Sustained low disease activity measured by ASDAS slow radiographic spinal progression in axial spondyloarthritis patients treated with TNF-inhibitors: data from REGISPONSERBIO

Abstract

Background To evaluate the influence of the disease activity on radiographic progression in axial spondyloarthritis (axSpA) patients treated with TNF inhibitors (TNFi). Methods The study included 101 axSpA patients from the Spanish Register of Biological Therapy in Spondyloarthritides (REGISPONSERBIO), which had clinical data and radiographic assessment available. Patients were classified into 2 groups based on the duration of TNFi treatment at baseline: (i) long-term treatment (≥4 years) and (ii) no long-term treatment (< 4 years). Radiographs were scored by two readers according to the modified Stoke Ankylosing Spondylitis Spine Score (mSASSS) with known chronology. Disease activity differences between patients’ groups at each time point were assessed using a linear mixed-effect model. Results Radiographic progression was defined as an increase in ≥2 mSASSS units. At inclusion, approximately half of the patients (45.5%) were receiving long-term treatment with TNFi (≥4 years). In this group of subjects, a significant difference in averaged Ankylosing Spondylitis disease Activity Score (ASDAS) across follow-up was found between progressors and non-progressors (2.33 vs 1.76, p=0.027, respectively). In patients not under long-term TNFi treatment (54.5%) though, no significant ASDAS differences were observed between progressors and non-progressors until the third year of follow-up. Furthermore, no significant differences were found in progression status, when disease activity was measured by Bath Ankylosing spondylitis Disease Activity Index (BASDAI) and C reactive protein (CRP). Conclusions Patients on long-term TNFi treatment with a mean sustained low disease activity measures by ASDAS presented lower radiographic progression than those with active disease.

The roles of Single Nucleotide Polymorphism (SNP) Endoplasmic Reticulum Aminopeptidase 1 (ERAP 1) gene in axial spondyloarthritis Indonesian adults

“…The normal section is given a value of 0. If erosion, sclerosis, or squaring is found, it is given a value of 1, the presence of syndesmophyte is given a value of 2, and the presence of complete bridging is given a value of 3 with a value range of 0–72 [ 8 , 17 ]. Measuring the mSASSS score was carried out based on lumbosacral and cervical radiology with two rheumatologists with inter-observer assessment (Kappa test = 86%) [ 8 , 18 ].…”

Disease modification in axial spondyloarthritis – still a controversy?

“…However, these studies do not give a conclusive answer, as there are methodological issues in several of these studies [37]. Interestingly, it was confirmed that reduction in structural progression was mediated by reduction in ASDAS [15,17,38].…”

“…In addition, both inflammatory and structural lesions in the axial skeleton are associated with decreased functional status and restricted spinal mobility, affecting daily activities of patients with axSpA [12,13]. Moreover, literature showed that disease activity measured by Axial Spondyloarthritis Disease Activity Score (ASDAS), but not by Bath Ankylosing Spondylitis Disease Activity Index or C reactive protein alone, is longitudinally associated with progression of radiographic spinal progression [14][15][16][17]. Naturally disease-modifying interventions in axSpA concentrate on preventing deterioration in the factors associated with this structural progression paradigm.…”

Bone Involvement in Rheumatoid Arthritis and Spondyloartritis: An Updated Review

“…Therefore, while some studies suggest the existence of a coupling between inflammation-and disease activity-and new bone formation in patients with AS [196][197][198], others demonstrate that ossification progresses independently from the suppression of inflammation involving adjacent but distinct sites [199,200]. Moreover, most findings from clinical trials show less bone formation in patients with axSpA treated with bDMARDs whose disease is well controlled by the therapy, suggesting that new bone formation in the context of a clinically controlled disease could be explained by a subclinical, persistent, non-detectable joint inflammation [201,202].…”