SAT0156 EFFECTIVE OF BARICITINIB ON RADIOGRAPHIC PROGRESSION OF STRUCTURAL JOINT DAMAGE AT 48 WEEKS IN PATIENTS WITH RHEUMATOID ARTHRITIS IN REAL-WORLD MULTICENTER CLINICAL DATA
Authors: E. Torikai, Y. Hirano, D. Suzuki, Y. Kanayama
Journal: Annals of the Rheumatic Diseases (2020)

Background: Baricitinib (bari) is an oral Janus kinase 1 (JAK1)/JAK2 selective inhibitor that has demonstrated good efficacy in patients with rheumatoid arthritis (RA) and adequate response to conventional synthetic (cs) DMARDs in some clinical trials [1,2]. We report the efficacy and safety of bari within 24 weeks in real-world clinical data at EULAR2019. Objectives: To evaluate the radiographic progression of structural joint damage at 48 weeks in Japanese patients with RA in real-world multicenter clinical data. Methods: We included 53 Japanese patients with RA who showed an inadequate response to csDMARDs or biologic (b) DMARDs. Patients were scheduled to receive a once-daily dose of 4 or 2 mg/day bari as monotherapy or in combination with other csDMARDs. We divided the patients into two groups: those treated with 2 mg/day of bari (2mg-group; n = 27) and those treated with 4 mg/day of bari (4-mg group; n = 26) throughout the observation period. Patients were allowed to decrease their predonisolone and csDMARDs combined with bari treatment if their disease activity improved. First, we evaluated changes in CDAI and HAQ-DI after 48 weeks. Second, we evaluated the change in the van der Heijdge modified total sharp score (ΔmTSS), erosion score (ΔERN), and joint space narrowing score (ΔJSN). In addition, we assessed predictors for suppression of joint destruction at 48 weeks after bari treatment. Results: The baseline characteristics of the patients were as summarized in Table 1. There were no significant differences in any items. CDAI scores significantly improved 4 weeks after the treatment. This tendency continued until the final evaluation (Table 2). At 48 weeks, remission and low disease activity rates were 37.0% and 74.1% in the 2-mg group and 38.4% and 76.9% in the 4-mg group, respectively. Structural remission (mTSS ≤ 0.5) was noted in 21 patients (80.8%) and 21 patients (77.8%) in 4-mg group and 2-mg group, respectively (Figure). Mean scores (ΔmTSS, ΔERN, and ΔJSN) of all patients in the 2-mg group and 4-mg groups were (0.26, 0.15, and 0.11), (0.30, 0.17, and 0.13) and (0.23, 0.13, and 0.10), respectively (Figure). There were no significant differences in ΔmTSS scores between the two groups. A matrix metalloproteinase-3 score within the standard value at 12 weeks after the treatment was associated with a predictor for suppression of joint destruction at 48 weeks (logistic regression analysis; odds ratio = 11.6, 95% confidence interval: 1.5–112.4, P = 0.020). Table 1. Characteristics of patients at baricitinib initiation 2mg-group (n=27) 4mg-group (n=26) p-value Age (years) 69.1 (12.0) 65.6 (10.3) 0.20 Gender, female, n (%) 19 (73.1) 23 (85.2) 0.28 Disease duration (years), 9.7 (10.4) 5.7 (7.4) 0.23 Prior use of biologics, (0/1/2/3) (18/6/2/1) (18/2/5/1) ------ MTX (mg/week), 4.5 (3.7) 6.5 (4.29) 0.08 PSL (mg/day) 1.0 (1.9) 1.2 (1.8) 0.49 RF, U/ml 254 (372) 134 (222) 0.21 ACPA, U/m 152 (176) 133 (301) 0.45 MMP-3 196 (220) 215 (221) 0.43 Table 2. Serial change of clinical assessment 2mg-group Baseline 4 week 12 week 24 week 48 week CDAI 22.5 (9.2) 7.4 (7.7) 6.7 (6.9) 6.9 (6.8) 6.9 (6.8) HAQ-DI 0.88 (0.51) 0.45 (0.47) 0.53 (0.58) 0.56 (0.56) 0.56 (0.56) MMP-3 196 (221) 98.9 (62.2) 115 (164) 106 (78) 106 (78) 4mg-group Baseline 4 week 12 week 24 week 48 week CDAI 24.4 (9.7) 9.4 (5.7) 8.6 (6.3) 6.7 (8.6) 6.8 (8.6) HAQ-DI 1.01 (0.51) 0.58 (0.48) 0.54 (0.60) 0.45 (0.49) 0.44 (0.45) MMP-3 216 (222) 99 (62) 101 (123) 89 (72) 95 (81) Conclusion: The data showed that bari has a favorable effect on the radiographic progression of structural joint damage regardless of its dose in a real-world clinical setting. In consideration of the risk/benefit balance, we suggest that the dose of bari could be reduced in patients with favorable disease activity. References: [1]Tanaka Y et al. Mod Rheumatol. 2018;28:583-91 [2]Tanaka Y et al. Mod Rheumatol. 2018;28:20-9 Disclosure of Interests: Eiji Torikai: None declared, Yuji Hirano Speakers bureau: Tanabe-Mitsubishi, Pfizer, Eisai, Abbie, Chugai, Bristol-Meyers, Jansen, Astellas, UCB, Eli-Lilly, Asahikasei, Daiichi-Sankyo, Amgen, Daisuke Suzuki: None declared, Yasuhide Kanayama: None declared