ObjectivesTumour necrosis factor inhibitors (TNFis) have been suggested to slow radiographic progression in patients with ankylosing spondylitis. However, limitations such as variations in disease activity, complex drug administration and short follow-up duration make it difficult to determine the effect of TNFis on radiographic progression. The aim of the study was to investigate whether long-term treatment with TNFis can reduce radiographic progression in patients with ankylosing spondylitis using 18-year longitudinal real-world data.MethodsThis retrospective study was conducted between January 2001 and December 2018 at a single centre. Among the 1280 patients whose electronic medical records were reviewed, data of 595 patients exposed to TNFis at least once were included. Among them, time intervals of TNFi exposure or non-exposure were determined in 338 patients (‘on the TNFis’ or ‘off the TNFis’ intervals, respectively). The difference in the modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS) change rate between ‘on the TNFis’ and ‘off the TNFis’ intervals was investigated.ResultsWe obtained 2364 intervals of 338 patients (1281 ‘on the TNFis’ and 1083 ‘off the TNFis’ intervals). In the marginal structural model for inverse probability of treatment weighting, the change rate of mSASSS significantly decreased with the use of TNFis (β=−0.112, p=0.004), and the adjusted mSASSS changes were 0.848 and 0.960 per year during ‘on the TNFis’ and ‘off the TNFis’ intervals, respectively.ConclusionCompared with treatment without TNFis, treatment with TNFis slowed radiologic progression significantly.
Aim: This study investigated the use of fat fraction (FF) measurements in the sacroiliac (SI) joint to determine radiologic progression in patients with spondyloarthritis (SpA). Method:A total of 138 patients who underwent pelvic magnetic resonance imaging (MRI) between September 2014 and March 2015 were retrospectively evaluated.The FF based upon fat deposition (%) using fat signaling on T1 and T2 weighted images in the sacroiliac joint was quantified using a 6-echo variant of the modified Dixon technique. We defined the normal bone marrow as normal FF, bone marrow edema as active inflammatory FF, and fat metaplasia as post-inflammatory FF. Results:The mean FF of normal marrow was 52.0% ± 10.4% and 50.5% ± 10.1% in the left and right SI joints, respectively. The mean FF of post-inflammatory fat deposition was 81.9% ± 9.7% and 82.3% ± 9.6% in the left and right SI joints, respectively.The mean FF of active inflammatory fat deposition was 15.8% ± 5.9% and 13.5% ± 6.7% in the left and right SI joints, respectively. In multiple linear regression, post-inflammatory FF was found to be significantly associated with radiologic progression, such as symptom duration, SI joint grade, and modified Stoke Ankylosing Spondylitis Spine Score. Conclusion:Post-inflammatory FF indicates the chronicity of SpA. Evaluating FF using MRI in the SI joint will help to determine radiologic progression. K E Y W O R D S fat fraction, magnetic resonance imaging, modified Dixon, sacroiliac joint, spondyloarthritis S U PP O RTI N G I N FO R M ATI O N Additional supporting information may be found online in the Supporting Information section at the end of the article. How to cite this article: Koo BS, Song Y, Shin JH, Lee S, Kim T-H. Evaluation of disease chronicity by bone marrow fat fraction using sacroiliac joint magnetic resonance imaging in patients with spondyloarthritis: A retrospective study. Int J Rheum Dis. 2019;22:734-741. https://doi.
Objective To determine the relationship between inflammation and radiographic progression over time in patients with ankylosing spondylitis (AS) attaining a Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) of <4 during tumor necrosis factor inhibitor (TNFi) treatment. Methods Medical records data of patients with AS with BASDAI scores of <4 during TNFi treatment were analyzed at 6-month intervals from January 2001 to December 2018. To determine the relationship between the modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS) and C-reactive protein (CRP) over time, we fitted linear mixed models with mSASSS as the response variable, baseline mSASSS and the cumulative sum of CRP with different lag times (6, 12, 18, 24, 30, and 36 months) as fixed effects, and patients as random effects. Associations between mSASSS and the cumulative sum of CRP or the lag times with the highest beta coefficients were further investigated with linear mixed models that included additional clinical variables. Results A total of 2,956 intervals were obtained from 333 patients. Among different lag times, the cumulative sum of log CRP in the previous 18–36 months and mSASSS showed significant beta coefficients. In the final linear mixed model, the cumulative sum of log CRP in the previous 24 months was significantly associated with mSASSS at 24 months (β=0.043, 95% CI: 0.014–0.071, p=0.004). Conclusion Remnant inflammation correlates with radiographic progression even in patients attaining a BASDAI of <4 during TNFi treatment. CRP is a surrogate marker for radiographic progression despite clinical improvement with TNFi treatment.
Aim Predicting radiographic progression is vital for assessing the prognosis of patients with radiographic axial spondyloarthritis, and C‐reactive protein (CRP) may be a valuable biomarker for this purpose. This study aimed to investigate the relationship between changes in the CRP level and spinal radiographic progression in patients with radiographic axial spondyloarthritis who were initially treated with non‐biologics. Methods Patients with radiographic axial spondyloarthritis who were followed up for 18 years at a single center and initially treated with nonsteroidal anti‐inflammatory drugs and/or conventional disease‐modifying antirheumatic drugs for 3 months were included. Patients with a CRP level of <0.8 mg/dL or 50% of the baseline CRP at 3 months were assigned to the controlled CRP group (n = 351), and the remaining patients were assigned to the uncontrolled CRP group (n = 452). A generalized estimating equation was used to analyze the differences in the modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS) between the 2 groups. Results The increase in the mSASSS was slower in the controlled CRP group than in the uncontrolled CRP group (interaction term β = −.499, 95% confidence interval −0.699 to −0.300). Conclusion Controlled CRP achieved in response to initial treatment with non‐biologic agents for 3 months was significantly associated with a slower rate of spinal radiographic change in patients with radiographic axial spondyloarthritis. The CRP level at 3 months after initial non‐biologic treatment is a good predictor of radiographic progression.
ObjectivesTo identify clinical and genetic factors associated with severe radiographic damage in patients with ankylosing spondylitis (AS).MethodsWe newly generated genome-wide single nucleotide polymorphism data (833K) for 444 patients with AS. The severity of radiographic damage was assessed using the modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS). To identify clinical and genetic factors associated with severe radiographic damage, multiple linear regression analyses were performed. Human AS-osteoprogenitor and control-osteoprogenitor cells were used for functional validation.ResultsThe significant clinical factors of final mSASSS were baseline mSASSS (β=0.796, p=3.22×10−75), peripheral joint arthritis (β=−0.246, p=6.85×10−6), uveitis (β=0.157, p=1.95×10−3), and smoking (β=0.130, p=2.72×10−2) after adjusting for sex, age and disease duration. After adjusting significant clinical factors, theRyanodine receptor 3(RYR3) gene was associated with severe radiographic damage (p=1.00×10−6). For pathway analysis, the PI3K-Akt signalling pathway was associated with severe radiographic damage in AS (p=2.21×10−4, false discovery rate=0.040). Treatment with rhodamine B, a ligand of RYR3, dose-dependently induced matrix mineralisation of AS osteoprogenitors. However, the rhodamine B-induced accelerated matrix mineralisation was not definitive in control osteoprogenitors. Knockdown of RYR3 inhibited matrix mineralisation in SaOS2 cell lines.ConclusionsThis study identified clinical and genetic factors that contributed to better understanding of the pathogenesis and biology associated with radiographic damage in AS.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.