 24, and 52. Mean BASDAI component scores through Wk52 are reported by treatment group. Pooled data from the two studies are reported. Mean BASDAI component scores are reported using observed data; total BASDAI scores with missing components were set to missing. The proportion of pts achieving ≥50% improvement in BASDAI (BASDAI 50) was also determined; pts with missing data or who met the treatment failure criteria (discontinued study agent or used prohibited medications) were considered nonresponders at all subsequent timepoints.Results:These analyses included 312 pts from DISCOVER-1&amp;2 (103 GUS Q4W, 91 GUS Q8W, 118 PBO); mean total BASDAI scores at Wk0 were 6.4, 6.5, and 6.6, respectively. Demographics and mean baseline BASDAI component scores (ie, fatigue, spinal pain, joint pain, enthesitis, qualitative morning stiffness, and quantitative morning stiffness) were similar across treatment groups (Table 1). In comparison with the total study population, this subgroup of pts had a higher mean C-reactive protein level at baseline and a higher proportion of pts with enthesitis and included a slightly higher proportion of males. Mean scores for all six BASDAI components, including spinal pain, decreased through Wk24 in GUS-treated pts, with separation from PBO observed as early as Wk8; improvements were maintained at Wk52. At Wk24, BASDAI 50 response rates were higher in the Q4W and Q8W groups vs PBO (38% and 40% vs 19%).1 At WK52, mean BASDAI component scores for PBO pts who crossed over to GUS Q4W at Wk24 were similar to those for pts who were randomized to GUS.2 A similar trend was observed for BASDAI50 response.Conclusion:Among PsA pts with axial symptoms and sacroiliitis (via investigator-confirmed imaging) in the DISCOVER-1&amp;2 trials, GUS treatment resulted in lower mean scores for all six BASDAI components compared with PBO as early as Wk 8 and through Wk24, with mean scores maintained at Wk52.

POS0195 GUSELKUMAB TREATMENT MODULATES CORE PSORIATIC ARTHRITIS GENE EXPRESSION IN TWO PHASE 3 CLINICAL TRIALS (DISCOVER-1 AND -2)

Background:Guselkumab (GUS), an interleukin-23 p19-subunit monoclonal antibody, demonstrated efficacy compared with placebo (PBO) in reducing signs and symptoms of psoriatic arthritis (PsA) in the phase 3 DISCOVER-1 &amp; 2 studies.1,2Objectives:To evaluate gene expression in the blood of PsA patients (pts) in the DISCOVER-1 &amp; -2 studies and the impact of GUS on the expression of these genes.Methods:Pts were treated with GUS 100 mg every 4 weeks (Q4W); GUS 100 mg at W0, W4, then Q8W; or matching PBO. Whole transcriptome profiling by RNA-sequencing was performed using the Novaseq platform on blood samples obtained from a subset of 673 pts with PsA at baseline across the 2 DISCOVER studies, as well as from 21 demographically (age, sex, and ethnicity) matched healthy controls procured independently of the clinical program. A subgroup (N=227) also had serial blood samples (W0/W4/W24) evaluated; the subgroup pts were selected based on having baseline characteristics (demographics, disease activity, medication use) representative of the overall cross-study PsA population. Significance of differentially expressed genes (DEGs) between PsA and healthy controls was defined by a false discovery rate (FDR) &lt;0.05 based on a log-linear model using edgeR. Top genes were defined by significance and |logFC| &gt;1. For cell type analysis, genes that changed with GUS treatment were tested for enrichment using Cibersort. Gene enrichment scores were calculated using Gene Set Variation Analysis (GSVA).Results:To define disease genes, we compared genes at baseline in pts with active PsA vs. healthy control whole blood transcriptomes and detected 355 upregulated and 314 downregulated (top genes shown in Table 1), defined here as core disease genes. Upregulated genes were largely related to neutrophils, monocytes, macrophages, and extracellular matrix, whereas downregulated genes were related to T cells. The upregulated disease genes were significantly decreased and the downregulated disease genes were significantly increased by GUS treatment vs. PBO at W4 and W24 (Fig 1). Upon stratification by Psoriasis Area and Severity Index 75% response and American College of Rheumatology 20% response, changes in core disease gene expression from W0 were statistically significant among responders, but not in non-responders, at W4 and W24 (data not shown). We then performed the second differential expression analysis comparing baseline to W4 and W24 for both PBO and GUS treatment arms to define genes that change with treatment arm over time. At W4 and W24 we found many DEGs from baseline with GUS treatment and none with PBO. These included genes related to B-, T-, NK-, and plasma cells (increased by GUS) and neutrophils, monocytes, eosinophils, and macrophages (decreased by GUS), suggestive of a partial normalization of immune cell composition in whole blood.Conclusion:Using whole transcriptome profiling, we detected DEGs in blood samples obtained from PsA pts vs. healthy controls, suggesting a dysregulation of immune cell profiles in PsA. The majority of these disease-associated genes were modulated by GUS, with directionality toward a normalization of whole blood transcriptomic signatures.

OP0054 EFFICACY OF GUSELKUMAB, A MONOCLONAL ANTIBODY THAT SPECIFICALLY BINDS TO THE P19-SUBUNIT OF IL-23, ON ENDPOINTS RELATED TO AXIAL INVOLVEMENT IN PATIENTS WITH ACTIVE PSA WITH IMAGING-CONFIRMED SACROILIITIS: WEEK-24 RESULTS FROM TWO PHASE 3, RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED STUDIES

Background:Guselkumab (GUS), an interleukin-23 inhibitor, was efficacious in reducing signs and symptoms of active psoriatic arthritis (PsA) in patients (pts) in two phase 3 trials (DISCOVER-1 and DISCOVER-2).Objectives:To evaluate the efficacy of GUS in PsA pts with imaging-confirmed axial involvement consistent with sacroiliitis in DISCOVER-1&amp;2.Methods:In DISCOVER-1, 381 pts with active PsA (≥ 3 swollen joints, ≥ 3 tender joints; C-reactive protein ≥ 0.3mg/dL despite standard therapies) and in DISCOVER-2, 739 pts with active PsA (≥ 5 swollen joints, ≥ 5 tender joints, CRP ≥ 0.6mg/dL despite standard therapies) were randomized 1:1:1 to GUS 100mg Q4W, GUS 100mg Q8W (Wk0, Wk4, then Q8W), or PBO. This analysis included pts with sacroiliitis at baseline who had either documented imaging confirmation of sacroiliitis in the past or pelvic X-ray confirmation of sacroiliitis at screening (pooled data from DISCOVER-1&amp;2) based on investigators’ judgment of presence/absence of sacroiliitis. Efficacy was assessed by BASDAI score, BASDAI50, modified BASDAI (mBASDAI; excludes Q#3), spinal pain (BASDAI Q#2), ASDAS-CRP score, and ASDAS responses of inactive disease (&lt;1.3), major improvement (decrease ≥2.0), and clinically important improvement (decrease ≥1.1). Pts with missing data at wk24 were classified as nonresponders.Results:312 pts presented with axial involvement (PBO, n= 118; GUS q8w, n = 91; GUS q4w, n = 103). The LS mean changes from baseline to wk24 in BASDAI, spinal pain, mBASDAI, and ASDAS-CRP were greater in the two GUS groups vs PBO (Table). Greater proportions of GUS-treated pts achieved BASDAI50 (Table) and ASDAS responses of inactive disease, major improvement, and clinically important improvement (Figure) at wk24 vs PBO.Conclusion:GUS improved axial symptoms over 24 weeks in active PsA patients with imaging-confirmed sacroiliitis.Table.Efficacy of GUS in PsA patients with axial involvement at week 24.aPBO(n=118)GUS 100 mg every 8 weeks(n=91)GUS100 mg every 4 weeks(n=103)LS Mean change in BASDAI-1.35-2.67*-2.68*LS Mean change in spinal painb-1.30-2.73*-2.48*BASDAI50c, %21/110 (19.1%)34/84 (40.5%)**36/95 (37.9%)**LS Mean change in modified BASDAId-1.13-2.16*-2.18*LS Mean change in ASDAS-CRP-0.71-1.43*-1.46*aPts with axial involvement consistent with sacroiliitis at baseline and either a history of imaging confirmation or pelvic X-ray at screening (pooled data from DISCOVER-1 &amp; 2)bQuestion 2 of the BASDAI.cPts with BASDAI &gt; 0 at baseline.dExcludes question 3 of the BASDAI.Unadjusted p-values as noted: *p &lt; 0.001, ** p &lt; 0.01Acknowledgments:NoneDisclosure of Interests:Philip Helliwell: None declared, Dafna D Gladman Grant/research support from: AbbVie, Amgen Inc., BMS, Celgene Corporation, Janssen, Novartis, Pfizer, UCB – grant/research support, Consultant of: AbbVie, Amgen Inc., BMS, Celgene Corporation, Janssen, Novartis, Pfizer, UCB – consultant, Denis Poddubnyy Grant/research support from: AbbVie, MSD, Novartis, and Pfizer, Consultant of: AbbVie, Bristol-Myers Squibb, Eli Lilly, MSD, Novartis, Pfizer, Roche, UCB, Speakers bureau: AbbVie, Bristol-Myers Squibb, Eli Lilly, MSD, Novartis, Pfizer, Roche, UCB, Philip J Mease Grant/research support from: AbbVie, Amgen, Bristol-Myers Squibb, Janssen, Eli Lilly, Novartis, Pfizer, Sun Pharma, UCB Pharma, Consultant of: AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Janssen, Eli Lilly, Galapagos, Gilead, Novartis, Pfizer, Sun Pharma, UCB Pharma, Speakers bureau: AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Genentech, Janssen, Novartis, Pfizer, UCB Pharma, Xenofon Baraliakos Grant/research support from: Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Consultant of: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Alexa Kollmeier Shareholder of: Johnson &amp; Johnson, Employee of: Janssen Research &amp; Development, LLC, Elizabeth C Hsia Shareholder of: Johnson &amp; Johnson, Employee of: Janssen Research &amp; Development, LLC, Xie L Xu Shareholder of: Johnson &amp; Johnson, Employee of: Janssen Research &amp; Development, LLC, Shihong Sheng Shareholder of: Johnson &amp; Johnson, Employee of: Janssen Research &amp; Development, LLC, Prasheen Agarwal Shareholder of: Johnson &amp; Johnson, Employee of: Janssen Research &amp; Development, LLC, Bei Zhou Shareholder of: Johnson &amp; Johnson, Employee of: Janssen Research &amp; Development, LLC, Soumya D Chakravarty Shareholder of: Johnson &amp; Johnson, Employee of: Janssen Scientific Affairs, LLC, May Shawi Shareholder of: Johnson &amp; Johnson, Employee of: Janssen Research &amp; Development, LLC, Chetan Karyekar Shareholder of: Johnson &amp; Johnson, Consultant of: Janssen, Employee of: Janssen Global Services, LLC. Previously, Novartis, Bristol-Myers Squibb, and Abbott Labs., Atul Deodhar Grant/research support from: AbbVie, Eli Lilly, GSK, Novartis, Pfizer, UCB, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myer Squibb (BMS), Eli Lilly, GSK, Janssen, Novartis, Pfizer, UCB, Speakers bureau: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myer Squibb (BMS), Eli Lilly, GSK, Janssen, Novartis, Pfizer, UCB, Désirée van der Heijde Consultant of: AbbVie, Amgen, Astellas, AstraZeneca, BMS, Boehringer Ingelheim, Celgene, Cyxone, Daiichi, Eisai, Eli-Lilly, Galapagos, Gilead Sciences, Inc., Glaxo-Smith-Kline, Janssen, Merck, Novartis, Pfizer, Regeneron, Roche, Sanofi, Takeda, UCB Pharma; Director of Imaging Rheumatology BV

OP0053 SECUKINUMAB IMPROVES CLINICAL AND IMAGING OUTCOMES IN PATIENTS WITH PSORIATIC ARTHRITIS AND AXIAL MANIFESTATIONS WITH INADEQUATE RESPONSE TO NSAIDS: WEEK 52 RESULTS FROM THE MAXIMISE TRIAL

Background:Although axial disease may affect up to 70% of patients (pts) with Psoriatic Arthritis (PsA), evidence on the efficacy of biologics in the treatment of axial manifestations in such pts is limited,1particularly as validated classification criteria for this subtype of PsA are not yet available. MAXIMISE (NCT02721966) is the first randomised controlled trial evaluating the efficacy of a biologic in the management of the axial manifestations of PsA and showed that secukinumab (SEC) 300 and 150 mg provided rapid and significant improvement in ASAS20 responses in these pts through week (Wk) 12.2Objectives:To present 52 wks efficacy results and imaging data from the MAXIMISE trial.Methods:This phase 3b, double-blind, placebo (PBO)-controlled, multicentre 52-wk trial included 498 pts (aged ≥18 years) with a diagnosis of PsA and classified by CASPAR criteria, spinal pain VAS score ≥ 40/100 and BASDAI score ≥ 4 despite use of at least two NSAIDs. Pts were randomised to SEC 300 mg (N=167) or SEC 150 mg (N=165) or PBO (N=166) wkly for 4 wks and every 4 wks thereafter. At Wk 12, PBO pts were re-randomised to SEC 300/150 mg. The primary endpoint was ASAS20 response with SEC 300 mg at Wk 12. The key secondary endpoint was ASAS20 response with SEC 150 mg at Wk 12. Wk 52 data are presented as observed. Bone marrow oedema of the entire spine and sacroiliac joints were assessed centrally with Berlin MRI scores at Baseline, Wk 12 and Wk 52.Results:Primary and key secondary endpoints were met; ASAS20 responses were sustained and increased further through Wk 52. 75%/79.7% of the PBO pts re-randomised at Wk 12 to SEC 300/150 mg achieved ASAS20 response at Wk 52 (Figure 1). ASAS40 responses at Wk 52 were 69.1% [SEC 300 mg], 64.5% [SEC 150 mg], 62.5% [PBO-SEC 300 mg], and 54.1% [PBO-SEC 150 mg]. At baseline, 59.5% [SEC 300 mg], 53.5% [SEC 150 mg] and 64.2% [PBO] of the pts had positive MRIs for the sacroiliac joints and/or the spine with Berlin MRI score ≥1. The reductions of Berlin MRI score for entire spine and sacroiliac joints were statistically significant for pts treated with SEC 300/150 mg vs. placebo (Figure 2a and b). There were no new or unexpected safety findings.Figure 1.ASAS20 Response over 52 Wks*Figure 2.Total Berlin MRI score for the Entire Spine and Sacroiliac Joints at Wk 12Conclusion:Secukinumab improved all evaluated ASAS responses through Wk 52 in PsA pts with axial manifestations and inadequate responses to NSAIDs and led to significant reduction of inflammatory MRI lesions in the spine and the Sacroiliac Joints. The safety profile of secukinumab through Wk 52 was consistent with previous reports.3-4

OP0050 ADALIMUMAB INTRODUCTION VERSUS METHOTREXATE DOSE ESCALATION IN PATIENTS WITH INADEQUATELY CONTROLLED PSORIATIC ARTHRITIS: RESULTS FROM RANDOMIZED PHASE 4 CONTROL STUDY

Background:Methotrexate (MTX) is often used as first-line therapy for patients (pts) with psoriatic arthritis (PsA) despite limited efficacy and data on appropriate dosage. Minimal Disease Activity (MDA) is suggested as an optimal treat-to-target outcome. Biologic disease-modifying antirheumatic drugs (bDMARDs) have demonstrated improved outcomes (including MDA rates) over MTX. However, more data are needed to define the optimal timing of bDMARD initiation and characterize efficacy of MTX dose escalation, to achieve optimal outcomes.Objectives:To compare achievement of MDA between adding adalimumab (ADA) vs escalating MTX dose in PsA pts with inadequate disease control after initial MTX therapy.Methods:The open-label, 2-part CONTROL study enrolled bDMARD-naive adult pts with active PsA (not in MDA at screening and ≥3 tender and ≥3 swollen joints) despite MTX 15 mg every wk (ew) for ≥4 wks. Pts were randomized to ADA 40 mg every other wk + MTX 15 mg (ADA+MTX) or escalated MTX to 20–25 mg ew or highest tolerable dose during 16-wk part 1 (Fig 1). The primary endpoint was achievement of MDA, defined as fulfilling ≥5 of the 7 criteria: tender joint count 68 (TJC68) ≤1, swollen joint count 66 (SJC66) ≤1, Psoriasis Area Severity Index (PASI) ≤1 or body surface area (BSA) ≤3%, pt’s pain (visual analogue scale [VAS] 0–100) ≤15, Pt’s Global Assessment of disease activity (PtGA) VAS ≤20, Health Assessment Questionnaire Disability Index (HAQ-DI) ≤0.5 and tender entheseal points (0–8) ≤1. Key secondary efficacy endpoints were achievement of ACR20 and PASI75 and change from baseline in HAQ-DI and Leeds Enthesitis Index (LEI) at wk 16.Results:Overall, 246 pts were randomized; 245 received treatment (ADA+MTX, n=123; escalated MTX, n=122); 117 (95%) pts and 110 (90%) pts, respectively, completed part 1. Baseline characteristics were similar between groups (Table). During part 1, the average dose of MTX was 21.8 mg/wk (55% on oral MTX) in the escalated MTX group. Significantly higher proportion of pts in ADA+MTX (42%) vs escalated MTX (13%) group achieved MDA at wk 16 (non-responder imputation [NRI]; difference [95% CI] 28% [18%–39%];P&lt;0.001;Fig 2). Observed case analysis confirmed the NRI analysis. Lower MDA rates at wk 16 were observed in the escalated MTX arm regardless of prior MTX duration (Fig 2). Significant improvements in key secondary endpoints were also observed with ADA+MTX vs escalated MTX (allP&lt;0.05;Fig 2). In part 1, the proportion of patients with adverse events was similar between groups (ADA+MTX, 62% vs escalated MTX, 57%); no opportunistic infections, tuberculosis, malignancies, or deaths were reported during part 1.Conclusion:A significantly higher proportion of pts achieved MDA at wk 16 after introducing ADA compared with escalating MTX dose; higher rates were observed regardless of prior MTX duration. Significantly higher responses in musculoskeletal, skin, and quality of life measures were observed with ADA+MTX vs escalated MTX. No new safety signals with ADA were identified in this pt population.Table 1.Baseline DemographicsCharacteristics, mean (SD)ADA+MTXn=123Escalated MTXn=122Female, n (%)64 (52.0)59 (48.4)Age, y51.4 (12.2)48.8 (12.7)BSA &gt;3%, n (%)74 (60.2)78 (63.9)Pt pain63.7 (19.5)62.3 (20.9)PtGA65.0 (19.9)62.9 (20.9)HAQ-DI1.2 (0.6)1.2 (0.7)LEI + plantar count3.5 (2.1)3.5 (2.1)Disclosure of Interests:Laura C Coates: None declared, William Tillett Grant/research support from: AbbVie, Celgene, Eli Lilly, Janssen, Novartis, Pfizer Inc, UCB, Consultant of: AbbVie, Amgen, Celgene, Lilly, Janssen, Novartis, MSD, Pfizer Inc, UCB, Speakers bureau: AbbVie, Amgen, Celgene, Lilly, Janssen, Novartis, Pfizer Inc, UCB, Maria Antonietta D’Agostino Consultant of: AbbVie, BMS, Novartis, and Roche, Speakers bureau: AbbVie, BMS, Novartis, and Roche, Proton Rahman Grant/research support from: Janssen and Novartis, Consultant of: Abbott, AbbVie, Amgen, BMS, Celgene, Lilly, Janssen, Novartis, and Pfizer., Speakers bureau: Abbott, AbbVie, Amgen, BMS, Celgene, Lilly, Janssen, Novartis, Pfizer, Frank Behrens Grant/research support from: Pfizer, Janssen, Chugai, Celgene, Lilly and Roche, Consultant of: Pfizer, AbbVie, Sanofi, Lilly, Novartis, Genzyme, Boehringer, Janssen, MSD, Celgene, Roche and Chugai, Philip G Conaghan Consultant of: AbbVie, BMS, Eli Lilly, EMD Serono, Flexion Therapeutics, Galapagos, GSK, Novartis, Pfizer, Speakers bureau: AbbVie, Eli Lilly, Novartis, Pfizer, Erin McDearmon-Blondell Shareholder of: AbbVie, Employee of: AbbVie, Xianwei Bu Shareholder of: AbbVie, Employee of: AbbVie, Liang Chen Shareholder of: AbbVie, Employee of: AbbVie, Mudra Kapoor Shareholder of: AbbVie, Employee of: AbbVie, Philip J Mease Grant/research support from: Abbott, Amgen, Biogen Idec, BMS, Celgene Corporation, Eli Lilly, Novartis, Pfizer, Sun Pharmaceutical, UCB – grant/research support, Consultant of: Abbott, Amgen, Biogen Idec, BMS, Celgene Corporation, Eli Lilly, Novartis, Pfizer, Sun Pharmaceutical, UCB – consultant, Speakers bureau: Abbott, Amgen, Biogen Idec, BMS, Eli Lilly, Genentech, Janssen, Pfizer, UCB – speakers bureau

OP0225 TOFACITINIB AS MONOTHERAPY FOLLOWING METHOTREXATE WITHDRAWAL IN PATIENTS WITH PSORIATIC ARTHRITIS PREVIOUSLY TREATED WITH OPEN-LABEL TOFACITINIB + METHOTREXATE: A RANDOMISED, PLACEBO-CONTROLLED SUBSTUDY OF OPAL BALANCE

Background:Tofacitinib is an oral JAK inhibitor for the treatment of psoriatic arthritis (PsA).Objectives:To assess tofacitinib 5 mg BID as monotherapy after methotrexate (MTX) withdrawal vs with continued background MTX in patients (pts) with PsA.Methods:OPAL Balance (NCT01976364) was an open-label (OL) long-term extension (LTE) study of tofacitinib in pts with PsA who participated in Phase (P)3 studies (OPAL Broaden,NCT01877668; OPAL Beyond,NCT01882439). Pts who completed ≥24 months’ tofacitinib treatment in the LTE (stable 5 mg BID for ≥3 months) and were receiving oral MTX (7.5–20 mg/week; stable for ≥4 weeks) entered the multicentre, 12-month, double-blind, MTX withdrawal substudy. Pts remained on OL tofacitinib 5 mg BID and were randomised 1:1 to receive placebo (tofacitinib monotherapy, ie, blinded MTX withdrawal) or MTX (tofacitinib + MTX; same stable doses). Primary endpoints were changes from substudy baseline (Δ) in PASDAS and HAQ-DI at Month (M)6. Secondary efficacy endpoints were assessed at all time points. Safety was assessed throughout the substudy.Results:Of 180 pts randomised, 179 were treated (tofacitinib monotherapy n=90; tofacitinib + MTX n=89). Pt characteristics were similar between treatment arms. At M6, least squares mean (LSM) (standard error [SE]) ΔPASDAS was 0.229 (0.079) for tofacitinib monotherapy and 0.138 (0.081) for tofacitinib + MTX, and LSM (SE) ΔHAQ-DI was 0.043 (0.027) and 0.017 (0.028), respectively (Figure 1); no clinically meaningful differences were observed. Efficacy and pt-reported outcomes were generally similar between treatment arms at M6 and M12 (data not shown). Rates of pts achieving minimal disease activity, and maintaining an absence of enthesitis and dactylitis, were sustained to M12 in both treatment arms (Figure 2). Adverse event rates (Table) and laboratory parameters were comparable between treatment arms, but liver enzyme elevations were more common with tofacitinib + MTX.Conclusion:No clinically meaningful differences in efficacy and safety were observed in PsA pts who received OL tofacitinib 5 mg BID as monotherapy after MTX withdrawal vs with continued MTX. Safety was consistent with previous P3 studies. The substudy was an estimation study and not powered for hypothesis testing.Table.Safety outcomes to Month 12Pts with events, n (%) AEs of special interestTofacitinib monotherapy N=90Tofacitinib + MTXN=89AE43 (47.8)41 (46.1)Serious AE4 (4.4)3 (3.4)Discontinuations due to AE3 (3.3)4 (4.5)Death00 Herpes zoster (serious/non-serious)1 (1.1)2 (2.2) Serious infection02 (2.2) Opportunistic infectiona01 (1.1) Malignancy (excl. NMSC)a1 (1.1)1 (1.1) NMSCa00 Major adverse cardiovascular eventa00 Venous thromboembolismc00 Arterial thromboembolismc1 (1.1)0 Gastrointestinal perforationa00 Interstitial lung diseaseb00Laboratory parametersdALT ≥3×ULN05 (5.6) ALT (IU/L), mean (SE)-2.7 (1.6)2.5 (1.3)AST ≥3×ULN03 (3.4) AST (IU/L), mean (SE)-1.5 (1.2)1.7 (0.8)Reviewed by independentaexternal/binternal adjudication committeecPer Standardised MedDRA Query termsdWithout regard to baseline abnormalityALT, alanine aminotransferase; AST, aspartate aminotransferase; ULN, upper limit of normalAcknowledgments:Study sponsored by Pfizer Inc. Medical writing support was provided by Christina Viegelmann of CMC Connect and funded by Pfizer Inc.Disclosure of Interests:Peter Nash Grant/research support from: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly and Company, Gilead, Janssen, MSD, Novartis, Pfizer Inc, Roche, Sanofi, UCB, Consultant of: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly, Gilead, Janssen, MSD, Novartis, Pfizer Inc, Roche, Sanofi, UCB, Speakers bureau: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly, Gilead, Janssen, MSD, Novartis, Pfizer Inc, Roche, Sanofi, UCB, Laura C Coates: None declared, Philip J Mease Grant/research support from: Abbott, Amgen, Biogen Idec, BMS, Celgene Corporation, Eli Lilly, Novartis, Pfizer, Sun Pharmaceutical, UCB – grant/research support, Consultant of: Abbott, Amgen, Biogen Idec, BMS, Celgene Corporation, Eli Lilly, Novartis, Pfizer, Sun Pharmaceutical, UCB – consultant, Speakers bureau: Abbott, Amgen, Biogen Idec, BMS, Eli Lilly, Genentech, Janssen, Pfizer, UCB – speakers bureau, Alan Kivitz Shareholder of: AbbVie, Amgen, Gilead, GSK, Pfizer Inc, Sanofi, Consultant of: AbbVie, Boehringer Ingelheim,,Flexion, Genzyme, Gilead, Janssen, Novartis, Pfizer Inc, Regeneron, Sanofi, SUN Pharma Advanced Research, UCB, Paid instructor for: Celgene, Genzyme, Horizon, Merck, Novartis, Pfizer, Regeneron, Sanofi, Speakers bureau: AbbVie, Celgene, Flexion, Genzyme, Horizon, Merck, Novartis, Pfizer Inc, Regeneron, Sanofi, Dafna D Gladman Grant/research support from: AbbVie, Amgen Inc., BMS, Celgene Corporation, Janssen, Novartis, Pfizer, UCB – grant/research support, Consultant of: AbbVie, Amgen Inc., BMS, Celgene Corporation, Janssen, Novartis, Pfizer, UCB – consultant, Frank Behrens Grant/research support from: Pfizer, Janssen, Chugai, Celgene, Lilly and Roche, Consultant of: Pfizer, AbbVie, Sanofi, Lilly, Novartis, Genzyme, Boehringer, Janssen, MSD, Celgene, Roche and Chugai, James Cheng-Chung Wei Grant/research support from: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly, Janssen, Novartis, Pfizer Inc, UCB, Consultant of: AbbVie, Bristol-Myers Squibb, Celgene, Chugai, Eisai, Janssen, Novartis, Pfizer Inc, Sanofi-Aventis, UCB Pharma, Dona Fleishaker Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Joseph Wu Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Cunshan Wang Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Ana Belen Romero Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Lara Fallon Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Ming-Ann Hsu Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Keith Kanik Shareholder of: Pfizer Inc, Employee of: Pfizer Inc

AB0801 EFFECTS OF GUSELKUMAB, A MONOCLONAL ANTIBODY THAT SPECIFICALLY BINDS TO THE P19-SUBUNIT OF INTERLEUKIN-23, ON DACTYLITIS AND ENTHESITIS IN PATIENTS WITH ACTIVE PSORIATIC ARTHRITIS: POOLED RESULTS THROUGH WEEK 24 FROM TWO PHASE 3 STUDIES

Background:Guselkumab (GUS), a novel monoclonal antibody that specifically binds to the p19-subunit of IL-23, demonstrated efficacy in the Ph 3 DISCOVER-1 (D1) &amp; DISCOVER-2 (D2) trials of pts with active psoriatic arthritis (PsA).1,2Dactylitis &amp; enthesitis, key PsA clinical manifestations, can be difficult to treat and may portend more significant disease burden.3,4Objectives:In pts with dactylitis or enthesitis at baseline, assess: 1) changes in symptoms over time and 2) relationships between improvements in dactylitis or enthesitis and other PsA domains.Methods:Adults with active PsA despite standard therapies were eligible for D1 &amp; D2. Approx. 30% of D1 pts previously received 1-2 TNF inhibitors; D2 pts were biologic-naïve. Pts were randomized 1:1:1 to GUS 100mg Q4W; GUS 100mg at W0, W4, Q8W; or PBO. Independent assessors evaluated dactylitis (total score: 0-60) &amp; enthesitis (Leeds Enthesitis Index [LEI]; total score 0-6). Dactylitis and enthesitis findings through W24 were prespecified to be pooled across D1 &amp; D2. P-values are unadjusted. We assessed changes in dactylitis and LEI scores over time (ANCOVA); associations between dactylitis or enthesitis resolution and ACR/PASI responses at W24 (Chi-square); and correlations between dactylitis or LEI and HAQ-DI/SF-36 change scores at W24 (Spearman’s correlation). AEs through W24 were reported.1,2Results:At W0, 42% of pooled D1+D2 pts had dactylitis; 65% had enthesitis. GUS improved dactylitis and LEI scores vs PBO at W8, W16, W24. GUS vs PBO differences were significant for dactylitis changes at W16 &amp; W24 and LEI changes at W8 (Q4W only), W16 &amp; W24; no dose response was observed (Fig). Rates of dactylitis or enthesitis resolution by W24 were consistently significantly (p&lt;0.001) associated with ACR20/50/70 and PASI75/90 response (Table). In GUS-treated pts at W24, significant correlations were observed between dactylitis change scores and PASI (p&lt;0.001 Q4W; p=0.006 Q8W) and SF-36 MCS (p=0.038 Q4W; p=0.003 Q8W) changes, and between LEI and HAQ-DI change scores (p&lt;0.001 Q4W; p=0.005 Q8W). No consistent correlations/associations were observed between dactylitis or LEI scores and other clinical outcomes.Conclusion:In PsA pts with dactylitis or enthesitis at W0, GUS improved dactylitis or LEI scores vs PBO by W8; treatment differences were significant at W16 &amp; W24. Resolution of dactylitis or enthesitis was significantly associated with clinically meaningful improvements in PsA joint &amp; skin symptoms. Improved dactylitis scores correlated with improved skin symptoms and mental health; improved LEI scores correlated with improved physical function.

P261 Continuing versus withdrawing ixekizumab in patients with PsA who achieved sustained minimal disease activity: results from the SPIRIT-P3 study

Abstract Background This study evaluated efficacy and safety of continuing vs. withdrawing ixekizumab (IXE), an IL-17A antagonist, in psoriatic arthritis (PsA) patients who achieved sustained minimal disease activity (MDA) on IXE and re-treating with IXE if required. Methods SPIRIT-P3 (NCT02584855) was a multicentre phase 3b study enrolling biologic-naïve patients with active PsA (diagnosis for ≥6 months, meeting classification criteria for psoriatic arthritis, ≥3/68 tender joints, ≥3/66 swollen joints) and previous inadequate response to conventional synthetic DMARDs (csDMARDs). Patients entered a 36-week, open-label (OL) treatment period with IXE every 2 weeks. Between Weeks 36-64, patients were randomised 1:1 to IXE or placebo (PBO) at the visit for which randomisation criteria were met (sustained MDA for at least 4 visits over 3 consecutive months) and evaluated up to Week 104. Patients not meeting randomisation criteria by Week 64 continued IXE up to Week 104. Maintenance of treatment response was measured by time to loss of sustained MDA (relapse) during randomised withdrawal (RW) period. The proportion of patients who relapsed during the first 40 weeks of RW period and time to regain MDA after re-treatment with IXE in relapsed patients were assessed. The Kaplan-Meier product limit method was used to estimate survival curves for time-to variables. Treatment comparisons were performed using a log-rank test adjusting for geographic region and csDMARD use as factors. Cumulative proportion of relapse was analysed using a logistic regression model with treatment, geographic region, and csDMARD use as factors. Safety data were summarised for the entire study period for patients who received ≥1 dose of IXE. Results In total, 394 patients entered the OL treatment period; 158 (40%) achieved sustained MDA criteria and were randomised to IXE (N = 79) or PBO (N = 79). Baseline characteristics were similar between groups. Time to relapse on PBO was significantly shorter than for IXE (p &amp;lt; 0.001) during RW period, with a median time to relapse of 22.3 weeks in the PBO group. The cumulative relapse rate during the first 40 weeks of RW period was 73% for PBO vs. 34% for IXE (p &amp;lt; 0.001). Of those who relapsed on PBO, 96% regained MDA following re-treatment with IXE. The median time to regain MDA was 4.1 weeks (95%CI 4.14-4.29) for PBO and 4.7 weeks (95%CI 4.14-8.29) for IXE. Safety data were consistent with previous IXE PsA studies with no unexpected safety signals. Conclusion Continued IXE therapy was superior to PBO in maintaining MDA in biologic-naïve PsA pts who achieved sustained MDA on initial IXE treatment. A vast majority of patients who lost MDA after IXE withdrawal regained MDA with IXE re-treatment. Continuous IXE treatment is optimal for maintaining MDA; however, patients can regain MDA after re-treatment with IXE in case of treatment interruption. Disclosures L.C. Coates: Corporate appointments; L. Coates is a consultant for: AbbVie, Amgen, Boehringer Ingelheim, Celgene, Eli Lilly and Company, Janssen, MSD, Novartis, Pfizer, Prothena, Sun Pharma, and UCB. Consultancies: L. Coates is a consultant for: AbbVie, Amgen, Boehringer Ingelheim, Celgene, Eli Lilly and Company, Janssen, MSD, Novartis, Pfizer, Prothena, Sun Pharma, and UCB. S.G. Pillai: Corporate appointments; S.G.P. is an employee and shareholder of Eli Lilly and Company. L. Zhang: Corporate appointments; Employee and shareholder of Eli Lilly and Company. D. Adams: Corporate appointments; Employee and shareholder of Eli Lilly and Company. L. Kerr: Corporate appointments; Employee and shareholder of Eli Lilly and Company. M. Hojnik: Corporate appointments; Employee and shareholder of Eli Lilly and Company. G. Gallo: Corporate appointments; Employee and shareholder of Eli Lilly and Company. I. Valter: None. H. Tahir: Grants/research support; H. Tahir has received grants/research support from: AbbVie, Celgene, Eli Lilly and Company, Janssen, and Novartis. V. Chandran: Grants/research support; V. Chandran has received grant/research support from AbbVie, is a consultant for: AbbVie, Amgen, Celgene, Eli Lilly and Company, Janssen, Novartis, Pfizer, and UCB. P. Mease: Consultancies; P. J. Mease is a consultant for and has received grant/research support from: AbbVie, Amgen, BMS, Celgene, Crescendo, Eli Lilly and Company, Genentech, Janssen, Merck, Novartis, Pfizer, UCB, is on the. A. Kavanaugh: Consultancies; A. Kavanaugh is a consultant for Eli Lilly and Company.

THU0171 Which Adverse Events (AES) of Biological Therapy (BT) Led to Discontinuation of Treatment in A Cohort of 377 JIA Patients in Comparison to 1115 Patients Affected by Ra, As, PSA in the Department of Rheumatology of G. Pini Institute

ObjectivesTo report adverse events (AEs), which led to discontinuation of biologics agents, in a large cohort of patients with Juvenile Idiopathic Arthritis (JIA), Rheumatoid Arthritis (RA), Ankylosing Spondylitis (AS) and...