Background MMP-3 is an enzyme produced by synoviocytes, and is a marker of synovitis that gives a more direct indication of actual joint destruction than either C-reactive protein (CRP)in patients with rheumatoid arthritis (RA).
Objectives Our aim in this study is to investigate the impact of the trend of MMP-3 and CRP during the treatment Adalimumub (ADA) and Abatacept (ABT) in the early stage of RA patients.
Methods Among 295 patients with active RA (DAS28-CRP≥2.7) who were recruited in the multicenter study group (Tsurumai Biologics Communication Registry; TBCR), 154 patients were received ADA (40mg subcutaneously every other week) and 141 patients were received ABT therapy (500mg for<60 kg; 750 mg for 60 kg-100 kg; and 1 gram for>100 kg infusion at week 0, 2, 4 and every 4 weeks). DAS28-CRP remission (DAS28-CRP<2.3) rates at 24 weeks were 34.2% (38/111) for ADA therapy and 19.7% (23/117) for ABT therapy. We analyzed 61patients who had DAS28-CRP remission at 24 weeks, consisting of 38 patients in ADA group and 23 patients in ABT group respectively. We compared the change in serum MMP-3 and CRP levels from first administration to 24 weeks between the two groups.
Results While there was significant baseline difference in age, methotrexate (MTX) use between the two groups, there was no significant baseline difference in serum MMP-3 and CRP levels between the two groups (Table). Serum MMP-3 and CRP levels decreased promptly at 4 weeks. The change in serum MMP-3 levels at 4, 12, and 24 weeks was significantly greater in the ADA group than in the ABT group (Fig. 1). However, the change in CRP levels at 4, 12, and 24 weeks had no significant deference between the two groups (Fig. 2). Similarly the % change in serum MMP-3 levels at 4, 12, and 24 weeks was significantly greater in the ADA group than in the ABT group (Fig. 3) and there was no difference in the % change in CRP levels at 4, 12, and 24 weeks between the two groups (Fig. 4).
Conclusions ADA showed improvements in serum MMP-3 levels from an early stage in 24 weeks in a comparison with ABT. ADA can suppress synovitis and therefore the progression of joint destruction by strongly inhibiting MMP-3 when it is administered from an early stage.
Disclosure of Interest: Y. Hattori: None Declared, T. Kojima Speakers bureau: Mitsubishi Tanabe Pharma Corporation, Takeda Pharma Corporation, Eisai Pharma Corporation, Chugai Pharma Corporation, Abbott, Bristol-Myers Squibb and Pfizer, N. Takahashi: None Declared, K. Funahashi: None Declared, D. Kato: None Declared, M. Hanabayashi: None Declared, N. Ishiguro Speakers bureau: Mitsubishi Tanabe Pharma Corporation, Takeda Pharma Corporation, Eisai Pharma Corporation, Chugai Pharma Corporation, Abbott, Bristol-Myers Squibb and Pfizer