<b>Radiographic sacroiliitis progression in axial spondyloarthritis: central reading of 5</b> <b>year follow-up data from the Assessment of SpondyloArthritis international Society cohort</b>

Low but still detectable progression of radiographic sacroiliitis is observed in patients with axial spondyloarthritis. Dear Editor, In a previous analysis performed using the Assessment of SpondyloArthritis international Society (ASAS) cohort [1] and based on the local reading of radiographs, a total of 35 of 125 (28%) patients with axial SpA (axSpA) changed from modified New York criteria (mNY) negative to mNY positive after a mean of 4.6 years, while 11 (8.8%) changed in the opposite direction, resulting in a net percentage of progression of 19.2% [2]. There is often a substantial discrepancy between the heterogeneous local and more homogeneous central assessment of radiographic sacroiliitis [3]. In the present work we analysed radiographic progression in the SI joints in patients with axSpA included in the ASAS cohort, based on the central reading of conventional pelvic radiographs. The study complies with the Declaration of Helsinki. It was approved by the ethics committee of the Charité-Universitätsmedizin Berlin and by local ethics committees of the participating centres. All patients gave written informed consent before any study-related procedures. A detailed description of the ASAS cohort has been reported elsewhere [1]. In the analysis of radiographic sacroiliitis progression, we included a total of 106 patients diagnosed with axSpA with pelvic radiographs from baseline and follow-up (after a mean of 4.4 years) available for the central reading. The baseline characteristics of this subgroup were comparable to the entire group of 445 patients with axSpA in this cohort. The baseline characteristics of the included patients and treatment during the follow-up are shown in Supplementary Table S1, available at Rheumatology online. Pelvic radiographs were scored independently by two trained central readers (M.P., F.P.), blinded to the chronology of the radiographs and clinical information, according to the mNY scoring system (grade 0–4 for each SIJ). Patients with bilateral sacroiliitis grade ≥2 or unilateral grade ≥3 were classified as radiographic axSpA (r-axSpA) and if not as non-radiographic axSpA (nr-axSpA). In case of disagreement in the classification (nr-axSpA or r-axSpA) between the two primary readers, the image was scored by a third reader (D.P.) who defined the final classification. A sacroiliitis sum score (SSS) was calculated as the sum of mean sacroiliitis grades for the left and right SI joints derived from two or three reads, giving a total range of 0–8 [4]. Based on the central reading, 57 (53.8%) and 59 (55.7%) patients were classified as r-axSpA at baseline and follow-up, respectively. There was poor agreement between the local and central classification at baseline [κ = 0.18 (95% CI 0.08, 0.27)] and moderate agreement at follow-up [κ = 0.58 (95% CI 0.73, 0.44)]. The agreement between both primary central readers was moderate at both time points [κ = 0.61 (95% CI 0.46, 0.79) and 0.69 (95% CI 0.55, 0.83) for baseline and follow-up, respectively]. A total of 8 of 49 patients (16.3%) with nr-axSpA at baseline were classified as r-axSpA at follow-up, while 6 of 57 patients (10.5%) were reclassified from r-axSpA to nr-axSpA (Fig. 1). The net progression rate [5] was therefore (8 − 6)/106 = 0.019 (1.9%). The analysis of the SSS also revealed more progression than regression. The mean SSS increased from 3.8 (s.d. 1.8) at baseline to 4.0 (s.d. 1.8) at follow-up, giving a mean progression of 0.2. An increase (Δ >0) of the SSS was observed in 43 (40.6%) patients and a decrease (Δ <0) in 21 (19.8%) patients (Fig. 1), giving a net progression rate of (43 − 21)/106 = 0.208 (20.8%). Progression of radiographic sacroiliitis in the ASAS cohort Progression of radiographic sacroiliitis in the ASAS cohort In the univariable logistic regression analysis, the presence of definite radiographic sacroiliitis (classification as r-axSpA) at follow-up was associated with male sex, younger age at baseline, HLA-B27 positivity, the presence of inflammatory back pain according to the ASAS definition [6] at baseline and active inflammatory and structural changes on MRI of the SI joints at baseline (MRI assessment is described elsewhere [7]). In the multivariable logistic regression analysis, all mentioned parameters but sex remained significantly associated with the r-axSpA classification at follow-up (Supplementary Table S2, available at Rheumatology online). Of note, C-reactive protein levels were not associated with the r-axSpA classification at follow-up, although it was previously shown to be associated with a higher chance of spinal radiographic progression [8]. In conclusion, the central analysis of sacroiliac radiographs of the ASAS cohort showed a rather low, yet detectable progression signal of radiographic sacroiliitis after 4.4 years of follow-up, with a net progression of 1.9% for the progression from nr-axSpA to r-axSpA, 0.2 grades worsening of the mean SSS and a net progression of 20.8% for SSS. Younger age at baseline, HLA-B27 positivity, the presence of inflammatory back pain at baseline and active inflammatory and structural changes on MRIs of the SI joints were associated with a classification of r-axSpA at follow-up. We would like to thank the following investigators who included patients in the ASAS cohort: N. Akkoc, Izmir, Turkey; J. Brandt, Berlin, Germany; F. Heldmann and J. Braun, Herne, Germany; E. Collantes-Estevez, Cordóba, Spain; C.-T. Chou, Taipei, Taiwan; J. Darmawan, Semarang, Indonesia; C. Hudry and M. Dougados, Paris, France; T. Duruöz, Manisa, Turkey; O. Fitzgerald, Dublin, Ireland; J. Gu, Guangzhou, China; F. Huang, Beijing, China; Y. Kirazli, Izmir, Turkey; R. Landewé and D. van der Heijde, Maastricht, The Netherlands; A. Linnssen, Ijmuiden, The Netherlands; W. Maksymowych, Edmonton, Alberta, Canada; M. Matucci-Cerinic, Firenze, Italy; F. van den Bosch and H. Mielants, Ghent, Belgium; M. Østergaard, Hvidovre, Denmark; S. Ozgocmen, Elazig, Turkey; M. Rudwaleit and J. Sieper, Berlin, Germany; E. Roussou, London, UK; C. Naclerio and S. Scarpato, Scafati, Italy; I.J. Sørensen, Copenhagen, Denmark; R. Valle-Oňate, Bogotá, Colombia; U. Weber, Balgrist, Switzerland; and J. Wei, Taichung, Taiwan. We would also like to thank the readers assessing the MRIs of the SIJs within the MRImagine project: W. Maksymowych, Edmonton, Alberta, Canada; U. Weber, Sønderborg, Denmark; P. Machado, London, UK; S.J. Pedersen, Copenhagen, Denmark; X. Baraliakos, Herne, Germany; M. Østergaard, Copenhagen, Denmark; and R. Lambert, Edmonton, Alberta, Canada. All authors contributed to acquisition, analysis and interpretation of the data and drafting the manuscript. Funding: This work was supported by the ASAS. The research project was supported by a 2016 ASAS Research Internship Grant (to M.P.). Disclosure statement: M.P. has received speaker and consulting fees from AbbVie and Novartis. F.P. has received research grants from Novartis and speaker and consulting fees from AbbVie, Amgen, Bristol-Myers Squibb, MSD, Novartis, Pfizer, Roche and UCB Pharma. A.S. has received speaker and consulting fees from Novartis and UCB. R.L. is the Director of Rheumatology Consultancy and has received speaker and consulting fees from AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly, Galapagos, Gilead, GlaxoSmithKline, Janssen, Merck, Novartis, Pfizer, Roche and UCB Pharma. D.v.d.H. is the Director of Imaging Rheumatology and has received speaker and consulting fees from AbbVie, Amgen, Astellas, AstraZeneca, Bristol-Myers Squibb, Boehringer Ingelheim, Celgene, Daiichi, Eli Lilly, Galapagos, Gilead, GlaxoSmithKline, Janssen, Merck, Novartis, Pfizer, Regeneron, Roche, Sanofi, Takeda and UCB Pharma. W.P.M. has received speaker and consulting fees from AbbVie, Boehringer Ingelheim, Celgene, Galapagos, Janssen, Eli Lilly, Novartis, Pfizer and UCB Pharma and research and/or educational grants from AbbVie, Novartis and Pfizer. X.B. has received research grants from AbbVie, MSD and Novartis and speaker and consulting fees from AbbVie, Bristol-Myers Squibb, Celgene, Chugai, Janssen, MSD, Novartis, Pfizer and UCB Pharma. J.S. has received speaker and consulting fees from AbbVie, Boehringer Ingelheim, Eli Lilly, Janssen, Merck, Novartis, Pfizer, Roche and UCB Pharma. M.R. has received speaker and consulting fees from AbbVie, Bristol-Myers Squibb, Celgene, Chugai/Roche, Janssen, Eli Lilly, MSD, Novartis, Pfizer and UCB Pharma. D.P. has received research grants from AbbVie, MSD, Novartis and Pfizer and speaker and consulting fees from AbbVie, BIOCAD, Bristol-Myers Squibb, Eli Lilly, Gilead, MSD, Novartis, Pfizer, Roche and UCB Pharma. The data underlying this article are available from the corresponding author on reasonable request. Supplementary data are available at Rheumatology online.

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