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Background:Oral Janus kinase inhibitors (JAKi) have dramatically altered outcomes in patients with rheumatoid arthritis (RA). However, there remains some proportion of patients who respond to inadequately JAKi treatment (JAKi-IR) [1,2]. The characteristics in RA patients associated with JAKi-IR have not been fully demonstrated.Objectives:To clarify the characteristics of JAKi-IR in patients with RA by cluster analysis.Methods:This retrospective study comprised 120 RA patients who were treated with JAKi (Tofacitinib or Baricitinib) between July 2013 and September 2019 in five facilities. The disease status at the baseline, at 12 weeks after JAKi treatment and at the time point of withdrawing JAKi was assessed using the Disease Activity Score (DAS28) and the American College of Rheumatology (ACR) response criteria. JAKi-IR was defined as follows, primary non-response at 12 weeks after JAKi treatment: withdrawal of JAKi with ACR20 non-response or non-improvement in DAS28-CRP (ΔDAS28-CRPResults:The 120 enrolled patients were classified into 4 groups by cluster analysis(Figure1), The characteristics of each group are as follows, Group A(n=21): female + bone erosion + RF/ACPA positive + AID + MTX non-user, Group B(n=36): male + older age + RA-ILD + RF/ACPA positive + MTX non-user, Group C(n=35): RF/ACPA positive + absence of RA-ILD + MTX user, Group D (n=28): seronegative + MTX user + absence of RA-ILD + history of biologic DMARDs failure. The rate of JAKi-IR was A:9%, B:8%, C:20%, D:32%, and the significant difference between Group B and D was identified (p=0.02). In multiple comparison of 4 groups, no significant difference was identified (p=0.06) (Figure2).Conclusion:JAKi-IR would be more likely to be seronegative, MTX use, absence of RA-ILD and history of biologic DMARDs failure. Cluster analysis is an exploratory tool that aids in the analysis of huge amount of data.References:[1] Takeuchi T, Yamanaka H, Yamaoka K, Arai S, Toyoizumi S, DeMasi R, et al. Efficacy and safety of tofacitinib in Japanese patients with rheumatoid arthritis by background methotrexate dose: A post hoc analysis of clinical trial data. Mod Rheumatol. 2019;29(5):756-66.[2] Tanaka Y, Atsumi T, Amano K, Harigai M, Ishii T, Kawaguchi O, et al. Efficacy and safety of baricitinib in Japanese patients with rheumatoid arthritis: Subgroup analyses of four multinational phase 3 randomized trials. Mod Rheumatol. 2018;28(4):583-91.Disclosure of Interests:Masanari Sugawara: None declared, Yuichiro Fujieda: None declared, Atsushi Noguchi: None declared, Shun Tanimura: None declared, Yuka Shimizu: None declared, Ikuma Nakagawa: None declared, Michihito Kono: None declared, Masaru Kato: None declared, Kenji Oku: None declared, Tatsuya Atsumi Grant/research support from: Eli Lily Japan K.K., Alexion Pharmaceuticals, Inc., Bristol-Myers Squibb Co., AbbVie Inc., Daiichi Sankyo Co., Ltd., Pfizer Inc., Chugai Pharmaceutical Co., Ltd., Mitsubishi Tanabe Pharma Co., Astellas Pharma Inc., Consultant of: Gilead Sciences, Inc., Eli Lilly Japan K.K., UCB Japan Co. Ltd., AbbVie Inc., Daiichi Sankyo Co., Ltd., Pfizer Inc., Chugai Pharmaceutical Co., Ltd., Speakers bureau: Eli Lilly Japan K.K., UCB Japan Co. Ltd., Bristol-Myers Squibb Co., AbbVie Inc., Eisai Co. Ltd., Otsuka Pharmaceutical Co., Ltd., Daiichi Sankyo Co., Ltd., Pfizer Inc., Chugai Pharmaceutical Co., Ltd., Mitsubishi Tanabe Pharma Co., Takeda Pharmaceutical Co., Ltd., Astellas Pharma Inc.

Background Thrombocytopenia is a non-criteria manifestation of antiphospholipid syndrome (APS). Antiphospholipid antibodies (aPL) have been shown to activate platelet through multiple mechanisms. In patients with idiopathic/immune thrombocytopenia, aPL have been shown to increase the risk of thrombosis. Conversely, it remains unclear whether thrombocytopenia increases the risk of thrombosis in patients who have aPL. Objectives To evaluate the relationship between thrombocytopenia and thrombosis in patients who have aPL. Methods A single center retrospective study comprising 670 consecutive patients who underwent testing for aPL including lupus anticoagulant, anticardiolipin antibodies (IgG and M), anti-β2-glycoprotein I antibodies (IgG and M), and phosphatidylserine-dependent antiprothrombin antibodies (IgG and M) between January 2004 and December 2006. Excluded were patients who had been followed-up for ≤1 year. Results Of 524 patients included in this study, 187 had systemic lupus erythematosus, 70 rheumatoid arthritis, and 33 primary APS. At least one of aPL was positive in 241 patients. The prevalence of thrombocytopenia was not different in aPL positive and negative patients (24% vs 18%, p=0.11). In aPL positive group, patients with thrombocytopenia experienced arterial thrombosis (46% vs. 17%, p Conclusions Our data indicate that thrombocytopenia is associated with the risk of thrombosis in aPL positive patients providing new insight into the pathophysiology of aPL mediated platelet activation. Disclosure of Interest None declared

Background Thrombosis is one of the most frequent manifestations in patients with systemic lupus erythematosus (SLE). In this study, we examined the several risk factors for thrombosis in patients with SLE. Further, we investigated whether some factors could play a protective thrombotic role in SLE. Objectives To identify risk and protective factors for thrombosis in SLE. Methods Ninety-seven newly diagnosed consecutive patients with SLE without history of thrombotic events were recruited at our hospital from 2001 to 2012. All patients, 87 woman and 10 men, fulfilled the 1997 American College of Rheumatology revised criteria for SLE. Fifty-four patients (55.7%) had antiphospholipid antibodies (aPL). All patients were follow-up since the inclusion until December, 2012. The development of thrombosis were defined as the study endpoint. Results The median follow-up period in all patients was 46 months (IQR 17-84 months). In 54 patients with aPL, the median follow-up period was 57 months (IQR 28-99 months). 10 patients with aPL (18.5%) developed thrombosis during the follow-up period. Cerebral infarction (CI) was observed in 5 patients, pulmonary embolism (PE) in 4 and deep vein thrombosis in 3. Multivariate analysis with Cox’s proportional hazards model showed that older age at SLE onset and anticardiolipin antibodies (aCL)-IgG positivity, (HR 1.89 for every ten age, 95%C.I. 1.07-3.33) and (HR 5.68, 95%C.I. 1.28-25.3), respectively, are statistically significant risk factor for thrombosis. Statin therapy appears as a statistically significant protective thrombotic factor (HR 0.093, 95%C.I. 0.01-0.82) (Figure 1.). Disease activity, anti-thrombotic agents and risk factors for atherosclerosis were not related to thrombosis. On the other hand, in 43 patients without aPL (median follow-up period 26 months, IQR 12-66 months), 4 patients (9.3%) developed thrombosis. Three patients had CI and one PE. None of the evaluated risk factors correlated to the development of thrombosis in aPL-negative patients. Image/graph Conclusions This study suggests that, in patients with aPL, the late disease onset and the presence of aCL-IgG represent additional risk factors for thrombosis. Statin treatment appears as a thrombotic protective factor. Disclosure of Interest : None Declared