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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.<\/jats:p>\n                <jats:p>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.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>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\u2122 Dysbiosis Test was used, grading gut microbiota aberrations on a 1-5 scale, where \u22653 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).<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>Gut dysbiosis was more frequent in AS than controls (36% versus 17%, <jats:italic>p<\/jats:italic>=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\u20130.9); BASDAI 1.6 (0.8\u20132.4); evaluator\u2019s global disease activity assessment (Likert scale 0\u20134) 0.3 (0.1\u20130.5), BASFI 1.5 (0.6\u20132.4), and VAS pain (cm) 1.3 (0.4\u20132.2). Differences remained significant after adjustment for demographics, lifestyle factors, treatments, gut inflammation (fecal calprotectin \u226550 mg\/kg), and gut symptoms, except for VAS pain. BASMI and CRP were not associated with dysbiosis.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>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.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s13075-022-02733-w","type":"journal-article","created":{"date-parts":[[2022,2,12]],"date-time":"2022-02-12T07:02:43Z","timestamp":1644649363000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":27,"title":["Gut dysbiosis associated with worse disease activity and physical function in axial spondyloarthritis"],"prefix":"10.1186","volume":"24","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7227-0665","authenticated-orcid":false,"given":"Jonas","family":"Sagard","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tor","family":"Olofsson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elisabeth","family":"Mogard","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jan","family":"Marsal","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristofer","family":"Andr\u00e9asson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mats","family":"Geijer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lars Erik","family":"Kristensen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elisabet","family":"Lindqvist","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johan K.","family":"Wallman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2022,2,12]]},"reference":[{"key":"2733_CR1","doi-asserted-by":"publisher","first-page":"65","DOI":"10.1136\/annrheumdis-2013-203582","volume":"74","author":"C Stolwijk","year":"2015","unstructured":"Stolwijk C, van Tubergen A, Castillo-Ortiz JD, Boonen A. 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Oral and written informed consent was acquired from all patients and controls before entry into the study, which was performed in accordance with the Helsinki Declaration.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethics approval and consent to participate"}},{"value":"Not applicable.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent for publication"}},{"value":"JS: None declared. TO: Consultant of Eli Lilly, Merck Sharp & Dohme. EM: Consultant of Novartis. JM: Speakers bureau of AbbVie, Bristol-Myers Squibb, Ferring, Janssen Pharmaceuticals, Pfizer, Takeda, Tillotts; Consultant of AbbVie, Janssen Pharmaceuticals, Pfizer, Takeda; Grant\/research support from AbbVie, Ferring, Pfizer, Takeda. KA: None declared. MG: Speakers bureau of AbbVie, Novartis, Pfizer, UCB Pharma. LEK: Speakers bureau of AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Eli Lilly, Janssen Pharmaceuticals, Merck Sharp & Dohme, Novartis, Pfizer, UCB Pharma; Consultant of AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Eli Lilly, Janssen Pharmaceuticals, Merck Sharp & Dohme, Novartis, Pfizer, UCB Pharma; EL: None declared. JKW: Consultant of AbbVie, Amgen, Celgene, Eli Lilly, Novartis.","order":4,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"42"}}