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Gut dysbiosis associated with worse disease activity and physical function in axial spondyloarthritis

Sagard, Jonas (författare)
Lund University,Lunds universitet,Reumatologi och molekylär skelettbiologi,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Rheumatology,Section III,Department of Clinical Sciences, Lund,Faculty of Medicine,Skåne University Hospital
Olofsson, Tor (författare)
Lund University,Lunds universitet,Tillämpad epidemiologi,Forskargrupper vid Lunds universitet,Lund Arthritis Research Group (LARG),Applied epidemiology,Lund University Research Groups,Skåne University Hospital
Mogard, Elisabeth (författare)
Lund University,Lunds universitet,Reumatologi och molekylär skelettbiologi,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Rheumatology,Section III,Department of Clinical Sciences, Lund,Faculty of Medicine,Skåne University Hospital
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Marsal, Jan (författare)
Lund University,Lunds universitet,Adaptivt immunförsvar,Forskargrupper vid Lunds universitet,Gastro,Adaptive Immunity,Lund University Research Groups,Skåne University Hospital
Andréasson, Kristofer (författare)
Lund University,Lunds universitet,Forskargruppen för systemisk skleros, Lund,Forskargrupper vid Lunds universitet,Lund Systemic Sclerosis Research Group,Lund University Research Groups,Skåne University Hospital
Geijer, Mats, 1957 (författare)
University of Gothenburg,Lund University,Lunds universitet,Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper, Avdelningen för radiologi,Institute of Clinical Sciences, Department of Radiology,Diagnostisk radiologi, Lund,Sektion V,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Diagnostic Radiology, (Lund),Section V,Department of Clinical Sciences, Lund,Faculty of Medicine,Sahlgrenska University Hospital
Kristensen, Lars Erik (författare)
Lund University,Lunds universitet,Reumatologi och molekylär skelettbiologi,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Rheumatology,Section III,Department of Clinical Sciences, Lund,Faculty of Medicine,Copenhagen University Hospital
Lindqvist, Elisabet (författare)
Lund University,Lunds universitet,Lund Arthritis Research Group (LARG),Forskargrupper vid Lunds universitet,Lund University Research Groups,Skåne University Hospital
Wallman, Johan K (författare)
Lund University,Lunds universitet,Lund Arthritis Research Group (LARG),Forskargrupper vid Lunds universitet,Lund University Research Groups,Skåne University Hospital
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 (creator_code:org_t)
2022-02-12
2022
Engelska.
Ingår i: Arthritis Research & Therapy. - : Springer Science and Business Media LLC. - 1478-6354 .- 1478-6362. ; 24:1
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • 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 (TM) 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.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Reumatologi och inflammation (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Rheumatology and Autoimmunity (hsv//eng)

Nyckelord

Spondyloarthritis
Ankylosing spondylitis (AS)
Non-radiographic axial
spondyloarthritis (nr-axSpA)
Physical function
Microbiota
Disease
activity
Dysbiosis
Gut inflammation
Inflammatory bowel disease
ankylosing-spondylitis
classification criteria
bowel inflammation
fecal microbiota
back-pain
reveals
pathogenesis
genetics
Rheumatology
Axial Spondyloarthritis
Humans
Leukocyte L1 Antigen Complex
Spondylarthritis/diagnosis
Spondylitis, Ankylosing/diagnosis

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