THU0164 Efficacy of Infliximab for Suppressing Radiographic Progression of Cervical Lesions in Patients with Rheumatoid Arthritis Comparison with Methotrexate; Two Years of Follow-Up – A Multicenter Registry Study
Authors: Y. Kanayama, T. Kojima, Y. Hirano, N. Takahashi, Y. Yabe, N. Ishiguro
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> Cervical lesions are known to occur at high frequency as a complication of rheumatoid arthritis (RA). Treatment with biological agents are more clinically effective than the DMARDs that were in use previously, in particular, with their efficacy in suppressing joint destruction having been emphasized. We reported the efficacy of infliximab (IFX), anti-tumor necrosis factor antibodies for suppressing the radiographic progression of RA cervical lesions at ACR2009, EULAR2010, 11, 12, 13 and 14. However there is still few studies of efficacy of against RA cervical lesions of IFX comparison with methotrexate (MTX). <h3>Objectives</h3> To evaluate the efficacy of IFX for suppressing the radiographic progression of RA cervical lesions comparison with MTX for 2 years. <h3>Methods</h3> We used MTX or MTX+IFX for treating Japanese patients with active RA who fulfilled the ACR criteria in 1987. The final study cohort of each 40 and 88 patients received continuous MTX and IFX treatment for at least 2 years. MTX was used in all patients receiving IFX. For evaluation of cervical lesions, the atlanto-dental interval (ADI), the space available for the spinal cord (SAC), and the Ranawat value were measured by plain lateral radiographs in the flexion position, at initiation and Year 1,2. <h3>Results</h3> In the patients receiving MTX (n=40) and IFX (n=88), the number of female were each 33 (83%) and 75 (85%) cases (p=0.794). The mean age was 62.5 ± 10.7 and 53.9 ± 12.9 years old (p&lt;0.001); disease duration was 9.3 ± 10.0 and 10.7 ± 9.2 years (p=0.127) and the mean dose of MTX was 7.3 ± 2.4 and 7.8 ± 2.1 mg/w (p=0.414). Clinical findings related to RA were as follows; CRP 1.3± 2.0 and 3.1± 2.8 mg/dl (p&lt;0.001); ESR 28.1 ± 21.1 and 49.9 ± 29.1mm/h (p&lt;0.001); MMP3 170 ± 303 and 337 ± 309ng/ml (p&lt;0.001); DAS28 4.07 ± 1.42 and 5.47 ± 1.25 (p&lt;0.001); ADI 2.6 ± 1.6 and 3.6 ± 1.9mm (p=0.001); SAC 20.2 ± 2.7 and 18.1 ± 2.7mm (p&lt;0.001) and Ranawat value 16.0 ± 1.5 and 14.5 ± 2.2mm (p&lt;0.001). The respective changes in cervical lesion parameters after 1 year were as follows: ADI: 0.25 ± 0.44 and 0.22 ± 0.44 mm (p=0.591); SAC: −0.18 ± 0.39 and −0.16 ± 0.40 mm (p=0.716); and Ranawat value: −0.13 ± 0.34 and −0.15 ± 0.36 mm (p=0.733). The respective changes in cervical lesion parameters after 2 years were as follows: ADI: 0.53 ± 0.72 and 0.35 ± 0.59 mm (p=0.193); SAC: −0.48 ± 0.64 and −0.27 ± 0.60 mm (p=0.038); and Ranawat value: −0.35 ± 0.58 and −0.26 ± 0.47 mm (p=0.486) (Fig. 1). The numbers of patients who did not showed progression in ADI, SAC and Ranawat value were each 24 (60%) and 62 (70%) cases (p=0.310); 24 (60%) and 67 (76%) cases (p=0.058) and 28 (70%) and 66 (75%) cases (p=0.666) after 2 years. Also the number who was able to suppress progression in all three parameters were each 24 cases (60%) receiving MTX and 58 cases (66%) receiving IFX (p=0.555) after 2 years (Fig. 2). <h3>Conclusions</h3> This study suggested that IFX treatment can be used to suppress the progression of RA cervical lesions more than MTX treatment. <h3>Disclosure of Interest</h3> Y. Kanayama: None declared, T. Kojima Speakers bureau: Mitsubishi Tanabe Pharma, Takeda Pharma, Eisai Pharma, AbbVie,Bristol-Myers Squibb, and Pfizer, Janssenn Pharmaceutical Companies, Astellas Pharma and Chugai Pharma., Y. Hirano Speakers bureau: Abbvie Japan, Eisai, Mitsubishi Tanabe Pharma, Pfizer, Chugai Pharmaceutical, and Bristol-Myers Squibb., N. Takahashi Speakers bureau: Abbvie Japan Co. Ltd, Eisai Co. Ltd, UCB Japan Co. Ltd, Mitsubishi Tanabe Pharma Corporation, Takeda Pharmaceutical Company Ltd, Pfizer Co. Ltd, Chugai Pharmaceutical Co. Ltd,Janssen Pharmaceutical K.K., and Bristol-Myers Squibb Co. Ltd., Y. Yabe: None declared, N. Ishiguro Grant/research support from: Daiichi Sankyo, Takeda Pharmaceutical, Hisamitsu Pharmaceutical, Otsuka Pharmaceutical, TaishoToyama Pharmaceutical, Kaken Pharmaceutical, Eisai, Janssen Pharmaceutical, Bristol-Myers Squibb, AbbVie, Chugai Pharmaceutical, Mitsubishi Tanabe Pharmaceutical, Astellas Pharma, and Pfizer Japan, Speakers bureau: Daiichi Sankyo, Takeda Pharmaceutical, Hisamitsu Pharmaceutical, Otsuka Pharmaceutical, Taisho Toyama Pharmaceutical, Kaken Pharmaceutical, Eisai, Janssen Pharmaceutical, Bristol-Myers Squibb, AbbVie, Chugai Pharmaceutical, Mitsubishi Tanabe Pharmaceutical, Astellas Pharma, and Pfizer Japan.