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Irritable bowel syndrome symptoms in axial spondyloarthritis more common than among healthy controls: is it an overlooked comorbidity?
  1. Johan Karlsson Wallman1,2,
  2. Elisabeth Mogard1,2,
  3. Jan Marsal3,4,
  4. Kristofer Andréasson1,2,
  5. Anna Jöud5,
  6. Mats Geijer6,7,
  7. Lars Erik Kristensen8,
  8. Elisabet Lindqvist1,2,
  9. Tor Olofsson1,2
  1. 1 Department of Clinical Sciences Lund, Rheumatology, Lund University, Lund, Sweden
  2. 2 Department of Rheumatology, Skåne University Hospital Lund, Lund, Sweden
  3. 3 Department of Clinical Sciences Lund, Gastroenterology, Lund University, Lund, Sweden
  4. 4 Department of Gastroenterology, Skåne University Hospital Lund, Lund, Sweden
  5. 5 Department of Laboratory Medicine, Division of Occupational and Environmental Medicine, Lund University, Lund, Sweden
  6. 6 Department of Radiology, Sahlgrenska University Hospital, Region Västra Götaland and Department of Radiology, Institute of Clinical Sciences, University of Gothenburg, Sahlgrenska Academy, Gothenburg, Sweden
  7. 7 Department of Clinical Sciences Lund, Diagnostic Radiology, Lund University, Lund, Sweden
  8. 8 Department of Rheumatology, Copenhagen University Hospital, Frederiksberg and Bispebjerg, Parker Institute, Copenhagen, Denmark
  1. Correspondence to Dr Johan Karlsson Wallman, Department of Rheumatology, Skåne University Hospital Lund, Lund 22185, Sweden; johan.81.karlsson{at}gmail.com

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The link between spondyloarthritis and inflammatory bowel disease (IBD) is well-established, with 5%–10% of patients with axial spondyloarthritis (axSpA) having concurrent IBD. Beyond that, ~50%–60% display microscopic gut inflammation,1 and faecal calprotectin (F-calprotectin) is elevated,2 although neither of these findings have been clearly linked to gut symptoms.1 2 Nevertheless, >50% of patients with ankylosing spondylitis (AS) report frequent gut pain/diarrhoea.3 This calls for investigating other potential causes, including irritable bowel syndrome (IBS), for which data in axSpA remain sparse. IBS (general population prevalence ~11%4) is thought to arise through mechanisms similar to fibromyalgia, common in axSpA (affecting up to 25% versus ~2% in the general population).

We aimed to compare the prevalence of gut symptoms meeting ROME III criteria for IBS between patients with axSpA and healthy controls.5 Hence, 182 consecutive patients with well-characterised axSpA without known IBD from the population-based SPARTAKUS study,2 and 50 controls, frequency-matched for sex/age, without rheumatic disease or IBD, were included (online supplementary table S1). For SPARTAKUS protocol/classification algorithm details, see online supplementary file 1.

Supplemental material

[annrheumdis-2019-216134supp001.pdf]

We found that gut symptoms meeting IBS criteria were significantly more frequent among patients with axSpA (30%) than controls (16%; OR: 2.5 (95% CI 1.1 to 5.7); p=0.036) by sex/age-adjusted logistic regression (figure 1A). Additional adjustments for F-calprotectin levels and non-steroidal anti-inflammatory drug (NSAID)-use, respectively, as well as excluding patients/controls reporting ‘alarm symptoms’ (frequent bloody/black stools; unexplained weight-loss), yielded similar OR-estimates for the patients/controls difference (online supplementary file 1).

Figure 1

Proportions of patients with axSpA and controls reporting gut symptoms …

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Footnotes

  • Handling editor Josef S Smolen

  • Contributors TO and JKW participated in study design, acquisition of data, analysis and interpretation of data and draft and revision of the manuscript. EM and EL participated in study design, acquisition and interpretation of data and revision of the manuscript. JM, KA, AJ, MG and LEK participated in study design, interpretation of data and revision of the manuscript. All authors read and approved the final manuscript.

  • Funding This study was supported by unrestricted grants from Skåne University Hospital, the Swedish Rheumatism Association, the Anna-Greta Crafoord Foundation, the Kock Foundation and the Lundgren Foundation. Funding from the Faculty of Medicine, Lund University, contributed to financing EM’s research time. Funding from the Hedlund Foundation and the Österlund Foundation contributed to financing JM’s research time. Grants to researchers in public healthcare from the Swedish government (ALF) contributed to financing JKW’s, JM’s, KA’s and TO’s research time.

  • Disclaimer The sponsors had no role in study design, data collection, data analysis, data interpretation or writing of the report.

  • Competing interests JKW has received consultancy fees from AbbVie, Celgene, Eli Lilly, Novartis and UCB Pharma (unrelated to the present work). JM has received investigator-initiated study funding from AbbVie, Ferring, Pfizer and Takeda and has served as a speaker, a consultant and/or an advisory board member for AbbVie, Ferring, Janssen-Cilag, Svar/EuroDiagnostica, Takeda and Tillotts (unrelated to the present work). MG has received consultancy fees from AbbVie, Novartis and Pfizer (unrelated to the present work). LEK has received consultancy and speaker’s bureau fees from AbbVie, Amgen, Biogen, Bristol-Myers Squibb (BMS), Celgene, Eli Lilly, Janssen Pharmaceuticals, Merck, Sharp & Dohme (MSD), Novartis, Pfizer, Roche, Sanofi and UCB Pharma (unrelated to the present work). Remaining authors report no competing interests.

  • Patient consent for publication Not required.

  • Ethics approval Ethical approval for the SPARTAKUS study has been granted by the Regional Ethics Committee in Lund, Sweden (Dnr. 2015/436 with amendment Dnr. 2018/238). Oral and written informed consent was granted by all patients and controls before entry in the study.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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