Effect of Anticitrullinated Protein Antibody Status on Response to Abatacept or Antitumor Necrosis Factor-α Therapy in Patients with Rheumatoid Arthritis: A US National Observational Study

被引:53
作者
Harrold, Leslie R. [1 ,2 ]
Litman, Heather J. [2 ]
Connolly, Sean E. [3 ]
Kelly, Sheila [3 ]
Hua, Winnie [2 ]
Alemao, Evo [3 ]
Rosenblatt, Lisa [3 ]
Rebello, Sabrina [2 ]
Kremer, Joel M. [2 ,4 ,5 ]
机构
[1] Univ Massachusetts, Sch Med, Worcester, MA 01605 USA
[2] Corrona LLC, Southborough, MA USA
[3] Bristol Myers Squibb, Princeton, NJ USA
[4] Albany Med Coll, Albany, NY 12208 USA
[5] Ctr Rheumatol, Albany, NY USA
关键词
DISEASE-MODIFYING ANTIRHEUMATIC DRUGS; RHEUMATOID ARTHRITIS; ANTICYCLIC CITRULLINATED ANTIBODIES; ANTI-TUMOR NECROSIS FACTOR; AMERICAN-COLLEGE; AUTOANTIBODIES; METHOTREXATE; SPECIFICITY; OUTCOMES;
D O I
10.3899/jrheum.170007
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective. Assess whether baseline anticyclic citrullinated peptide antibodies (anti-CCP) status is associated with treatment response in patients with rheumatoid arthritis (RA) initiating abatacept (ABA) or a tumor necrosis factor-alpha inhibitor (TNFi). Methods. Using the Corrona RA registry, patients were identified who initiated ABA or a TNFi (June 2004-January 2015), had a followup visit 6 months (+/- 3 mos) after initiation, and anti-CCP measured at or prior to initiation. Primary outcome was mean change in Clinical Disease Activity Index (CDAI) from initiation to 6 months. Treatment response was evaluated based on a typical patient profile (female, aged 57 yrs, body mass index of 30 kg/m(2), baseline CDAI of 20, 1 prior biologic, and no comorbidities other than RA). Secondary outcomes included remission and low disease activity. Results. There were 566 ABA initiators [anti-CCP + (>= 20 units/ml): n = 362; anti-CCP-(< 20 units/ml): n = 204] and 1715 TNFi initiators (anti-CCP+: n = 1113; anti-CCP-: n = 602). Differences between treatment groups included baseline disease duration, CDAI, and prior biologic use. At 6 months, anti-CCP+ ABA initiators were associated with significantly greater CDAI response versus anti-CCP-ABA initiators; no significant difference was observed for TNFi initiators. When considering a typical RA patient profile, CDAI response was greater in anti-CCP+ versus anti-CCP-ABA initiators; anti-CCP+ versus anti-CCP TNFi initiators were similar. Secondary outcome responses were also greater in anti-CCP+ versus anti-CCP-ABA initiators; TNFi initiators did not differ by anti-CCP status. Conclusion. In a US-based clinical practice setting, anti-CCP status was associated with a differential treatment response to ABA, but not TNFi.
引用
收藏
页码:32 / 39
页数:8
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