Background: A randomized, placebo-controlled phase 3 trial of subcutaneous abatacept and standard of care (SOC) was conducted in patients with idiopathic inflammatory myopathy (IIM; NCT02971683). 52-week results for the global population were reported (primary endpoint not met).1 Patients who enrolled at Japanese study sites were required to complete an additional 24 weeks of treatment and observation. Objectives: To evaluate the efficacy and safety of abatacept in patients enrolled at Japanese sites through the full 76 weeks of treatment. Methods: Adults with active, treatment-refractory IIM received 125 mg weekly subcutaneous abatacept+SOC or placebo+SOC in the double-blind period (weeks 0–24). In the 28-week open-label period (weeks 24–52, data not shown), patients receiving placebo were switched to abatacept+SOC. In the 24-week open-label extension (weeks 52–76), all patients randomized in Japan continued abatacept+SOC. The primary endpoint was the proportion meeting International Myositis Assessment and Clinical Studies definition of improvement (IMACS DOI). Secondary endpoints and safety/tolerability were assessed. Here we report results from the full 76-week observation period for the subset of patients at Japanese sites. Results: Of 148 patients randomized, 21 were from Japanese sites (abatacept, n=11; placebo, n=10) and 19 out of 21 completed the open-label extension. Baseline demographics and disease characteristics were similar to those of the full study population. Distribution of IIM disease subtypes was similar in both treatment groups (abatacept vs placebo: dermatomyositis 7 vs 7, polymyositis 3 vs 3, autoimmune necrotizing myopathy 1 vs 0). Proportions of abatacept vs placebo patients achieving IMACS DOI at week 24 were 72.7% vs 50%, and, at week 76, 90% vs 87.5% (Table 1), demonstrating a sustained benefit of continuing abatacept (abatacept group) and an improvement after switching to abatacept (placebo/abatacept group). Adjusted mean Myositis Response Criteria Total Improvement Scores were no different between groups at week 24; at week 76, values were 46.8 and 55.3 in the abatacept and placebo/abatacept groups, respectively (Table 1). The proportions of patients with Myositis Response Criteria moderate/major responses at week 76 were 70% and 100% in the abatacept and placebo/abatacept groups, respectively. Improvements were seen in most secondary endpoints when continuing abatacept and switching to abatacept (Table 1). The safety and tolerability of abatacept in this subset of patients from Japan were consistent with the full study population. Conclusion: Throughout the 76-week study, patients in Japan tolerated abatacept well and showed continued clinical responses with abatacept treatment, consistent with findings from the full study population. REFERENCES: [1] Aggarwal R, et al. Arthritis Rheumatol 2022;74 (suppl 9): abstract 2237. Acknowledgements: Study funded by Bristol Myers Squibb, executed by Sandra Overfield and Robin Scully. Medical writing: Joanna Wright (Caudex, a division of IPG Health Medical Communications), funded by Bristol Myers Squibb. Disclosure of Interests: Michael A. Maldonado Bristol Myers Squibb, Bristol Myers Squibb, Rohit Aggarwal Actigraph, Alexion, ANI Pharmaceuticals, Argenx, AstraZeneca, Boehringer-Ingelheim, Bristol Myers Squibb, CabalettaBio, Capella Bioscience, Corbus, CSL Behring, EMD Serono, Galapagos, Horizon Therapeutics, I-Cell, Immunovant, Janssen, Kezar, Kyverna, Merck, Novartis, Nuvig Therapeutics, Octapharma, Pfizer, Regeneron, Roivant, Sanofi, Teva, Boehringer Ingelheim (BI), Bristol Myers Squibb, EMD Serono, Janssen, Mallinckrodt, Pfizer, Q32, Takahisa Gono Asahi Kasei Pharma, Astellas, Boehringer-Ingelheim, Bristol Myers Squibb, Chugai, Eli Lily, Ono Pharmaceuticals, and Tanabe-Mitsubishi, Ingrid E. Lundberg Boehringer Ingelheim, Roche, Novartis, Pfizer, Chugai, Janssen, Serono, Yeong Wook Song: None declared, Aziz Shaibani: None declared, Victoria P Werth Janssen, Lilly, Pfizer, Biogen, BMS, Gilead, Amgen, Nektar, Incyte, EMD Sorona, CSL Behring, Crisalis, Viela Bio, Argenx, Kwoya Kirin, Regeneron, AstraZeneca, Abbvie, Octapharma, GSK, Astra-Zeneca, Cugene, UCB, Corcept, Beacon Bioscience, Rome Pharmaceuticals, Horizon, Merck, Kezar, Sanofi, Bayer, Akari, Calyx, Cabaletta Bio, Nuvig Pharmaceuticals, Pfizer, Biogen, Gilead, Corbus Pharmaceuticals, Genentech, Viela, Amgen, Regeneron, Argenx, CSL Behring, Ventus, q32 Bio, BMS, Horizon, Rome Pharmaceuticals, Priovant

OBJECTIVES:To evaluate the similarities between LBAL (adalimumab biosimilar candidate) and the adalimumab reference product (ADL) in terms of efficacy and safety, including immunogenicity, in patients with active rheumatoid arthritis despite methotrexate treatment.METHODS:This phase III, multicentre, randomised, double-blind, parallel-group, 56-week study was conducted in Japan and Korea. During the first 24 weeks, patients subcutaneously received 40 mg of LBAL or ADL every two weeks (LBAL and ADL groups). During the subsequent 28 weeks, the LBAL group patients and half of the ADL group patients received LBAL (L-L and A-L arms). The remaining ADL group patients continued to receive ADL (A-A arm). The primary efficacy endpoint was the change from baseline in disease activity score 28-erythrocyte sedimentation rate (DAS28-ESR) at Week 24. American College of Rheumatology (ACR) response rates, adverse events (AEs), and anti-drug antibody (ADA) were also assessed.RESULTS:In total, 383 patients were randomised. The least squares (LS) mean changes from baseline in DAS28-ESR at Week 24 were -2.45 and -2.53 in the LBAL (n=191) and ADL (n=190) groups, respectively. The 95% confidence interval (CI; -0.139, 0.304) of the difference (0.08) was within the pre-specified equivalence margin (-0.6, 0.6). Up to Week 52, the decreases in DAS28-ESR were maintained in all three arms. No notable differences in ACR20/50/70 were observed. The AE and ADA incidences were comparable between the arms.CONCLUSIONS:LBAL was equivalent in efficacy and comparable in safety, including immunogenicity, to ADL. Switching from ADL to LBAL did not impact on efficacy and safety.

Background: Vasculopathies are a heterogeneous group of morphologically and pathogenetically distinct vascular diseases. They include both non-inflammatory and inflammatory vasculopathies. Patients with connective tissue disease (CTD), including systemic sclerosis (SSc), dermatomyositis (DM), and polymyositis (PM), can develop a non-thrombotic proliferative vasculopathy (NTPV), a distinctive disease entity characterized by vascular wall proliferation without overt evidence of vascular inflammation and intraluminal thrombosis. Objectives: This study aimed to analyze the angiographic features of NTPV in patients with CTD, including SSc, DM, and PM in comparison to polyarteritis nodosa (PAN). Methods: Angiograms of 47 extremities (24 upper and 23 lower extremities) of 11 patients with CTD (6 SSc, 4 DM, and 1 PM), and 12 patients with PAN who presented with critical digital ischemia between January 2001 and May 2020 were analyzed. The degree and pattern of stenosis, occlusion, aneurysms, and neovascularization in proximal arteries (defined as arteries above the wrist and ankle) and distal arteries (defined as those at or below the wrist and ankle) were compared between CTD-vasculopathy and PAN. Results: Diffuse narrowing was significantly more frequent (66.1% vs. 38.0%; p=0.001), whereas multifocal stenosis was significantly less frequent (6.5% vs. 26.8%, p=0.002) in the CTD group than in the PAN group. All patients with CTD and 72.0% with PAN had diffuse narrowing in the distal arteries (p =0.010). Tapered occlusion was more frequent than abrupt occlusion in patients with CTD (43.5% vs. 11.3%). Abrupt occlusion (11.3% vs. 29.6%, p=0.010) and aneurysm formation (1.6% vs. 11.3%; p=0.037) were significantly less frequent in the CTD than in the PAN group. After 1 year, three patients (27.3%) in the CTD group and seven (58.3%) in the PAN group showed improvements in digital ischemia. Moreover, four patients (36.4%) in the CTD group and two (16.7%) in the PAN group underwent auto- or surgical amputation. Conclusion: Patients with CTD-vasculopathy exhibit more frequently diffuse smooth narrowing, tapered occlusion and delayed distal blood flow on conventional angiograms and worse outcomes than with PAN patients. Larger studies are needed to confirm the current findings. References: [1]Kahaleh MB. Vascular involvement in systemic sclerosis (SSc). Clin Exp Rheumatol. 2004;22(3 Suppl 33):S19-23. [2]Lee JS, Kim H, Lee EB, Song YW, Park JK. Nonthrombotic proliferative vasculopathy associated with antiphospholipid antibodies: A case report and literature review. Mod Rheumatol. 2019;29(2):388-92. Figure 1. Angiographic features of CTD-vasculopathy and PAN. Arteries in the (A) upper extremities and (B) lower extremities of patients with CTD-vasculopathy and PAN. Diffuse narrowing is indicated by white arrowheads; tapered occlusion by white arrows; multifocal stenosis by black arrowheads; abrupt occlusion by black arrows; aneurysmal changes by empty arrows; grade 2 tortuosity by white stars; and grade 3 tortuosity by black stars. CTD, connective tissue disease; PAN, polyarteritis nodosa. Table 1. Comparison of angiographic parameters between CTD-vasculopathy and PAN. CTD (upper 14, lower 8 ) PAN (upper 10, lower 15 ) p -value Total number of images 62 71 Shoulder/elbow/wrist and hand 11/14/14 8/10/10 Femoral/knee/ankle and foot 7/8/8 13/15/15 Stenosis Diffuse narrowing 41/62 (66.1%) 27/71 (38.0%) 0.001 Focal stenosis 13/62 (21.0%) 10/71 (14.1%) 0.295 Multifocal stenosis 4/62 (6.5%) 19/71 (26.8%) 0.002 Occlusion Tapered occlusion 27/62 (43.5%) 23/71 (32.4%) 0.185 Abrupt occlusion 7/62 (11.3%) 21/71 (29.6%) 0.010 Aneurysm 1/62 (1.6%) 8/71 (11.3%) 0.037 Neovascularization in muscular branch Tortuosity Grade 1 45/62 (72.6%) 30/68 (39.1%) 0.002 Grade 2 11/62 (17.7%) 14/68 (23.9%) Grade 3 6/62 (9.7%) 24/68 (37.0%) Tortuosity grade 1, normal; grade 2, mild to moderate; grade 3, severe (hypertortuosity). CTD, connective tissue disease; PAN, polyarteritis nodosa. Disclosure of Interests: Jina Yeo: None declared, Eun-Ah Park: None declared, Eun Bong Lee Consultant of: Pfizer, Grant/research support from: GC Pharma and Handok Inc., Yeong Wook Song: None declared, Jin Kyun Park: None declared

Background:CT-P13, an infliximab biosimilar, is effective for treating ankylosing spondylitis (AS) at a dose of 5 mg/kg infused once every 6–8 weeks. Evidence suggests that patients with AS may benefit from a lower dose, and individualised dose/interval adjustments should be based on treatment response.Objectives:To analyse real-world treatment patterns (doses and infusion intervals) and outcomes for CT-P13-treated patients with AS over 5 years.Methods:The RAAS study collected medical record data for adults with AS treated with CT-P13 at five referral hospitals in the Republic of Korea (2012–2017). Patients were infliximab naïve at CT-P13 initiation (‘naïve’) or had switched to CT-P13 from reference infliximab (‘switched’). Patients were analysed by baseline dose (BD) (<4 mg/kg; ≥4–<5 mg/kg; ≥5 mg/kg), defined as the third (naïve) or first (switched) infusion dose. Baseline infusion intervals were the average of the three infusion intervals after BD. Over time, patients with both constant dose and infusion interval were compared with those with changes in dose and/or infusion interval. Data were analysed by Kruskal–Wallis test, chi-squared test and one-way analysis of variance, and drug survival by log-rank test.Results:Overall, 337 patients (219 naïve; 118 switched) were identified. Of those with BD data, 71, 117 and 82 patients had BDs of <4 mg/kg, ≥4–<5 mg/kg and ≥5 mg/kg, respectively. Most patients were male (74.8%). Patients with higher BDs tended to have higher Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) scores; switched patients had lower scores than naïve patients. Of 186 evaluable patients (118 naïve; 68 switched), 85 (46 naïve; 39 switched) did not have dose and/or interval changes (‘combined constant’ group). More naïve (n=72; 61.0%) versus switched (n=29; 42.6%) patients had dose and/or interval changes (‘combined changed’ group). Considering dose and interval separately, 18/235 evaluable patients (152 naïve; 83 switched) had dose changes (12 increased; 6 decreased) and 110/224 evaluable patients (140 naïve; 84 switched) had interval changes (79 increased; 31 decreased). Cumulative annual doses were similar between naïve and switched patients; switched patients had longer infusion intervals than naïve patients (Figure 1). There were no significant differences in drug survival between BD groups overall or for naïve and switched patients. BASDAI scores over time showed that disease activity was well controlled (Table 1). Patients in the combined changed versus combined constant group had greater improvements in BASDAI score.Table 1.BASDAI scoresGroupStatisticW0W54W102W156W210Combined constantTotal (N=85)n7273574231Mean (SD)5.50 (3.12)2.50 (1.71)2.35 (1.66)2.42 (1.66)2.36 (1.68)Median6.322.602.402.552.60Naïve (n=46)n3939261812Mean (SD)7.86 (1.45)2.49 (1.82)2.41 (1.75)2.34 (1.70)1.94 (1.58)Median7.802.201.751.901.44Switched (n=39)n3334312419Mean (SD)2.71 (2.07)2.50 (1.60)2.31 (1.60)2.48 (1.67)2.63 (1.73)Median2.582.752.502.802.70Combined changedTotal (N=101)n8785765335Mean (SD)5.68 (2.89)1.81 (1.45)1.58 (1.27)1.49 (1.34)1.40 (1.24)Median6.701.321.191.201.00Naïve (n=72)n6360543418Mean (SD)7.18 (1.37)2.01 (1.44)1.65 (1.22)1.54 (1.26)1.52 (0.97)Median7.301.831.351.311.35Switched (n=29)n2425221917Mean (SD)1.74 (1.94)1.33 (1.36)1.42 (1.41)1.39 (1.50)1.28 (1.50)Median0.920.800.850.700.58SD, standard deviation; W, WeekConclusion:These real-world data demonstrate that adjusting dose and infusion interval can improve clinical outcomes for CT-P13-treated patients with AS. Drug survival and BASDAI results show that patients with lower baseline BASDAI receiving low CT-P13 doses can achieve the same outcomes as those dosed with ≥5 mg/kg. Findings support the lack of impact of switching from reference infliximab to CT-P13 on efficacy, underlining conclusions previously drawn for efficacy and safety.1References:[1]Kim T-H, et al. Clin Drug Investig 2020;40:541–53.Acknowledgements:Funding: This study was supported by Celltrion Healthcare Co., Ltd. (Incheon, Republic of Korea). Medical writing support was provided by Beatrice Tyrrell, DPhil (Aspire Scientific, Bollington, UK), and funded by Celltrion Healthcare Co., Ltd. (Incheon, Republic of Korea).Disclosure of Interests:Shin-Seok Lee: None declared, Tae-Hwan Kim: None declared, Won Park Consultant of: Celltrion, Inc., Yeong Wook Song: None declared, Chang-Hee Suh Speakers bureau: AbbVie Inc., Astellas Pharma Inc., Samsung Bioepis Co., Ltd, Consultant of: Celltrion Healthcare Co., Ltd., Eli Lilly and Company, GlaxoSmithKline plc, Janssen Pharmaceuticals, Yungjin Pharmaceutical, Co., Ltd, SooKyoung Kim Shareholder of: Celltrion Healthcare Co., Ltd., Employee of: Celltrion Healthcare Co., Ltd., DaeHyun Yoo Speakers bureau: Celltrion, Consultant of: Celltrion, Grant/research support from: Celltrion

Background: Semaphorin 4D (SEMA4D) / CD100, known as a subfamily of axonal guidance proteins, has also been reported to act as an immunoregulator in several infectious and inflammatory diseases [1]. Sjögren’s syndrome (SS) is a systemic autoimmune disease that primarily affects the exocrine glands by infiltrated lymphocytes resulting in dryness of mouth and eyes. IL-17 was reported to impair the integrity of tight junction barrier and attenuate the expression of aquaporin 5 (AQP5), causing salivary gland dysfunction in SS [2]. Objectives: This study was aimed to evaluate the role of SEMA4D in patients with SS and investigate the effect of SEMA4D on human salivary gland epithelial cell (SGEC) and T cell. Methods: Soluble SEMA4D levels in plasma were measured by enzyme-linked immunosorbent assay (ELISA) from patients with SS, non-SS sicca and healthy controls. Immortalized human SGECs, originated from acini (NS-SV-AC) and duct (NS-SV-DC), were used to evaluate the effects of SEMA4D. CD4 + T cells from human peripheral blood were isolated to determine the secretion of cytokines in response to SEMA4D. IFN-γ and IL-17 were used to determine the effects on AQP5 expression of SGEC. Results: The levels of soluble SEMA4D in plasma were increased in patients with SS (median [interquartile range]: 1221.3 [393.5] pg/mL) compared to non-SS sicca (940.2 [355.1] pg/mL, p = 0.006) or healthy controls (909.5 [108.0] pg/mL, p < 0.0001). The levels of soluble SEMA4D in plasma were correlated with the levels of several autoantibodies including anti-SSA (Spearman’s rho = 0.358, p = 0.006), anti-SSB (rho = 0.350, p = 0.007), and anti-muscarinic receptor 3 (M3R) Ab (rho = 0.495, p < 0.001), and also correlated with total IgG (rho = 0.431, p = 0.002). SEMA4D-stimulated SGECs showed decreased expression of tight junctions such as occludin and Zo-1. CD4 + T cells secreted IFN-γ ( p = 0.025), IL-17 ( p = 0.028), and IL-21 ( p = 0.007) with SEMA4D stimulation. IFN-γ and IL-17 decreased AQP5 expression in SGECs. Conclusion: SEMA4D contributed to decreased expression of tight junction in SGECs. SEMA4D induced production of IFN-γ and IL-17 in CD4 + T cells and these cytokine decreased AQP5 expression in SGECs. References: [1]Worzfeld T, Offermanns S. Nat Rev Drug Discov. 2014;13(8):603-21. [2]Bhattarai KR, Junjappa R, Handigund M, Kim HR, Chae HJ. Autoimmun Rev. 2018;17(4):376-90. Disclosure of Interests: None declared

Background: Polymyositis (PM) is a chronic inflammatory myopathy that impairs muscle functions. While the treatment with glucocorticoids (GC) has been the cornerstone of the treatment for PM to suppress immune-mediated muscle injury, some patients suffer from glucocorticoid-induced myopathy during the treatment, which further deteriorates the muscle weakness. It has been reported that significant disability and muscle weakness persist in a quarter of the patients even after successful treatment with the immunosuppressive therapy 1 . Ultimately, new therapeutic strategies to preserve and recover muscle strength as well as to suppress immune-mediated muscle injury are needed. Glucagon-like peptide-1 (GLP-1) is a peptide hormone with a variety of functions. Although GLP-1 receptor (GLP-1R) agonists have been developed as an anti-diabetic therapy to promote insulin secretion, emerging data suggest that they have pleiotropic actions including anti-inflammatory effects and suppression of muscle wasting 2 . We presumed that GLP-1R agonists have beneficial effect on PM to preserve and recover muscle strength. Objectives: To examine the effect of a GLP-1R agonist on C protein-induced myositis (CIM), a murine model of polymyositis 3 , in monotherapy or in combination with prednisolone (PSL). Methods: Muscle specimens of PM patients and CIM were examined with immunohistological staining for the expression of GLP-1R. The therapeutic effect of PF1801 (ImmunoForge), a GLP-1R agonist (5 mg/kg body weight (BW)/day), in monotherapy or in combination with PSL (20 mg/kg BW/day) on CIM was examined for grip strength, muscle weight and histological muscle inflammation. Results: GLP-1R was expressed on the plasma membrane of muscle cells of PM patients and CIM. The expression levels were high in the area where inflammatory infiltrates were observed. The treatment of CIM with PF1801 in monotherapy or in combination with PSL suppressed the CIM-induced decrease in grip strength on day 14. The combination therapy with PF1801 and PSL ameliorated the CIM-induced muscle weight loss in quadriceps, while the monotherapy with PF1801 or PSL did not. The histological analysis of muscle specimens on day 14 of CIM revealed that the muscle inflammation was suppressed by the treatments with PF1801, PSL, or the combination of PF1801 and PSL. None of the mice in the combination therapy group developed histologically evident myositis, while the myositis was observed in 90%, 40% and 40 % of the mice in vehicle treated group, PF1801 treated group, and PSL treated group, respectively. The necrotic area of the muscle in CIM was also reduced in the mice treated with PF1801, PSL, or the combination of PSL and PF1801. The CIM-induced increase in spleen weight was suppressed by PF1801, PSL, or the combination of PSL and PF1801. The additive effect of PSL and PF1801 on the suppression of CIM-induced increase in spleen weight was observed. Conclusion: PF1801 ameliorated CIM-induced muscle weakness and muscle inflammation in CIM. The combination therapy with PF1801 and PSL ameliorated CIM-induced muscle weight loss. PF1801 could be a novel therapy to recover muscle weakness and to suppress muscle inflammation in PM. References: [1]Bronner IM, et al. Ann Rheum Dis. 2006;65:1456–61. [2]Hong Y, et al. J Cachexia Sarcopenia Muscle . 2019;10:903-18. [3]Sugihara T, et al. Arthritis Rheum . 2007;56:1304-14. Disclosure of Interests: Mari Kamiya: None declared, Seon Uk Kim: None declared, Jeong Yeon Kim: None declared, Yeong Wook Song: None declared, Eun Young Lee: None declared, Fumitaka Mizoguchi Grant/research support from: ImmunoForge, Consultant of: ImmunoForge

Background: Frailty is defined as syndrome of physical decline in late life, characterized by marked vulnerability to adverse health outcomes. Knee osteoarthritis (OA) could be one of the major diseases related to frailty conditions. The prevalence and clinical features of frailty syndrome in knee OA and rheumatoid arthritis (RA) were not reported previously. Objectives: We studied the clinical features and nutritional status of knee OA and RA patients with frailty syndrome in nationwide survey data. Methods: Symptomatic knee osteoarthritis patients were defined who had knee joint pain accompanied with grade 2 or more Kellgren-Lawrence score in plain radiographic studies from the data of KNHANES (N=17,873, from 2010 to 2013). RA was defined who diagnosed by physician. We calculated the frailty index (score 0~1.0) using 46 items from the frailty related co-morbidities and laboratory abnormalities according to Rockwood clinical frailty scale. We analyzed the clinical features of three frailty groups [robust (≤0.10), pre-frail (0.1< * ≤0.21), and frail (>0.21)] in symptomatic radiographic knee OA patients and RA patients. Results: The prevalence of Knee OA patients was 8.59% [95% CI: 8.19-9.01]. Relative risk ratio is significantly increased in pre-frail (OA; 2.66 [2.26-3.14], RA;4.02 [3.07-5.27]) and frail group (OA; 6.27 [5.20-7.57], RA;7.00[5.03-9.74]) in polytomous logistic regression. Body mass index (BMI), white blood cell, platelet, and serum creatinine were significantly increased in knee OA and RA patients with frailty syndrome. But, hemoglobin, estimated GFR (CKD-EPI equation) and EQ-5D were significantly decreased in knee OA and RA patients with frailty syndrome (Table). The daily nutritional intakes of total calories, carbohydrate, protein, fat, sodium and potassium were significantly decreased in knee OA patients with the frailty syndrome. In RA patients, the significant decreased nutritional intakes of total calories, carbohydrate, protein and fat were observed. Conclusion: We showed increased BMI, decreased renal function and lower nutritional status in symptomatic radiographic knee OA and RA patients with frailty syndrome. Table. Robust Pre-frail Frail p Body mass index (kg/m 2 ) Knee OA 24.13 [23.74-24.53] 25.07 [24.83-25.32] 25.46 [25.14-25.78] < 0.0001 RA 23.73[23.04-24.42] 23.58 [23.20-23.97] 24.97 [24.28-25.66] 0.001 Hemoglobin, g/dL Knee OA 13.53 [13.36-13.70] 13.51 [13.42-13.61] 13.27 [13.14-13.40] 0.004 RA 13.63 [13.34-13.92 13.30 [13.14-13.46] 13.15 [12.85-13.45] 0.060 White blood cell, 10 3 /μL Knee OA 5.50 [5.29-5.71] 5.94 [5.81-6.07] 6.41 [6.24-6.58] < 0.0001 RA 5.47 [5.13-5.82] 5.85 [5.64-6.06] 6.68 [6.32-7.03] < 0.0001 Platelet, 10 3 /μL Knee OA 246.03 [238.52-253.53] 258.13 [253.44-262.82] 259.96 [253.40-266.53] 0.045 RA 237.49 [222.91-252.06] 255.30 [247.50-263.10] 262.04 [248.32-275.77] 0.038 Serum creatinine, mg/dL Knee OA 0.734 [0.712-0.756] 0.764 [0.751-0.777] 0.861 [0.826-0.895] < 0.0001 RA 0.732 [0.686-0.779] 0.783 [0.762-0.805] 0.917 [0.840-0.994] < 0.0001 CKD-EPI eGFR, ml/min Knee OA 88.54 [86.77-90.31] 83.89 [82.89-84.88] 76.22 [74.80-77.63] < 0.0001 RA 94.30 [90.77-97.82] 85.86 [84.00-87.73] 74.76 [70.91-78.61] < 0.0001 EQ-5D Knee OA 0.933 [0.921-0.944] 0.804 [0.793-0.815] 0.635 [0.616-0.653] < 0.0001 RA 0.966 [0.953-0.979] 0.857 [0.839-0.874] 0.666 [0.619 -0.713] < 0.0001 Acknowledgments: None Disclosure of Interests: None declared

Objective To evaluate the performance of the 2019 European League against Rheumatism/American College of Rheumatology (EULAR/ACR) classification criteria for systemic lupus erythematosus (SLE) in Asian patients. Methods We conducted an electronic medical chart review of patients with SLE and defined rheumatic diseases. Classification criteria of the 1997 ACR, 2012 Systemic Lupus International Collaborating Clinics (SLICC), and 2019 EULAR/ACR were examined based on sensitivity, specificity, positive predictive value, negative predicted value, and accuracy using clinical diagnosis as the gold standard. Results A total of 335 SLE patients and 337 non-SLE patients were analysed. Non-SLE patients included rheumatoid arthritis (RA) (n=92), anti-phospholipid syndrome (APS) (n=57), mixed connective tissue disease (n=52), systemic sclerosis (n=43), primary Sjogren's syndrome (SS) (n=39), undifferentiated connective tissue disease (n=28), RA with secondary SS (n=24), dermatomyositis (n= 1), and spondyloarthropathy (n=1). The sensitivity was 97.6% (95% confidence interval (CI): 0.954-0.989) for the 2019 EULAR/ACR criteria, 98.5% (95% CI: 0.966-0.995) for the 2012 SLICC criteria and 95.5% (95% CI: 0.927-0.975) for the 1997 ACR criteria. The specificity was 91.4% (95% CI: 0.879-0.942) for the 2019 EULAR/ACR criteria, 92.6% (95% CI: 0.892-0.951) for the 2012 SLICC criteria 93.8% (95% CI: 0.906-0.961) for the 1997 ACR criteria. Conclusion The 2019 EULAR/ACR criteria for SLE had comparable performance to the 2012 SLICC criteria regarding diagnostic sensitivity and specificity in Korean population of SLE and other rheumatic diseases. However, the new criteria could not reach higher specificity than the 2012 SLICC criteria.

Background: Rheumatoid arthritis (RA) is a chronic inflammatory disease associated with excess mortality. Objectives: To compare all-cause and cause-specific mortality between RA patients versus general population, using a nationally representative cohort from Korea National Health Insurance Service database (KNHIS). Methods: Patients with RA aged ≥ 40 years were identified from 2010-2016 KNHIS database and their annual cohorts were constructed per each calendar year. RA patients of each cohort were required to have prevalent RA on January 1 st of the given calendar year. The KNHIS were linked with Korea national mortality data to obtain cause of death information and to estimate expected deaths of RA patients in reference to mortality data of the general population in Korea. Standardized mortality ratio (SMR) with a 95% confidence interval (CI) was calculated to compare mortality of RA patients and general population. Results: A total of 6,404 deaths occurred among 79,440 RA patients during 2011-2016 period, showing all-cause SMR (95% CI) of 1.45 (1.42-1.49) compared to general population. The SMR was 1.72 (1.59-1.85) for biologics users and 1.43 (1.39-1.46) for non-users, versus general population. The annual SMR of RA patients showed a growing trend of mortality over time particularly among biologics users (Table 1). The SMRs for common causes of death among RA patients showed approximately tripled risk of dying due to pulmonary and infectious causes compared to general population (Table 2). There was approximately 20% increased risk of cardiovascular deaths but 8% decreased risk of cancer-related deaths among RA patients compared to general population (Table 2). Table 1. Annual all-cause SMR of RA patients compared to 2010 general population Calendar year 1 RA patients Biologics users Biologics non-users 2011 1.00 (0.92−1.07) 1.13 (0.87−1.39) 0.98 (0.90−1.06) 2012 1.13 (1.06−1.21) 0.98 (0.75−1.22) 1.15 (1.07−1.23) 2013 1.22 (1.14−1.30) 1.29 (1.04−1.54) 1.21 (1.13−1.29) 2014 1.30 (1.23−1.38) 1.53 (1.26−1.79) 1.28 (1.20−1.36) 2015 1.45 (1.38−1.53) 1.81 (1.53−2.09) 1.41 (1.33−1.50) 2016 1.45 (1.37−1.52) 1.94 (1.66−2.22) 1.39 (1.31−1.47) CI, confidence interval; RA, rheumatoid arthritis; SMR, standardized mortality ratio 1 2010 data were used to identify RA diagnosis dates but were not included for SMR estimation since diagnosis dates of RA were unclear for those who had RA in 2010. Table 2. Cause-specific SMR comparing RA patients versus general population Cause of death RA patients Biologics users Biologics non-users Infection 3.12 (2.93−3.13) 4.12 (3.36−4.88) 3.03 (2.83−3.23) Cancer 0.92 (0.87−0.97) 0.98 (0.81−1.14) 0.91 (0.85−0.96) Respiratory 1 3.14 (2.97−3.32) 4.64 (3.89−5.38) 3.01 (2.83−3.19) Cardiovascular 2 1.18 (1.12−1.25) 1.26 (1.03−1.50) 1.18 (1.11−1.25) CI, confidence interval; RA, rheumatoid arthritis; SMR, standardized mortality ratio 1 Includes pulmonary infections and chronic lung diseases (J00-J98, U04); 2 Includes atherosclerotic and non-atherosclerotic deaths (I00-I99). Conclusion: The all-cause mortality of RA patients during 2011-2016 was overall 45% greater than that of general Korean population, which increased annually over the study period. The increased mortality was more prominent among biologics users than non-users. The risk of infectious and respiratory deaths were tripled among RA patients compared to general population. References: [1]Sokka T, et al. Mortality in rheumatoid arthritis: 2008 update. Clin Exp Rheumatol. 2008;26(5 Suppl 51):S35-61. Acknowledgments: None Disclosure of Interests: None declared

Background: Based on the benefit of chemoprophylaxis among patients receiving biologics [1], Health Insurance Review and Assessment (HIRA) service of Korea requires patients to undergo latent tuberculosis (LT) screening before initiation of any biologics and to receive chemoprophylaxis for positive LT. Objectives: To assess the effect of chemoprophylaxis on tuberculosis infection (TI) risk among patients with rheumatoid arthritis (RA) receiving biologics in Korea Methods: Using 2002-2016 Korea National Health Insurance database, we conducted a cohort study on RA patients initiating biologic drugs (TNF inhibitors, abatacept, tocilizumab) to compare TI risk between those who started isoniazid and/or rifampin within 1 year before biologics initiation (prophylaxis group) versus those who did not (non-prophylaxis group). TI was defined by ICD10 codes plus anti-tuberculosis medications as previously described [2]. Patients were followed-up from biologics initiation to censoring events (TI occurrence, death, biologics discontinuation, initiation of anti-tuberculosis drug due to non-TI cause, and end of database). To control >50 baseline confounders, we used propensity score (PS)-based fine stratification and weighting. A weighted Cox proportional hazards model estimated hazard ratios (HRs) and 95% confidence intervals (CIs). Results: Before PS stratification (PSS) and weighting, we identified 2,250 and 7,259 RA patients for prophylaxis and non-prophylaxis group, respectively. Mean age was 57.6 years and 81.3% female. Three-fourths of patients in the prophylaxis group completed >70% of recommended treatment periods [3]. The incidence rate of TI per 100 person-years was 0.33 for prophylaxis group versus 0.57 for non-prophylaxis group. 28% of all TI cases (n=34) were extra-pulmonary with gastrointestinal (n=11) and miliary TI (n=9) being most common. The PSS-weighted HR (95% CI) of TI comparing prophylaxis versus non-prophylaxis group was 0.52 (0.32-0.86) (Table 1, Figure 1). Sensitivity analyses showed that the chemoprophylaxis was particularly effective for those with younger age (<65 years), male gender, or high comorbidity (≥ median value) (Table 1). Table 1. Comparative risk of tuberculosis infection between prophylaxis versus non-prophylaxis group Crude PSS-weighted N Events PY IR per 100 person-years HR (95% CI ) Primary as-treated analysis 1 Total P 2,250 18 5,532 0.33 0.52 (0.32-0.86) NP 7,259 100 17,503 0.64 ITT analyses 1 1 year ITT P 2,250 10 2,115 0.47 0.33 (0.17-0.64) NP 7,259 97 6,833 1.42 2 year ITT P 2,250 21 3,907 0.54 0.49 (0.31-0.78) NP 7,259 140 12,698 1.10 4 year ITT P 2,250 31 6,305 0.49 0.56 (0.38-0.82) NP 7,259 181 21,278 0.88 Sensitivity Analyses Age <65 years P 1,751 9 4,588 0.20 0.39 (0.19-0.78) NP 5,345 72 13,634 0.52 Male P 546 2 1,319 0.15 0.12 (0.03-0.50) NP 1,235 28 2,624 1.33 Comorbidity score ≥3 P 824 6 1,908 0.31 0.34 (0.15-0.79) NP 2,668 52 6,129 0.94 1 As-treated analysis censored patients when they discontinued biologics use, while ITT analysis did not. IR=incidence rate; ITT=intention-to-treat; HR=hazard ratio; PSS=propensity-score stratification; CI=confidence interval; PY=person-years; P=prophylaxis group; NP=non-prophylaxis group Conclusion: We found 48% risk reduction of TI by chemo-prophylaxis among RA patients receiving biologics. Due to HIRA requirements, a majority of non-prophylaxis group were considered negative for LT by screening at biologics initiation [4]. These findings indicate that the risk of TI during bDMARD treatment is still high among RA patients who were negative for LT at baseline but did not undergo chemoprophylaxis, which is double the risk among RA patients who had LT and underwent chemoprophylaxis. References: [1]Carmona L et al. Arthritis Rheum. 2005;52:1766-72. [2]Lee J et al. Ann Am Thorac Soc. 2017;14:690-697. [3]https://www.cdc.gov/tb/topic/treatment/ltbi.htm [4]Kim ES et al. World J Gastroenterol. 2015;21:3308-16. Disclosure of Interests: None declared

Objective Tofacitinib is an oral Janus kinase inhibitor for the treatment of rheumatoid arthritis (RA). Here we present data from the completed Phase 3 randomised controlled trial (RCT) ORAL Scan (NCT00847613), which evaluated the impact of tofacitinib on patient-reported outcomes (PROs) through 24 months in patients with active RA and inadequate responses to methotrexate (MTX-IR). Methods Patients were randomised 4:4:1:1 to receive tofacitinib 5 or 10 mg twice daily (BID), or placebo advanced to tofacitinib 5 or 10 mg, plus background MTX. Patients receiving placebo advanced to tofacitinib at month 3 (non-responders) or month 6 (remaining patients). Mean changes from baseline in PROs, assessed at months 1-24, included Health Assessment Questionnaire-Disability Index, Patient Global Assessment of disease activity (visual analogue scale [VAS]), Patient Assessment of Arthritis Pain (VAS), health-related quality of life (Short Form-36 version 2), Functional Assessment of Chronic Illness Therapy-Fatigue and Medical Outcomes Study-Sleep. Results Overall, 539/797 ( 67.6%) patients completed 24 months' treatment. At month 3, tofacitinib-treated patients reported significant (p<0.05) mean changes from baseline versus placebo across all PROs, and significantly more patients reported improvements = minimum clinically important differences versus placebo. Improvements in PROs with tofacitinib were sustained to month 24. Following advancement to tofacitinib, placebo-treated patients generally reported changes of similar magnitude to tofacitinib-treated patients. Conclusion Patients with RA and MTX-IR receiving tofacitinib 5 or 10 mg BID plus MTX reported significant and clinically meaningful improvements in PROs versus placebo at month 3, which were sustained through 24 months.

Background: Biological disease-modifying anti-rheumatic drugs (bDMARDs) have significantly improved clinical prospects for patients with rheumatoid arthritis (RA). Objectives: To identify predictors of bDMARDs initiation in RA patients. Methods: Using 2002-2016 Korea National Health Insurance Service database, we conducted a nested case-control study on RA patients. Four conventional DMARD (cDMARD) users were selected by risk set sampling per each bDMARD user, matched on the calendar year/month of RA diagnosis. Potential predictors were separately assessed for two periods, 1 year after RA diagnosis and 1 year prior to bDMARD initiation, by logistic regression analyses estimating odds ratio (OR) and 95% confidence interval (CI). Results: The study included 27,940 cDMARD users and 6,985 bDMARD users. Younger age, initial use of a less potent cDMARD (sulfasalazine), corticosteroid use, and higher maximal methotrexate (MTX) dose during 1 year post-diagnosis were positive predictors for later bDMARD initiation, while male gender, initial use of a potent cDMARD (MTX, leflunomide, or tacrolimus), initial MTX dose of ≥10mg/wk, and initial cDMARD combination were negative predictors (Table 1). Use of non-MTX DMARDs (leflunomide, sulfasalazine, or tacrolimus), higher # of cDMARD used, subcutaneous administration of MTX, corticosteroid therapy, and higher maximal MTX dose were positive predictors of subsequent bDMARD. Although higher comorbidity score during 1 year before bDMARD initiation was a positive predictor, the effect was heterogenous by involved systems (Table 2). Table 1. Predictors of bDMARD initiation among RA patients during 1-year post-diagnosis Predictors OR (95% CI) P-value Age (/1 year) 0.977 (0.974-0.980) <0.001 Sex (male vs. female) 0.850 (0.787-0.918) <0.001 1st cDMARD at RA diagnosis (yes vs. no) Methotrexate 0.540 (0.476-0.614) <0.001 Leflunomide 0.463 (0.388-0.552) <0.001 Sulfasalazine 1.305 (1.197-1.424) <0.001 Tacrolimus 0.181 (0.083-0.395) <0.001 Initial MTX dose (≥10mg/week vs. <10mg/week) 0.539 (0.506-0.575) <0.001 Initial cDMARD combination (yes vs. no) 0.621 (0.530-0.727) <0.001 Subcutaneous MTX use (yes vs. no) 1.456 (1.156-1.834) 0.001 Maximal MTX dose (/1mg) 1.012 (1.008-1.016) <0.001 Corticosteroids use (yes vs. no) 2.805 (2.345-3.355) <0.001 Table 2. Predictors of bDMARD initiation among RA patients during 1-year prior to bDMARD initiation Predictors OR (95% CI) P-value Age (/1 year) 0.970 (0.967-0.974) <0.001 Non-MTX cDMARD use (yes vs. no) 1 Leflunomide 1.765 (1.573-1.980) <0.001 Sulfasalazine 1.465 (1.297-1.654) <0.001 Tacrolimus 2.070 (1.796-2.387) <0.001 Subcutaneous MTX use (yes vs. no) 1.731 (1.577-1.900) <0.001 Maximal MTX dose (/1mg) 2.568 (1.921-3.433) <0.001 Glucocorticoid use (yes vs. no) 1.015 (1.010-1.021) <0.001 Comorbidity index (/1 point) 1.124 (1.076-1.175) <0.001 Individual comorbidities (yes vs. no) Stroke/ transient ischemic attack 0.764 (0.626-0.932) 0.008 Atrial fibrillation 0.666 (0.455-0.973) 0.036 Diabetes mellitus 1.208 (1.076-1.356) 0.001 Joint replacement therapy 1.788 (1.341-2.384) <0.001 Hepatitis B infection 1.559 (1.238-1.964) <0.001 Hepatitis C infection 2.117 (1.532-2.925) <0.001 Chronic obstructive pulmonary disease 1.118 (1.012-1.234) 0.028 1 MTX was excluded since all bDMARD initiators were required to use MTX before bDMARD initiation. Conclusion: In this population-based nationwide study, we identified period-specific predictors of bDMARD initiation among RA patients in Korea. Overall, initial aggressive RA treatment after RA diagnosis were associated with less use of later bDMARD, while highly intensive therapy observed just before bDMARD initiation reflects refractory nature of RA during this period. Disclosure of Interests: None declared

Background: Due to the shared mechanism of nontraumatic avascular necrosis (AVN) and endothelial dysfunction, the associations of AVN with increased cardiovascular and cerebrovascular events have been suggested in the several population-based studies. Objectives: This study aimed to estimate the prevalence and incidence of nontraumatic AVN in South Korea from the Korean National Health Insurance Service Sample Cohort Database 2.0 (2006-2015) and to evaluate the risk of major cardiovascular and cerebrovascular events among patients with nontraumatic AVN. Methods: We defined an incident case as a newly diagnosed and registered patient in the registry in that year, with a 2-year washout period. Prevalent cases were defined as all patients with nontraumatic AVN in the corresponding year. To evaluate the cardiovascular and cerebrovascular risks in patients with AVN, we set AVN group composed of patients with an initial diagnosis of non-traumatic AVN between 2008 and 2010 (n=1,150). The comparison group was composed of randomly selected subject (5 per patient with AVN; n = 5,750) who were matched to the AVN group according to age, sex, resident area, and year of AVN diagnosis. The development of major cardiovascular and cerebrovascular events was tracked in each sampled patient until 2015. Cox proportional hazard regressions were used to calculate the overall risks for the development of major cardiovascular and cerebrovascular events. Results: From 2008 to 2015, the prevalence of nontraumatic AVN increased gradually, but its incidence did not change, with an annual average incidence of 413 per 1 million population and the male-to-female ratio of 1.2:1. The peak incidence occurred in the 50-59 year age group. The incident AVN was more prevalent in male than in female under 70, but there was female predominance after the age of 70 (Figure 1). The patients with AVN had a higher cumulative incidence of major adverse cardiovascular and cerebrovascular events than controls (19.5% versus 14.9%; p = 0.017). Upon univariate Kaplan-Meier method with the log-rank test, there was a significant difference in major cardiovascular and cerebrovascular events-free survival rates between AVN group and control group (p <0.001). However, after adjusting for potential confounders including hypertension, diabetes, dyslipidemia, and use of steroid or statin, the association between AVN group and major adverse cardiovascular and cerebrovascular events was insignificant (adjusted HR 1.114, 95% CI 0.959-1.295, p=0.158) Conclusion: In this population-based cohort study, we provided the updated epidemiologic data of Korean patients with nontraumatic AVN. The increased risk for major cardiovascular and cerebrovascular events among AVN patients was not observed in the representative Korean population. References: [1]Kang JH, Lin HC. Increased risk for coronary heart disease after avascular necrosis of femoral head: a 3-year follow-up study. Am Heart J. 2010;159:803-8. [2]Sung PH, Yang YH, Chiang HJ, Chiang JY, Chen CJ, Yip HK, et al Cardiovascular and cerebrovascular events are associated with nontraumatic osteonecrosis of the femoral head. Clin Orthop Relat Res 2018;476:865-74. Figure 1. Age- and sex-distributed incidence of patients with nontraumatic avascular necrosis in Korea, 2008-2015 Disclosure of Interests: None declared

OBJECTIVES:To perform unbiased analysis of fever patterns and to investigate their association with clinical manifestations and outcome of patients with adult-onset Still's disease (AOSD). METHODS:AOSD patients who were treated as in-patients from 2004 through 2015 were grouped according to 24-hour body temperature (BT) by hierarchical clustering using a Euclidean distance metric with complete linkage. The clinical and laboratory characteristics of the groups were then examined. RESULTS:Hierarchical clustering partitioned 70 AOSD patients into three distinct groups. Group 1 (n=14) had the highest mean BT (38.1± 0.4°C) and the widest variation in BT (2.7±0.9°C). Group 2 (n=35) had a lower mean BT (37.4±0.3°C) and a smaller variation (2.1±0.7°C). Group 3 (n=21) had the lowest mean BT (36.7±0.3°C) and the smallest variation (1.5±0.6°C). Clinical features and extent of organ involvement did not differ significantly between groups. However, Group 1 had lower platelet counts and higher lactate dehydrogenase, ferritin levels, and prothrombin time than the other groups. In addition, Group 1 exhibited higher risk of having a macrophage activation syndrome (MAS) and tended to require more intense treatment with corticosteroids and immunosuppressant to achieve clinical remission as compared to other groups. CONCLUSIONS:Hierarchical clustering identified three distinct fever patterns in patients with AOSD. Higher BT was associated with wider variations in diurnal temperature, higher risk of developing MAS, more intense treatment, and longer time to clinical remission, suggesting that fever pattern is a prognostic factor for AOSD.

Background: Lipid metabolism appear to be changed in rheumatoid arthritis (RA) patients because of disease activity and inflammation. Objectives: It was not clear in the previous studies that lipid profiles status is associated with nutritional intake in RA patients. Methods: We analyzed RA, dyslipidemia, serum lipid profiles (total cholesterol, TG, HDL, and LDL) and nutritional intake data related lipid from the data of KNHANES (N=22,948, estimated population size=48,402,221). We analyzed the prevalence of RA and abnormal status of lipid profiles using general linear model and logistic regression with complex sample design method adjusted by age and sex and evaluated the association between RA and dyslipidemia including nutritional intake data. Results: The prevalence of RA was 1.21% [95% CI: 1.07–1.38]. The prevalence of dyslipidemia with RA (3.31% [95% CI: 2.63–4.17]) was significantly increased compared with that of dyslipidemia without RA (1.37% [95% CI: 1.17–1.59], p<0.001). LDL (RA vs. control: 117.77±3.87 mg/dL vs. 114.47±0.51 mg/dL, p<0.001) was significantly increased, whereas TG (RA vs. control: 129.21±6.38 mg/dL vs. 136.72±1.20 mg/dL, p<0.001) was significantly decreased in RA. Total cholesterol tended to be higher in RA (RA vs. control: 198.12±3.09 mg/dL vs. 188.11±0.39 mg/dL, p=0.051). but HDL (RA vs. control: 54.16±1.42 mg/dL vs. 52.46±0.15 mg/dL, p=0.98) was not different between two groups. There were no differences in nutritional intake volume including total diet volume, energy intake, water, carbohydrate, protein, fat, other fatty acids and dietary fiber (Table).Table 1 Nutritional intake difference between RA and control Conclusions: We showed increased prevalence of dyslipidemia patients in the individuals with RA than those without RA. Serum LDL levels was increased and TG was decreased in RA patients of the Korean population survey. Disclosure of Interest: None declared

Background Systemic sclerosis (SSc) is a rare autoimmune disease characterised by fibrosis of the skin and multiple internal organ involvement. Previous studies reported a poorer health-related quality of life (HRQoL) in patients with SSc compared to the general population. However, very little is known about HRQoL of SSc as compared with other systemic autoimmune diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and Sjogren’s syndrome (SJS) Objectives To compare the HRQoL of patients with SSc and other systemic autoimmune disease and general population. Methods HRQoL was captured by the Korean short form-36 health survey version 2 (SF-36), short form-6D (SF-6D) and 3 level version of EuroQol five-dimensional (EQ-5D) descriptive system (EQ-5D-3L). Between March and July 2017, consecutive patients with SSc, and randomly chosen patients with RA, SLE and SJS were recruited from the outpatient rheumatology clinics of Seoul National University Hospital, and were asked to answer SF-36 and EQ-5D. Disease activity of RA was evaluated by Disease Activity Score 28-ESR (DAS 28-ESR), SLE by Systemic Lupus Erythematosus Disease Activity Index-2k (SLEDAI-2k), and SJS by EULAR Sjogren’s syndrome disease activity index (ESSDAI). For patients with SSc, Korean version of Health Assessment Questionnaire Disability Index (HAQ-DI) and Systemic sclerosis HAQ-DI (SSc HAQ-DI) were also evaluated. Demographic, clinical, laboratory information were obtained through a medical chart review. Data on representative Korean healthy controls were obtained from a study of psychometric properties of the Korean SF-36 v2 for assessing the general population, which was performed on six hundred healthy Koreans. Results A total of 480 patients with SSc (n=120), RA (n=120), SLE (n=120) and SJS (n=120) and 600 healthy controls were included. The demographic features of patients were similar to the known features of each rheumatic disease group. Patients with rheumatic diseases had significantly lower SF-36 scores (p<0.001 in all domains), SF-6D scores (p<0.001), EQ-5D-3L index scores and EQ-VAS (p<0.001) than the healthy controls; adjustments for age and sex did not change those results. Patients with SSc showed significantly lower scores in the mental component summary scores compared with patients with RA (age and sex-adjusted scores, 43.0±0.9 vs 48.9±0.9; p<0.001). Specifically, domain of mental health was lower in SSc patients than RA patients (age and sex-adjusted scores, 61.3±1.8 vs 71.7±1.8, p<0.001). Among the physical domains scores, SSc patients showed lower score in general health domain than RA patients (age and sex-adjusted scores, 41.4±1.8 vs 51.3±1.8, p<0.001). Moreover, SSc patients reported remarkably lower scores of EQ-5D-3L index scores than all comparative rheumatic disease groups (RA, SLE, SJS) (p<0.001). HRQoL of patients with SSc was associated with HAQ-DI and SSc HAQ-DI. Conclusions HRQoL of patients with systemic autoimmune diseases is significantly worse and affects all health domains in comparison to healthy controls. Patients with SSc have poorer HRQoL than patients with other rheumatic diseases. Specifically, SSc patients have more impaired mental health than RA patients, and the perception of an individual’s general health is also poor compared to RA. Disclosure of Interest None declared

Lupus nephritis (LN) is a major complication of systemic lupus erythematosus (SLE). Conventional biomarkers for assessing renal disease activity are imperfect in predicting clinical outcomes associated with LN. The aim of this study is to identify urinary protein biomarkers that reliably reflect the disease activity or predict clinical outcomes. A quantitative proteomic analysis was performed to identify protein biomarker candidates that can differentiate between SLE patients with and without LN. Selected biomarker candidates were further verified by enzyme-linked immunosorbent assay using urine samples from a larger cohort of SLE patients (n=121) to investigate their predictive values for LN activity measure. Furthermore, the association between urinary levels of a selected panel of potential biomarkers and prognosis of LN was assessed with a four-year follow-up study of renal outcomes. Urinary vitamin D-binding protein (VDBP), transthyretin (TTR), retinol binding protein 4 (RBP4), and prostaglandin D synthase (PTGDS) were significantly elevated in SLE patients with LN, especially in patients with active LN (n=21). Among them, VDBP well correlated with severity of proteinuria (rho=0.661, p<0.001) and renal SLE Disease Activity Index (renal SLEDAI) (rho=0.520, p<0.001). In the four-year follow-up, VDBP was a significant risk factor (hazard ratio 9.627, 95% confidence interval 1.698 to 54.571, p=0.011) for the development of proteinuric flare in SLE patients without proteinuria (n=100) after adjustments for multiple confounders. Urinary VDBP correlated with proteinuria and renal SLEDAI, and predicted the development of proteinuria.

Background Gout is a form of inflammatory arthritis that develops in some people with hyperuricemia. Several drugs may induce hyperuricemia and gout attack. Some anti-tuberculosis (TB) medications are also known to increase uric acid level and trigger acute gout attack. However, there have been no well-described studies for gout during anti-TB therapy. Objectives To investigate the clinical features and risk factors of gout attacks following anti-TB treatment in South Korea. Methods We conducted the case-control study including 49 patients who developed gout attack following anti-TB medications and 147 age- and sex- matched TB controls without gout attack. Demographic, clinical features and laboratory findings of patients with gout attacks following anti-TB medication were analysed and compared to those of controls in order to establish risk factors associated with gout attack during anti-TB treatment. Results The mean age was 67.7±13.2 years and 39 patients (79.6%) were male. Twenty-four patients (49.0%) had a previous history of gout. The mean time interval to develop gout attack from the initiation of anti-TB therapy was 4.13±4.49 months. The attacks tended to involve lower extremity joints (43/49, 87.8%), especially the ankle and the first metatarsophalangeal joint. Factors associated with experiencing gout attack during anti-TB medication were higher body mass index (BMI, 23.7±3.6 vs 21.8±3.6, p=0.003), higher pre-treatment uric acid level (7.2±2.5 vs 6.2±1.7 mg/dL, p<0.001), previous history of gout (49.0% vs 1.4%, p<0.001), absence of dyslipidemia (4.1% vs 16.3%, p=0.008), and decreased renal function (eGFR 63.6±27.5 vs 82.6±29.9, p=0.003). In multivariate model, higher BMI, chronic kidney disease (CKD, eGFR <60 ml/min/1.73m2), previous history of gout, and pre-treatment hyperuricemia (uric acid ≥6.8 mg/dL) were found to be independent risk factors for gout attack following anti-TB medication (table 1). Conclusions TB patients with obesity, history of gout, pre-treatment hyperuricemia, and CKD have higher risk for having gout attack following anti-TB medication. When starting anti-TB therapy in TB patients with these risk factors, physicians should pay attention to the development of gout attack and educate the patients. References [1] Gerdan G, Nurullah A, Ucan ES, et al. Paradoxical increase in uric acid level with allopurinol use in pyrazinamide-induced hyperuricemia. Singapore Med J. 2013;54(6):e125–128. [2] Postlethwaite AE, Bartel AG, Kelley WN. Hyperuricemia due to ethambutol. N Engl J Med. 1972;286(14):761–762. [3] Ben Salem C, Slim R, Fathallah N, Hmouda H. Drug-induced hyperuricaemia and gout. Rheumatology (Oxford)2017;56(5):679–688. Disclosure of Interest None declared