FRI0205 Relationship between Anti-Citrullinated Protein Antibody Status and Response To Abatacept or Anti-Tumour Necrosis Factor Therapy in Patients with Rheumatoid Arthritis: A US National Observational Study

Background Anti-citrullinated protein antibodies (ACPA) are associated with more severe, erosive rheumatoid arthritis (RA), but the extent to which ACPA status predicts response to therapy is not known.1,2 Objectives To evaluate in a real-world, observational RA cohort whether baseline ACPA status is associated with response to biologics among patients with RA. Methods Using the Corrona RA registry, we identified patients with RA who initiated abatacept (ABA) or a tumour necrosis factor-alpha inhibitor (TNFi) between June 2002 and January 2015, had a follow-up visit 6 months (±3 months) after initiation and anti-cyclic citrullinated peptide (anti-CCP [a surrogate of ACPA]) measured at or prior to initiation. Anti-CCP positivity was defined as anti-CCP ≥20 U/mL. The primary outcome was mean change from baseline in Clinical Disease Activity Index (CDAI) at 6 months. Secondary outcomes at 6 months included: 1) achievement of low disease activity (LDA; CDAI ≤10) among those with moderate or high disease activity who initiated treatment; 2) achievement of remission (CDAI ≤2.8) in those with low, moderate or high disease activity who initiated treatment; 3) Minimally Important Clinical Difference (MCID) in CDAI; and 4) modified ACR20/50/70. Unadjusted and adjusted linear and logistic analyses were performed based on anti-CCP status (positive [+] vs negative [–]). Results 566 patients initiated ABA: 204 (36.0%) were anti-CCP– and 362 (64.0%) anti-CCP+. There were no differences by CCP status for age (mean 57–58 years), disease duration (median 7 years) or prior biologic use (0, 1 or ≥2 prior); however, median baseline CDAI was greater in anti-CCP– vs anti-CCP+ patients (21 vs 19, p=0.035). 1715 patients initiated a TNFi: 602 (35.1%) were anti-CCP– and 1113 (64.9%) anti-CCP+. There were no differences by CCP status for age (mean 55–56 years), prior biologic use or median baseline CDAI; however, median disease duration was greater in anti-CCP+ vs anti-CCP– patients (4 vs 3 years, p=0.021). In adjusted analyses, anti-CCP+ ABA initiators had a mean (SE) change in CDAI of –8.5 (0.6) vs –4.1 (0.8) for anti-CCP– (p Conclusions In a clinical practice setting, anti-CCP positivity was associated with a differential treatment response to abatacept, but not TNFis. These real-world data suggest that anti-CCP+ patients with RA show incremental improvements in response while receiving abatacept therapy compared with anti-CCP– patients. References Lv Q, et al. PLoS One 2014;9:e89442. Sokolove J, et al. Ann Rheum Dis 2015; doi:10.1136/annrheumdis-2015-207942. Disclosure of Interest L. R. Harrold Grant/research support from: Pfizer, H. J. Litman Employee of: Corrona, S. E. Connolly Shareholder of: Bristol-Myers Squibb, Employee of: Bristol-Myers Squibb, S. Kelly Shareholder of: Bristol-Myers Squibb, Employee of: Bristol-Myers Squibb, W. Hua Employee of: Corrona, E. Alemao Shareholder of: Bristol-Myers Squibb, Employee of: Bristol-Myers Squibb, L. Rosenblatt Shareholder of: Bristol-Myers Squibb, Employee of: Bristol-Myers Squibb, S. Rebello Employee of: Corrona, J. Kremer Shareholder of: Corrona, Grant/research support from: AbbVie, Bristol-Myers Squibb, Genentech, Lilly, Novartis, Pfizer, Employee of: Corrona, Speakers bureau: Genentech (non-branded talks only)