POS0011 FACTORS ASSOCIATED WITH THE EVOLUTION OF DEGENERATIVE SPINAL LESIONS IN AXIAL SPONDYLOARTHRITIS: 10-YEAR FOLLOW-UP OF THE DESIR COHORT
Authors: L. Pina Vegas, S. Ramiro, M. Van Lunteren, D. Loeuille, E. Newsum, C. Morizot, F. A. Van Gaalen, A. Saraux, P. Claudepierre, A. Feydy, D. Van der Heijde, M. Reijnierse
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> Radiographs and magnetic resonance imaging (MRI) are both used to screen for and diagnose axial spondyloarthritis (axSpA) but they also provide information about morphological and even biomechanical changes in the spinal components. The natural course of degenerative changes in the spine over a long period of observation has not been established in a large group of patients with axSpA. Moreover, it is not well-known which factors are associated with faster progression. <h3>Objectives:</h3> To investigate the evolution of degenerative spinal lesions in patients with axSpA over 10 years (10Y) of follow-up and the factors associated with progression. <h3>Methods:</h3> Whole spine MRI and cervical and lumbar spine radiographs at baseline, 2Y, 5Y and 10Y of patients diagnosed with axSpA in the DESIR cohort were assessed for degenerative lesions by 3 central readers blinded to timepoint and to clinical or any other imaging information[1]. All patients with degenerative lesions assessed at least at one time point were included. Degenerative lesions were defined at patient level and, for descriptive purposes, in consensus across central readers (≥2 out of 3 readers or average, as appropriate). To assess progression of degenerative lesions of both imaging modalities (disc height loss, osteophytes, sclerosis, disc degeneration [Pfirrmann &gt;2], high-intensity zone [HIZ], central and lateral/ neuroforaminal canal stenosis, disc protrusion or extrusion, Modic type I, II or III, facet joint osteoarthritis [FJOA], spondylolisthesis, Schmorl's node, Scheuermann's disease and total number of degenerative lesions per patient) over time, we used multilevel generalised estimating equation (GEE) models considering individual reader data and exchangeable working correlation structure to handle repeated observations over time for each degenerative lesion. The main variable of interest was time to reflect the 10Y progression of each lesion. Models were adjusted for sex, HLA-B27 status, body mass index (BMI), smoking (ever vs never) and job type (retired/no professional activity, white or blue collar) at baseline and biological disease-modifying antirheumatic drugs (bDMARDs) exposure (ever vs never) during the 10Y period. Odds ratios (OR) and 95% confidence intervals (95%CI) were reported for dichotomous outcomes and β coefficients and 95%CI for continuous outcomes. <h3>Results:</h3> Degenerative lesions on radiographs were available at at least one time point for 329 patients (34.5 [SD 8.6] years; 47% men) and on MRI for 327 patients (33.9 [8.6] years; 47% men). There was a mean of 1.6 (2.5) degenerative lesions per patient at baseline on radiographs; this number increased to 3.4 (3.9) at 10Y. On MRI, there was a mean of 7.5 (5.5) degenerative lesions per patient at baseline and 11.0 (7.1) at 10Y. A statistically significant progression, but with a very small effect size, was detected on radiographs over 10Y for disc height loss (adjusted OR=1.15, 95%CI 1.10-1.20), osteophytes (1.26, 1.21-1.32), sclerosis (1.08, 1.05-1.10) and FJOA (1.14, 1.09-1.18). The same trend in progression over 10Y was detected on MRI for disc degeneration (1.09, 1.07-1.12), HIZ (1.05, 1.04-1.14), central (1.02, 1.01-1.02) and lateral/neuroforaminal (1.03, 1.01-1.04) canal stenosis, disc protrusion (1.12, 1.07-1.17), disc extrusion (1.07, 1.04-1.10), Modic type I (1.11, 1.07-1.14) and type II (1.10, 1.07-1.13) (Table 1). We observed a statistically significant increase in the number of degenerative lesions on radiographs (β=1.81, 95%CI 1.48-2.14) and MRI (4.17, 3.49-4.84). Other factors associated with the increasing number of degenerative lesions over time in both imaging modalities were increasing BMI (0.15, 0.12-0.19 on radiographs; 0.35, 0.27-0.44 on MRI) and bDMARDs exposure (0.39, 0.13-0.66 on radiographs; 0.95, 0.34-1.55 on MRI) (Table 2). <h3>Conclusion:</h3> In an inception cohort of axSpA, degenerative spinal lesions, though common, progress very slowly over 10Y, both on radiographs and MRI. However, this progression appears to be faster in patients with a higher BMI and those exposed to bDMARDs, which likely indicates a more severe form of axSpA. <h3>REFERENCES:</h3> [1] de Bruin F <i>et al. RMD Open</i>. 2018;4(1):e000657. <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> Laura Pina Vegas: None declared, Sofia Ramiro: research grants and/or consulting fees from AbbVie, Eli Lilly, Galapagos, Janssen, MSD, Novartis, Pfizer, UCB, Sanofi, Miranda van Lunteren: None declared, Damien Loeuille: None declared, Esther Newsum: None declared, Caroline Morizot: None declared, F. A. van Gaalen: grant and/or consulting fees from, Abbvie, ASAS, BMS, Galapagos, Janssen, Lilly, Novartis, Pfizer, UCB, Alain Saraux: None declared, PASCAL CLAUDEPIERRE: consulting fees from AbbVie, Amgen, Biogen, Celltrion, Galapagos, Janssen, Lilly, MSD, Novartis, Pfizer and UCB (less than US$10 000 each); investigator for Abbvie, Janssen, Lilly, MSD, Novartis and Pfizer, Antoine Feydy: None declared, Désirée van der Heijde: consulting fees AbbVie, BMS, Galapagos, Glaxo-Smith-Kline, Janssen, Lilly, Novartis, Pfizer, Takeda UCB Pharma; director of Imaging Rheumatology bv, Monique Reijnierse: ASAS consultant; ISS research grant.