SAT0148 IMMUNOGLOBULIN A LEVELS IN ADDITION TO RHEUMATOID FACTOR PREDICTS REMISSION ACHIEVEMENT WITH ABATACEPT IN PATIENTS WITH EARLY RHEUMATOID ARTHRITIS
Authors: Jun Inamo, Yuko Kaneko, Jun Kikuchi, Tsutomu Takeuchi
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background</h3> Biological disease modifying antirheumatic drugs (bDMARDs) now play an important role of clinical practice for patients with rheumatoid arthritis (RA). Abatacept (ABT) has a biologic agent that has an unique mechanism of action suppressing T lymphocyte activation. Although many prediction studies about therapeutic responses to bDMARDs for RA have been conducted to date [1], few studies has focused on ABT. <h3>Objectives</h3> The aim of this study was to identify predictive clinical biomarkers for remission achievement with ABT in RA patients. <h3>Methods</h3> We retrospectively reviewed consecutive patients with RA who started ABT from 2010 through 2018 in Keio University Hospital. We defined early ABT use as the initiation of ABT within two years from diagnosis without radiographic progression in hand X rays, and stratified the patients into the early ABT users and the late ABT users. Baseline characteristics were compared between patients who achieved CDAI remission achievement at 6 months and those who did not in both groups. <h3>Results</h3> One hundred and seven RA patients who were treated with ABT with baseline information available were enrolled in the study. Among them, 15 patients were classified into the early ABT users and 92 were the late ABT users, and the remission rates at 6 months were 40% and 24%, respectively. In the early ABT users, patients who achieved CDAI remission at 6 months showed significantly higher IgA levels than those who did not achieve remission (390 mg/dL vs 279 mg/dL, P=0.04, respectively). The difference in IgA disappeared in the late ABT users (332 mg/dL vs 313 mg/dL, P=0.60, respectively). Principal component analysis revealed that in the early ABT users, patients who achieved remission and those who did not could be clearly separated by the levels of IgA, IgG, rheumatoid factor, and albumin (Figure), whereas those baseline characteristics were mostly overlapped in the late ABT users (cut-off value for predicting remission with sensitivity and specificity in the early ABT users; IgA 342 mg/dL with 83% and 100%, IgG 1880 mg/dL with 50% and 100%, rheumatoid factor 152 IU/mL with 50% and 100%, albumin 3.7 g/dL with 88% and 67%, respectively). The area under the curves of receiver operating characteristic curves to predict remission were 0.833 of IgA and 0.778 of rheumatoid factor titer. <h3>Conclusion</h3> We identified serum IgA titer was the novel predictive factor for response of ABT. <h3>Reference</h3> [1] Wijbrandts CA, Tak PP. Prediction of Response to Targeted Treatment in Rheumatoid Arthritis. Mayo Clin Proc. 2017;92:1129-1143. <h3>Disclosure of Interests</h3> Jun Inamo: None declared, Yuko Kaneko Grant/research support from: Abbvie, Eisai, Speakers bureau: AbbVie, Astellas, Ayumi, Bristol-Myers Squibb, Chugai, Eisai, Eli Lilly, Jansen, Kissei, Pfizer, Sanofi, Takeda, Tanabe-Mitsubishi, UCB, Jun Kikuchi: None declared, Tsutomu Takeuchi Grant/research support from: Astellas Pharma Inc, Chugai Pharmaceutical Co, Ltd., Daiichi Sankyo Co., Ltd., Takeda Pharmaceutical Co., Ltd., AbbVie GK, Asahikasei Pharma Corp., Mitsubishi Tanabe Pharma Co., Pfizer Japan Inc., Eisai Co., Ltd., AYUMI Pharmaceutical Corporation, Nipponkayaku Co. Ltd., Novartis Pharma K.K., Grant/research support from: AbbVie, Asahi Kasei, Astellas, AstraZeneca, AYUMI, Bristol-Myers Squibb, Chugai, Daiichi Sankyo, Eisai, Eli Lilly Japan, Janssen, Mitsubishi Tanabe, Nippon Kayaku, Novartis, Pfizer Japan Inc, Taiho, Taisho Toyama, Takeda, Teijin, Grant/research support from: Astellas Pharma Inc., Bristol Myers Squibb, Chugai Pharmaceutical Co., Ltd., Mitsubishi Tanabe Pharma Co., Pfizer Japan Inc., Santen Pharmaceutical Co., Ltd., Takeda Pharmaceutical Co., Ltd., Teijin Pharma Ltd., AbbVie GK, Asahi Kasei Pharma Corp., Taisho Toyama Pharmaceutical Co., Ltd., SymBio Pharmaceuticals Ltd., Janssen Pharmaceutical K.K., Celltrion Inc., Nipponkayaku Co. Ltd., and UCB Japan, Consultant for: Astra Zeneca K.K., Eli Lilly Japan K.K., Novartis Pharma K.K., Mitsubishi Tanabe Pharma Co., Abbivie GK, Nipponkayaku Co.Ltd, Janssen Pharmaceutical K.K., Astellas Pharma Inc., Taiho Pharmaceutical Co. Ltd., Chugai Pharmaceutical Co. Ltd., Taisho Toyama Pharmaceutical Co. Ltd., GlaxoSmithKline K.K., UCB Japan Co. Ltd., Consultant for: AbbVie, Asahi Kasei, Astellas, AstraZeneca, AYUMI, Bristol-Myers Squibb, Chugai, Daiichi Sankyo, Eisai, Eli Lilly Japan, Janssen, Mitsubishi Tanabe, Nippon Kayaku, Novartis, Pfizer Japan Inc, Taiho, Taisho Toyama, Takeda, Teijin, Consultant for: Astra Zeneca K.K., Eli Lilly Japan K.K., Novartis Pharma K.K., Mitsubishi Tanabe Pharma Co., Asahi Kasei Medical K.K., AbbVie GK, Daiichi Sankyo Co., Ltd., Bristol Myers Squibb, and Nipponkayaku Co. Ltd., Speakers bureau: Astellas Pharma Inc., Bristol Myers Squibb, Chugai Pharmaceutical Co., Ltd., Mitsubishi Tanabe Pharma Co., Pfizer Japan Inc., Santen Pharmaceutical Co., Ltd., Takeda Pharmaceutical Co., Ltd., Teijin Pharma Ltd., AbbVie GK, Asahi Kasei Pharma Corp., Taisho Toyama Pharmaceutical Co., Ltd., SymBio Pharmaceuticals Ltd., Janssen Pharmaceutical K.K., Celltrion Inc., Nipponkayaku Co. Ltd., and UCB Japan, Speakers bureau: AbbVie, Asahi Kasei, Astellas, AstraZeneca, AYUMI, Bristol-Myers Squibb, Chugai, Daiichi Sankyo, Eisai, Eli Lilly Japan, Janssen, Mitsubishi Tanabe, Nippon Kayaku, Novartis, Pfizer Japan Inc, Taiho, Taisho Toyama, Takeda, Teijin, Speakers bureau: AbbVie GK., Bristol–Myers K.K., Chugai Pharmaceutical Co. Ltd., Mitsubishi Tanabe Pharma Co., Pfizer Japan Inc., Astellas Pharma Inc, Diaichi Sankyo Co. Ltd., Eisai Co. Ltd., Sanofi K.K., Teijin Pharma Ltd., Takeda Pharmaceutical Co. Ltd., Novartis Pharma K.K.