Evidence map›Paper›PMID 32661321›Full record

ReviewNature reviews. Rheumatology2020

Revisiting the gut-joint axis: links between gut inflammation and spondyloarthritis.

Eric Gracey, Lars Vereecke, Dermot McGovern, Mareike Fröhling, Georg Schett, Silvio Danese, Martine De Vos, Filip Van den Bosch, Dirk Elewaut

Erratum issuedAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 115 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 4 pooled it
17.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

115 citing papers in PubMed, 4 syntheses or guidelines pooled it, 174 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Article
  7. [Psoriatic arthritis as MHC-I-associated disease].Zeitschrift fur Rheumatologie · 2026
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Intestinal microbiota and arthritis.EULAR rheumatology open · 2026
    Review
  14. The gut-joint axis in juvenile idiopathic arthritis.Arthritis research & therapy · 2026
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

55 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 4 countries.

Eric GraceyVIB Center for Inflammation Research, Ghent, Belgium. roberteric.gracey@ugent.be.ORCID http://orcid.org/0000-0003-0984-435X
Lars VereeckeVIB Center for Inflammation Research, Ghent, Belgium.
Dermot McGovernF. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Mareike FröhlingVIB Center for Inflammation Research, Ghent, Belgium.
Georg SchettFriedrich-Alexander University Erlangen-Nuremberg and Universitätsklinikum Erlangen, Erlangen, Germany.ORCID http://orcid.org/0000-0001-8740-9615
Silvio DaneseIBD Center, Department of Gastroenterology, Humanitas Clinical and Research Center - IRCCS -, Rozzano, Milan, Italy.ORCID http://orcid.org/0000-0001-7341-1351
Martine De VosGhent Gut Inflammation Group, Ghent University, Ghent, Belgium.
Filip Van den BoschVIB Center for Inflammation Research, Ghent, Belgium.
Dirk ElewautVIB Center for Inflammation Research, Ghent, Belgium. Dirk.Elewaut@UGent.be.ORCID http://orcid.org/0000-0002-7468-974X
Ghent University Hospital · BEGhent University · BECedars-Sinai Medical Center · USHumanitas University · ITUniversitätsklinikum Erlangen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gut inflammation is strongly associated with spondyloarthritis (SpA), as exemplified by the high prevalence of inflammatory bowel disease (IBD) and the even higher occurrence of subclinical gut inflammation in patients with SpA. The gut-joint axis of inflammation in SpA is further reinforced by similarities in immunopathogenesis at both anatomical sites and by the clinical success of therapies blocking TNF and IL-23 in IBD and in some forms of SpA. Many genetic risk factors are shared between SpA and IBD, and changes in the composition of gut microbiota are seen in both diseases. Current dogma is that inflammation in SpA initiates in the gut and leads to joint inflammation; however, although conceptually attractive, some research does not support this causal relationship. For example, therapies targeting IL-17A are efficacious in the joint but not the gut, and interfering with gut trafficking by targeting molecules such as α4β7 in IBD can lead to onset or flares of SpA. Several important knowledge gaps remain that must be addressed in future studies. Determining the true nature of the gut-joint axis has real-world implications for the treatment of patients with co-incident IBD and SpA and for the repurposing of therapeutics from one disease to the other.

Indexed as

Gastrointestinal MicrobiomeAnimalsGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansInflammatory Bowel DiseasesSpondylarthritis

Identifiers

PMID32661321
OpenAlexW3040904763

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.