Abstract
Background: Based on clinical and genetic associations, axial spondyloarthritis (axSpA) and inflammatory bowel disease (IBD) are suspected to have a linked pathogenesis. Gut dysbiosis, intrinsic to IBD, has also been observed in axSpA. It is, however, not established to what degree gut dysbiosis is associated with axSpA disease severity. The objective of this study was to compare gut dysbiosis frequency between controls, non-radiographic axial spondyloarthritis (nr-axSpA), and ankylosing spondylitis (AS) patients and investigate whether gut dysbiosis is cross-sectionally associated with axSpA disease activity, physical function, mobility, or pain. Methods: Gut dysbiosis was assessed by 16SrRNA analysis of feces from 44/88 nr-axSpA/AS patients (ASAS/mNY criteria) without inflammatory bowel disease (IBD) and 46 controls without IBD or rheumatic disease. The GA-map™ Dysbiosis Test was used, grading gut microbiota aberrations on a 1-5 scale, where ≥3 denotes dysbiosis. Proportions with dysbiosis were compared between the groups. Furthermore, standard axSpA measures of disease activity, function, mobility, and pain were compared between patients (nr-axSpA and AS combined) with and without dysbiosis, univariately, and adjusted for relevant confounders (ANCOVA). Results: Gut dysbiosis was more frequent in AS than controls (36% versus 17%, p=0.023), while nr-axSpA (25% dysbiosis) did not differ significantly from either AS or controls. Univariately, most axSpA measures were significantly worse in patients with dysbiosis versus those without: ASDAS-CRP between-group difference 0.6 (95% CI 0.2–0.9); BASDAI 1.6 (0.8–2.4); evaluator’s global disease activity assessment (Likert scale 0–4) 0.3 (0.1–0.5), BASFI 1.5 (0.6–2.4), and VAS pain (cm) 1.3 (0.4–2.2). Differences remained significant after adjustment for demographics, lifestyle factors, treatments, gut inflammation (fecal calprotectin ≥50 mg/kg), and gut symptoms, except for VAS pain. BASMI and CRP were not associated with dysbiosis. Conclusion: Gut dysbiosis, more frequent in AS patients than controls, is associated with worse axSpA disease activity and physical function, seemingly irrespective of both gut inflammation and treatments. This provides further evidence for an important link between disturbances in gastrointestinal homeostasis and axSpA.
| Originalsprog | Engelsk |
|---|---|
| Artikelnummer | 42 |
| Tidsskrift | Arthritis Research and Therapy |
| Vol/bind | 24 |
| Udgave nummer | 1 |
| Antal sider | 14 |
| ISSN | 1478-6354 |
| DOI | |
| Status | Udgivet - 2022 |
Bibliografisk note
Funding Information:Open access funding provided by Lund University. This study was supported by unrestricted grants from Skåne University Hospital, the Swedish Rheumatism Association, the Anna-Greta Crafoord Foundation, the Kock Foundation, The Österlund Foundation, the Nanna Svartz Foundation, and the Lundgren Foundation. Funding from the Hedlund Foundation and the Österlund Foundation contributed to financing JM’s research time. TO, JM, KA, and JKW received grants from the Swedish government to researchers in public health care (ALF). The sponsors had no role in study design, data collection, data analysis, data interpretation, or writing of the report.
Publisher Copyright:
© 2022, The Author(s).