FRI0385 LONG-TERM CERTOLIZUMAB PEGOL TREATMENT OF AXIAL SPONDYLOARTHRITIS IS ASSOCIATED WITH RAPID AND SUSTAINED REDUCTION OF ACTIVE INFLAMMATION AND MINIMAL STRUCTURAL CHANGES IN THE SPINE: 4-YEAR MRI RESULTS FROM RAPID-AXSPA. (June 2019)

• Record Type: Journal Article
• Authors: Baraliakos, Xenofon; Kruse, Sebastian; Auteri, Simone; Peyrecave, Natasha de; Nurminen, Tommi; Kumke, Thomas; Hoepken, Bengt; Braun, Juergen
• Is Part Of: Annals of the rheumatic diseases. Volume 78(2019)Supplement 2
• Page Start: 876
• Page End: 877
• Publication Date: 2019-06
• Subjects: Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2019-eular.689
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Background: In patients (pts) with axial spondyloarthritis (axSpA), inflammation of the spine is believed to trigger a repair mechanism that results in syndesmophyte formation. 1 Fatty lesions (FLs) in the bone marrow and erosions in the axial skeleton, both visible on magnetic resonance imaging (MRI) T1 sequences, are post–inflammatory changes that have been shown to contribute significantly to models predicting new bone formation. 2 It has previously been shown that resolution of inflammatory lesions (INFLs) in pts with axSpA treated with anti–TNF therapy may be associated with an increase in FLs. 3, 4 RAPID–axSpA was a long–term study in pts with radiographic (r)–axSpA (also known as ankylosing spondylitis) or non–radiographic (nr)–axSpA treated with certolizumab pegol (CZP), which rapidly suppressed active inflammation of the spine, with pts showing limited spinal radiographic progression over 4 years. 5 However, it is not known whether CZP treatment coincides with changes in FLs, sclerosis, and erosions. Objectives: To report the incidence and association of active inflammation and chronic lesions in the spine of pts with axSpA treated with CZP over 4 years Methods: RAPID–axSpA (NCT01087762 ) was double–blind and placebo (PBO)–controlled to Week (Wk)24, dose–blind to Wk48, and open–label to Wk204. CZP–randomised pts (either 200mg every 2 weeks [Q2W] or 400 mg Q4W) continued their assigned dose throughout; PBO–randomised pts received CZP from Wk24, or if non–responders, from Wk16 onwards. Blinded spinal MRI scans at baseline (BL) and Wk12, 48, 96, and 204 were assessed by 2 central readers to evaluate the presence/absence of active INFLs (Short T1 Inversion Recovery [STIR] sequence) and FLs, sclerosis and erosions (T1 sequence) in vertebral edges (VEs) (present if recorded so by both readers). Pts (r–axSpA and nr–axSpA combined) with valid assessments at BL and at least once post–BL were included. Mean lesion counts at the pt level were estimated from mixed models with repeated measures (MMRM), fitted on observed data from CZP–randomised pts. Associations between INFLs and FLs at the VE level for CZP–and PBO–randomised pts were described using cross–tabulations. Results: Of 325 randomised pts, 136 were eligible for these analyses. In pts randomised to CZP at Wk0 (n=89), active INFLs were reduced, and FL counts only slightly increased by Wk12; both were sustained at a low level to Wk204 (Table A ). Very few VEs with sclerosis and erosions were observed at BL, and no changes in their frequency were observed over 4 years' treatment (Table A ). Over 4 years' CZP treatment, the risk of developing a new FL was greater in VEs with vs without INFLs at BL, regardless of changes to INFLs in these VEs post–BL (Table B ). The prevalence of FLs was greater in pts with >3 vs ≤3 years' symptom duration and there were more new FLs in the >3 years subgroup during CZP treatment (data not shown) Conclusion: Long–term CZP treatment in axSpA pts was associated with rapid and sustained reduction in active inflammation and a negligible increase in FLs in VEs. More FLs developed in VEs with INFLs at BL than without, but this was not affected by resolution of INFLs. There was no increase in sclerosis and erosions in VEs over 4 years' CZP treatment. Reference: [1] Appel H. Curr Rheumatol Rep2008;10:356–63; 2. Poddubnyy D. Arthritis Rheum 2016;68:1899–903; 3. Maksymowych W. Ann Rheum Dis 2013;72:23–8; 4. Song I. Ann Rheum Dis 2011;70:1257–63; 5. van der Heijde D. Ann Rheum Dis2018;77:699–705. Acknowledgement: We thank the patients who participated. This study was funded by UCB Pharma, medical writing by Hinal Tanna, Costello Medical, UK. Disclosure of Interests: Xenofon Baraliakos Grant/research support from: AbbVie, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Centocor, Chugai, Janssen, MSD, Novartis, Pfizer Inc, Roche and UCB, Grant/research support from: AbbVie, Pfizer, Merck Sharp & Dohme, UCB Pharma, Novartis, Consultant for: AbbVie, Bristol-Myers Squibb, Boehringer Ingelheim, Celgene, Chugai, Janssen Biologics, Novartis, Pfizer, UCB Pharma, Galapagos, Speakers bureau: AbbVie, Chugai, Janssen, Novartis, Pfizer, UCB Pharma, Sebastian Kruse: None declared, Simone Auteri Employee of: Employee of UCB Pharma, Natasha de Peyrecave Employee of: Employee of UCB Pharma, Tommi Nurminen Employee of: Employee of UCB Pharma, Thomas Kumke Employee of: UCB Pharma, Bengt Hoepken Employee of: Employee of UCB Pharma, Juergen Braun Shareholder of: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB, Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB, Grant/research support from: Abbott, Bristol Myers Squibb, Celgene, Celltrion, Chugai, Johnson & Johnson, MSD, Novartis, Pfizer, Roche, UCB Pharma, Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB, Grant/research support from: Abbvie (Abbott), Amgen, Baxter, Biogen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, Hexal, Janssen, Lilly, Medac, MSD (Schering-Plough), Mylan, Mundipharma, Novartis, Pfizer (Wyeth, Hospira), Roche, Sanofi-Aventis and UCB, Consultant for: Abbvie (Abbott), Amgen, Baxter, Biogen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, Hexal, Janssen, Lilly, Medac, MSD (Schering-Plough), Mylan, Mundipharma, Novartis, Pfizer (Wyeth, Hospira), Roche, Sanofi-Aventis and UCB, Consultant for: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB, Consultant for: Abbott, Bristol Myers Squibb, Celgene, Celltrion, Chugai, Johnson & Johnson, MSD, Novartis, Pfizer, Roche, UCB Pharma, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB, Speakers bureau: Abbvie (Abbott), Amgen, Baxter, Biogen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, Hexal, Janssen, Lilly, Medac, MSD (Schering-Plough), Mylan, Mundipharma, Novartis, Pfizer (Wyeth, Hospira), Roche, Sanofi-Aventis and UCB, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB