Axial Spondyloarthritis
Read Time: 6 mins

Managing Inflammatory Bowel Disease in Spondyloarthritis

Copy Link
Published Online: Apr 24th 2023 touchREVIEWS in RMD. 2023;2(1):7–10 DOI:
Authors: Olivier Fakih
Quick Links:
Article Information

Spondyloarthritis is a chronic inflammatory rheumatism associated with a variety of extra-articular manifestations, including chronic inflammatory bowel disease (Crohn’s disease and ulcerative colitis). Subclinical gastrointestinal manifestations in patients with spondyloarthritis are common, and clinical involvement exists in a number of patients. The pathophysiology remains poorly understood and involves genetic and immunological factors, as well as the gut microbiome. Screening for inflammatory bowel disease in patients with spondyloarthritis is important because its occurence modifies the therapeutic management of these patients.


Spondyloarthritis, ankylosing spondylitis, inflammatory bowel disease, Crohn’s disease, ulcerative colitis, biological therapy


Spondyloarthritides are chronic rheumatic diseases associated with diverse extra-articular manifestations, such as psoriasis, uveitis and inflammatory bowel diseases (IBDs), namely Crohn’s disease (CD) and ulcerative colitis (UC). Historically, spondyloarthritis (SpA) was divided into several subcategories, namely, ankylosing spondylitis (AS), psoriatic arthritis, enteropathic arthritis, reactive arthritis and undifferentiated spondyloarthropathy. Given the possible overlap between these different entities, it is now preferred to use a phenotypic classification, associating the distribution of joint involvement (axial, peripheral or both) with any associated extra-articular manifestations, including IBD.


Clinical SpA occurs in up to 13% of patients with IBD, and CD in particular.1 However, in a Canadian cohort, subclinical sacroiliitis was found in 16% of cases, with no difference in prevalence between CD and UC.2 On the contrary, up to 60% of patients with SpA have subclinical, histological, gastrointestinal inflammation.3 IBD seems to be more associated with AS than with psoriatic arthritis.4 In a large British AS cohort, the prevalence of IBD at diagnosis was 3.7%, which was lower than the rate of acute anterior uveitis or psoriasis.5 The incidence rate was 2.4 per 1,000 person-years, giving a cumulative incidence at 20 years of 7.5%, with a higher risk in the first year after diagnosis. High Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) or Bath Ankylosing Spondylitis Disease Functional Index (BASFI) scores were associated with microscopic gut inflammation, without necessarily having a clinical impact.6 Interestingly, a study of the British BSRBR-AS cohort revealed that, overall, exposure to anti-tumour necrosis factor (TNF) therapy was associated with an increased risk of developing IBD compared with unexposed patients; however, this finding was only replicated in the observational studies and not in the randomized controlled trials included in the meta-analysis, possibly dye to unadjusted confounding factors.7


The relationship between SpA and IBD is complex and not yet fully understood. It involves both genetic and immunological mechanisms. Moreover, in recent years, the role of the gut microbiome has been increasingly studied. Genetically, human leukocyte antigen B27 (HLA-B27) is the most studied risk factor. Different theories have been formulated regarding its involvement in the pathogenesis of SpA. However, large genetic studies have shown that it is not a risk factor for the occurrence of IBD,8 which could suggest different pathophysiological pathways. A clinical study of Caucasian patients with AS showed that HLA-B27-negative patients had more extra-articular manifestations, besides uveitis, than HLA-B27-positive patients.9 Conversely, HLA-B27 was also associated with gut dysbiosis in patients with SpA, and these effects were highly dependent on host genetic background and environment.9 On the contrary, genomewide association studies have shown common genetic factors between SpA and IBD. The largest genome-wide association study explains 27.8% of the heritability of SpA, which is mostly related to major histocompatibility complex loci.10 Others, such as genes related to type 3 immunity and epithelial barrier integrity are shared risk factors for SpA and IBD. Some variants are associated with only one of the two diseases. Finally, some variants are a risk factor in one disease and protective in the other.3,10

Immunologically, type 3 immunity, which is involved in the integrity of the intestinal endothelial barrier, seems to play a major role in the development of both SpA and IBD.11 Apart from TNFα, the key cytokine in the pathophysiology of IBD is interleukin (IL)-23, whereas in SpA it is IL-17A. IL-23, produced by dendritic cells and macrophages, promotes differentiation and activation of several cell types, including Thelper lymphocytes type 17, which in turn produce TNFα and IL-17A. There is, therefore, an IL-23/IL-17A axis of inflammation, but it is not inflexible: treatments directed against IL-23 work well in both IBD and SpA, whereas treatments directed against IL-17A are effective in SpA but not in IBD. This could be explained by different interaction networks and cytokine effects depending on the tissue studied.11

Serum IL17A is also higher in patients with AS compared with both healthy controls and patients with IBD,12 and smallintestine IL23 concentrations are higher in patients with AS and CD than in healthy controls.13

The gut microbiome has been increasingly studied in SpA, but many questions remain unanswered. Several studies have shown variations in the diversity and composition of the gut microbiome in patients, with some bacteria even being associated with disease activity.14,15 In particular, an imbalance in the ratio of Firmicutes/Bacteroidetes could cause AS.16

These three mechanisms  genetic, immunological and microbiome  are strongly linked, altering the epithelial barrier, causing subclinical inflammation, and leading to recruitment of pro-inflammatory cells and cytokines in the axial and peripheral skeleton. It is therefore a real gutjoint axis.3

Recognizing inflammatory bowel disease in the context of spondyloarthritis

It is important for clinicans, including rheumatologists, to have good knowledge of the clinical signs and diagnosis of IBD, to ensure it is promptly diagnosed and treated. An Italian team proposed a set of criteria for referral to a gastroenterologist: chronic diarrhoea, rectal bleeding, perianal abscess/fistula, chronic abdominal pain and nocturnal symptoms were major criteria (one is sufficient for referral), while oral aphthosis, fever, anaemia, a family history of IBD, and weight loss were minor criteria (at least two criteria are necessary for referral).17 These signs should be assessed at each follow-up visit.

The diagnostic strategy for IBD in a patient with a history of SpA does not change from that for the general population. As mentioned in the European Crohn’s and Colitis Organisation (ECCO)/European Society of Gastrointestinal and Abdominal Radiology recommendations,18 no single test is diagnostic of IBD. Instead, diagnosis is based on a combination of clinical and paraclinical evidence. Faecal calprotectin is a sensitive marker of intestinal inflammation in IBD. However, its performance as a screening test in the context of SpA may be diminished due to the high prevalence of microscopic inflammation, which may not have a clinical impact.19 This marker could also define patients at risk of developing IBD.20 An ileocolonoscopy remains mandatory to diagnose IBD, with two biopsies in the inflamed zone and biopsies in each colonic segment, except in cases of acute severe colitis in which sigmoidoscopy may be sufficient.18 There are only few endoscopic studies in SpA. In a Korean series of 108 patients, lesions were found in 40 cases (37%).21 Ulceration was the most frequently found lesion, and the terminal ileum was the most frequently affected site.21 Small-bowel capsule endoscopy can also be used. Two studies have evaluated its use in SpA, in comparison with ileocolonoscopy. Eliakim et alshowed in 2005 that, in 20 patients, small-bowel capsule endoscopy uncovered more lesions than ileocolonoscopy (30% versus 5%, respectively).22 Similar results (42.2% versu10.9%, respectively) were found in a prospective study of 64 patients in 2018.23

Managing inflammatory bowel disease in the context of spondyloarthritis

Consideration of IBD is important for the therapeutic management of patients with SpA. Indeed, some treatments are not effective, or are even contraindicated, in the presence of this extra-articular manifestation. Disease activity at the articular and digestive levels is also an element to be taken into account.

Non-steroidal anti-inflammatory drugs (NSAIDs), the first-line treatment for SpA, are contraindicated in active IBD because of the risk of aggravating the digestive disease. However, some authors suggest that this relation is only the consequence of a residual bias,24 and there are more and more studies questioning this effect. In cases of quiescent IBD, treatment with NSAIDs may be proposed for a short period of time and with the agreement of the patient’s gastroenterologist. A selective cyclooxygenase-2 inhibitor may be preferred because of the absence of short-term exacerbation of IBD in two studies included in a Cochrane review.25

Systemic corticosteroids should not be used long term in pure axial involvement, and may be used with caution in psoriatic arthritis.26 Studies are rare, and have small sample sizes and short follow-up periods.27,28 ECCO guidelines suggest the use of systemic corticosteroids for inducing clinical response and remission in CD, but long-term use does not prevent relapse.29

Regarding conventional, synthetic, disease-modifying anti-rheumatic drugs, the latest European League Against Rheumatism (EULAR) recommendations suggest that they can be tried in cases of peripheral involvement, with preference given to sulfasalazine, which has demonstrated efficacy, unlike methotrexate.30 The ECCO guidelines are against the use of aminosalicylic acid (5-ASA) compounds due to lack of efficacy in CD.29 On the contrary, in UC, there is a strong recommendation to use 5-ASA orally and/or rectally for inducing remission, and a weak recommendation for maintaining remission.31 No agreement was reached regarding methotrexate in CD, but the authors state that this treatment can be considered in cases of moderate-to-severe disease when alternative options cannot be used.29 No study suggests its use in UC.

If disease activity persists despite conventional therapy, TNF inhibitors, IL17 inhibitors and Janus kinase (JAK) inhibitors are indicated in axial disease, with the usual practice of starting with TNF inhibitors or IL17 inhibitors. In peripheral SpA, IL23 inhibitors can also be considered. The Assessment of SpondyloArthritis International Society (ASAS)-EULAR guidelines also state that, in active IBD, a monoclonal antibody to TNF should be preferred.30 Indeed, various studies have shown the efficacy of anti-TNF antibodies in CD and UC, and the lack of efficacy of etanercept and secukinumab.32–35

Furthermore, the ASAS-EULAR guidelines do not suggest one anti-TNF antibody over another, but it should be noted that certolizumab is not approved for UC and golimumab is not approved for CD.30 In addition, a network meta-analysis showed superiority of infliximab plus azathioprine and of adalimumab monotherapy over certolizumab in inducing remission in patients with CD.36

The ineffectiveness of IL17 inhibitors in IBD, and their association with disease worsening, despite the IL23/IL17 pathway being involved in its occurrence and these treatments working in SpA, illustrates the complex links between type 3 immunity and the pathophysiology of IBD and SpA. Although no excess risk of developing de novo IBD has been definitively demonstrated, patients on anti-IL17 therapy should be carefully monitored for the occurrence of digestive signs.37

Ustekinumab, an anti-IL12/23 monoclonal antibody, has demonstrated efficacy38,39 and is recommended for the induction and maintenance of remission in both CD and UC.29,31 It is also effective in peripheral spondyloarthritis40 but not effective in axial involvement.41

Regarding JAK inhibitors, two are approved by the US Food and Drug Administration (FDA) for AS and psoriatic arthritis: tofacitinib (non-selective) and upadacitinib (JAK1-selective).42–45 Tofacitinib is approved for UC and recommended by ECCO.31 Upadacitinib is also approved for UC. However, evidence of an increased risk of major cardiovascular events in selected patients treated with JAK inhibitors versus TNF inhibitors for rheumatoid arthritis (age 50 years, and at least one additional cardiovascular risk factor)46 prompted the FDA and European Medicines Agency to issue a warning about the use of this treatment for all approved indications. Additional data are needed to clarify the safety and place of this therapeutic class in the management of SpA and IBD.

Finally, some treatments are recommended in IBD but not in SpA.47,48 In particular, vedolizumab, a monoclonal antibody directed against α4β7 integrin is effective in inducing and maintaining remission in CD and UC, thanks to gut-selective anti-inflammatory activity. The ECCO guidelines suggest the use of vedolizumab rather than adalimumab for inducing and maintaining remission in patients with moderately-to-severely active UC based on the results of a randomized controlled trial.31,49 Several authors have reported the occurrence of severe de novo SpA50 and isolated enthesitis51 following vedolizumab treatment.

Thiopurines such as azathioprine are also recommended for maintaining remission in patients with steroid-dependent CD or UC.29,31 However, they are not recommended in patients with newly diagnosed CD, as it has been speculated that early introduction of thiopurines may alter the course of the disease.

Thus, the clinical phenotype of SpA, the type of IBD and its activity, and previous treatments are all important to consider when making treatment decisions for patients with both SpA and IBD. In any case, clinical and biological evaluation before introducing immunosuppressive therapy, as well as regular monitoring of infection risk, should be performed, as in the case of SpA without associated IBD.


In conclusion, recognizing IBD in a patient with SpA is important. Indeed, IBD with clinical manifestations is not rare in patients with SpA, and some treatments are not effective on one or other of these pathologies. Collaboration with the gastroenterologist remains important for optimal patient management.

Article Information:

Olivier Fakih has no financial or non-financial relationships or activities to declare in relation to this article.

Compliance With Ethics

This article involves a review of the literature and did not involve any studies with human or animal subjects performed by the author.

Review Process

Double-blind peer review.


The named author meets the International Committee of Medical Journal Editors (ICMJE) criteria for authorship of this manuscript, takes responsibility for the integrity of the work as a whole, and has given final approval for the version to be published.


Dr Olivier Fakih, CHU de Besançon, 3 boulevard Fleming, 25030 Besançon Cedex, France. E:


No funding was received in the publication of this article.


This article is freely accessible at © Touch Medical Media 2023

Data Availability

Data sharing is not applicable to this article as no datasets were generated or analysed during the writing of this article.




1. Karreman MCLuime JJHazes JMWWeel AEAMThe prevalence and incidence of axial and peripheral spondyloarthritis in inflammatory bowel disease: A systematic review and meta-analysisJ Crohns Colitis2017;11:63142DOI10.1093/ecco-jcc/jjw199

2. Kelly OBLi NSmith Met alThe prevalence and clinical associations of subclinical sacroiliitis in inflammatory bowel diseaseInflamm Bowel Dis2019;25:106671DOI10.1093/ibd/izy339

3. Gracey EVereecke LMcGovern Det alRevisiting the gut-joint axis: Links between gut inflammation and spondyloarthritisNat Rev Rheumatol2020;16:41533DOI10.1038/s41584-020-0454-9

4. Bengtsson KForsblad-d’Elia HDeminger Aet alIncidence of extra-articular manifestations in ankylosing spondylitis, psoriatic arthritis and undifferentiated spondyloarthritis: Results from a national register-based cohort studyRheumatology (Oxford)2021;60:272534DOI10.1093/rheumatology/keaa692

5. Stolwijk CEssers Ivan Tubergen Aet alThe epidemiology of extra-articular manifestations in ankylosing spondylitis: A population-based matched cohort studyAnn Rheum Dis2015;74:13738DOI10.1136/annrheumdis-2014-205253

6. Van Praet LVan den Bosch FEJacques Pet alMicroscopic gut inflammation in axial spondyloarthritis: A multiparametric predictive modelAnn Rheum Dis2013;72:4147DOI10.1136/annrheumdis-2012-202135

7. Macfarlane GJBiallas RDean LEet alInflammatory bowel disease risk in patients with axial spondyloarthritis treated with biologic agents determined using the BSRBR-AS and a metaanalysisJ Rheumatol2023;50:17584DOI10.3899/jrheum.211034

8. Goyette PBoucher GMallon Det alHigh-density mapping of the MHC identifies a shared role for HLA-DRB1*01:03 in inflammatory bowel diseases and heterozygous advantage in ulcerative colitisNat Genet2015;47:1729DOI10.1038/ng.3176

9. Xu HYin JHLA risk alleles and gut microbiome in ankylosing spondylitis and rheumatoid arthritisBest Pract Res Clin Rheumatol2019;33:101499DOI10.1016/j.berh.2020.101499

10. Ellinghaus DJostins LSpain SLet alAnalysis of five chronic inflammatory diseases identifies 27 new associations and highlights disease-specific patterns at shared lociNat Genet2016;48:5108DOI10.1038/ng.3528

11. Schett GMcInnes IBNeurath MFReframing immune-mediated inflammatory diseases through signature cytokine hubsN Engl J Med2021;385:62839DOI10.1056/NEJMra1909094

12. Ciccia FBombardieri MPrincipato Aet alOverexpression of interleukin-23, but not interleukin-17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitisArthritis Rheum2009;60:95565DOI10.1002/art.24389

13. Gracey EYao YGreen Bet alSexual dimorphism in the Th17 signature of ankylosing spondylitisArthritis Rheumatol2016;68:67989DOI10.1002/art.39464

14. Zhou CZhao HXiao XYet alMetagenomic profiling of the pro-inflammatory gut microbiota in ankylosing spondylitisJ Autoimmun2020;107:102360DOI10.1016/j.jaut.2019.102360

15. Manasson JShen NGarcia Ferrer HRet alGut microbiota perturbations in reactive arthritis and postinfectious spondyloarthritisArthritis Rheumatol2018;70:24254DOI10.1002/art.40359

16. Liu GHao YYang QDeng SThe association of fecal microbiota in ankylosing spondylitis cases with C-reactive protein and erythrocyte sedimentation rateMediators Inflamm2020;2020:8884324DOI10.1155/2020/8884324

17. Felice CLeccese PScudeller Let alRed flags for appropriate referral to the gastroenterologist and the rheumatologist of patients with inflammatory bowel disease and spondyloarthritisClin Exp Immunol2019;196:12338DOI10.1111/cei.13246

18. Maaser CSturm AVavricka SRet alECCO-ESGAR guideline for diagnostic assessment in IBD Part 1: Initial diagnosis, monitoring of known IBD, detection of complicationsJ Crohns Colitis2019;13:14464DOI10.1093/ecco-jcc/jjy113

19. Campos JFResende GGBarbosa AJAet alFecal calprotectin as a biomarker of microscopic bowel inflammation in patients with spondyloarthritisInt J Rheum Dis2022;25:107886DOI10.1111/1756-185X.14388

20. Klingberg EStrid HStåhl Aet alA longitudinal study of fecal calprotectin and the development of inflammatory bowel disease in ankylosing spondylitisArthritis Res Ther2017;19:21DOI10.1186/s13075-017-1223-2

21. Ahn SMKim YGBae SHet alIleocolonoscopic findings in patients with ankylosing spondylitis: A single center retrospective studyKorean J Intern Med2017;32:91622DOI10.3904/kjim.2015.313

22. Eliakim RKarban AMarkovits Det alComparison of capsule endoscopy with ileocolonoscopy for detecting small-bowel lesions in patients with seronegative spondyloarthropathiesEndoscopy2005;37:11659DOI10.1055/s-2005-870559

23. Kopylov UStarr MWatts Cet alDetection of Crohn disease in patients with spondyloarthropathy: The space capsule studyJ Rheumatol2018;45:498505DOI10.3899/jrheum.161216

24. Cohen-Mekelburg SVan TWallace Bet alThe association between nonsteroidal anti-inflammatory drug use and inflammatory bowel disease exacerbations: A true association or residual bias? Am J Gastroenterol2022;117:18517DOI10.14309/ajg.0000000000001932

25. Miao XPLi JSOuyang Qet alTolerability of selective cyclooxygenase 2 inhibitors used for the treatment of rheumatological manifestations of inflammatory bowel diseaseCochrane Database Syst Rev2014:CD007744DOI10.1002/14651858.CD007744.pub2

26. Gossec LBaraliakos XKerschbaumer Aet alEULAR recommendations for the management of psoriatic arthritis with pharmacological therapies: 2019 updateAnn Rheum Dis2020;79:70012DOI10.1136/annrheumdis-2020-217159

27. Dhir VMishra DSamanta JGlucocorticoids in spondyloarthritis – systematic review and real-world analysisRheumatology (Oxford)2021;60:446375DOI10.1093/rheumatology/keab275

28. Haroon MAhmad MBaig MNet alInflammatory back pain in psoriatic arthritis is significantly more responsive to corticosteroids compared to back pain in ankylosing spondylitis: A prospective, open-labelled, controlled pilot studyArthritis Res Ther2018;20:73DOI10.1186/s13075-018-1565-4

29. Torres JBonovas SDoherty Get alECCO guidelines on therapeutics in Crohn’s disease: Medical treatmentJ Crohns Colitis2020;14:422DOI10.1093/ecco-jcc/jjz180

30. Ramiro SNikiphorou ESepriano Aet alASAS-EULAR recommendations for the management of axial spondyloarthritis: 2022 updateAnn Rheum Dis2023;82:1934DOI10.1136/ard-2022-223296

31. Raine TBonovas SBurisch Jet alECCO guidelines on therapeutics in ulcerative colitis: Medical treatmentJ Crohns Colitis2022;16:217DOI10.1093/ecco-jcc/jjab178

32. Stidham RWLee TCHHiggins PDRet alSystematic review with network meta-analysis: The efficacy of anti-TNF agents for the treatment of Crohn’s diseaseAliment Pharmacol Ther2014;39:134962DOI10.1111/apt.12749

33. Singh SMurad MHFumery Met alFirst- and second-line pharmacotherapies for patients with moderate to severely active ulcerative colitis: An updated network meta-analysisClin Gastroenterol Hepatol2020;18:217991DOI10.1016/j.cgh.2020.01.008

34. Sandborn WJHanauer SBKatz Set alEtanercept for active Crohn’s disease: A randomized, double-blind, placebo-controlled trialGastroenterology2001;121:108894DOI10.1053/gast.2001.28674

35. Hueber WSands BELewitzky Set al.Secukinumab in Crohn’s Disease Study GroupSecukinumab, a human anti-IL-17A monoclonal antibody, for moderate to severe Crohn’s disease: Unexpected results of a randomised, double-blind placebo-controlled trialGut2012;61:1693700DOI10.1136/gutjnl-2011-301668

36. Hazlewood GSRezaie ABorman Met alComparative effectiveness of immunosuppressants and biologics for inducing and maintaining remission in Crohn’s disease: A network meta-analysisGastroenterology2015;148:34454DOI10.1053/j.gastro.2014.10.011

37. Țiburcă LBembea MZaha DCet alThe treatment with interleukin 17 inhibitors and immune-mediated inflammatory diseasesCurr Issues Mol Biol2022;44:185166DOI10.3390/cimb44050127

38. Khanna RPreiss JCMacDonald JKTimmer AAnti-IL-12/23p40 antibodies for induction of remission in Crohn’s diseaseCochrane Database Syst Rev2015;CD007572:CD007572DOI10.1002/14651858.CD007572.pub2

39. Sands BESandborn WJPanaccione Ret alUstekinumab as induction and maintenance therapy for ulcerative colitisN Engl J Med2019;381:120114DOI10.1056/NEJMoa1900750

40. Matsumoto SMashima HEfficacy of ustekinumab against infliximab-induced psoriasis and arthritis associated with Crohn’s diseaseBiologics2018;12:6973DOI10.2147/BTT.S169326

41. Deodhar AGensler LSSieper Jet alThree multicenter, randomized, double-blind, placebo-controlled studies evaluating the efficacy and safety of ustekinumab in axial spondyloarthritisArthritis Rheumatol2019;71:25870DOI10.1002/art.40728

42. PfizerPfizer Announces FDA Approval of XELJANZ® (tofacitinib) and XELJANZ® XR for the Treatment of Active Psoriatic ArthritisAvailable (Date last accessed6 April 2023)

43. PfizerFDA Approves Pfizer’s XELJANZ® (tofacitinib) for the Treatment of Active Ankylosing SpondylitisAvailable (Date last accessed6 April 2023)

44. AbbVieRINVOQ® (upadacitinib) Receives U.S. FDA Approval for Active Psoriatic ArthritisAvailable at (Date last accessed6 April 2023)

45. AbbVieRINVOQ® (upadacitinib) Approved by U.S. FDA as an Oral Treatment for Adults with Active Ankylosing SpondylitisAvailable at (Date last accessed6 April 2023)

46. Ytterberg SRBhatt DLMikuls TRet alCardiovascular and cancer risk with tofacitinib in rheumatoid arthritisN Engl J Med2022;386:31626DOI10.1056/NEJMoa2109927

47. Sandborn WJFeagan BGRutgeerts Pet alVedolizumab as induction and maintenance therapy for Crohn’s diseaseNew Engl J Med2013;369:71121DOI10.1056/NEJMoa1215739

48. Feagan BGRutgeerts PSands BEet alVedolizumab as induction and maintenance therapy for ulcerative colitisN Engl J Med2013;369:699710DOI10.1056/NEJMoa1215734

49. Sands BEPeyrin-Biroulet LLoftus EV Jret alVedolizumab versus adalimumab for moderate-to-severe ulcerative colitisN Engl J Med2019;381:121526DOI10.1056/NEJMoa1905725

50. Felice CPugliese DPapparella LGet alClinical management of rheumatologic conditions co-occurring with inflammatory bowel diseasesExpert Rev Clin Immunol2018;14:7519DOI10.1080/1744666X.2018.1513329

51. Ruscio MDTinazzi IVariola Aet alPrevalence and real-world management of vedolizumab-associated enthesitis in successfully treated IBD patientsRheumatology2021;60:580913DOI10.1093/rheumatology/keab135

Further Resources

Share this Article
Related Content In Axial Spondyloarthritis
  • Copied to clipboard!
    accredited arrow-down-editablearrow-downarrow_leftarrow-right-bluearrow-right-dark-bluearrow-right-greenarrow-right-greyarrow-right-orangearrow-right-whitearrow-right-bluearrow-up-orangeavatarcalendarchevron-down consultant-pathologist-nurseconsultant-pathologistcrosscrossdownloademailexclaimationfeedbackfiltergraph-arrowinterviewslinkmdt_iconmenumore_dots nurse-consultantpadlock patient-advocate-pathologistpatient-consultantpatientperson pharmacist-nurseplay_buttonplay-colour-tmcplay-colourAsset 1podcastprinter scenerysearch share single-doctor social_facebooksocial_googleplussocial_instagramsocial_linkedin_altsocial_linkedin_altsocial_pinterestlogo-twitter-glyph-32social_youtubeshape-star (1)tick-bluetick-orangetick-red tick-whiteticktimetranscriptup-arrowwebinar Sponsored Department Location NEW TMM Corporate Services Icons-07NEW TMM Corporate Services Icons-08NEW TMM Corporate Services Icons-09NEW TMM Corporate Services Icons-10NEW TMM Corporate Services Icons-11NEW TMM Corporate Services Icons-12Salary £ TMM-Corp-Site-Icons-01TMM-Corp-Site-Icons-02TMM-Corp-Site-Icons-03TMM-Corp-Site-Icons-04TMM-Corp-Site-Icons-05TMM-Corp-Site-Icons-06TMM-Corp-Site-Icons-07TMM-Corp-Site-Icons-08TMM-Corp-Site-Icons-09TMM-Corp-Site-Icons-10TMM-Corp-Site-Icons-11TMM-Corp-Site-Icons-12TMM-Corp-Site-Icons-13TMM-Corp-Site-Icons-14TMM-Corp-Site-Icons-15TMM-Corp-Site-Icons-16TMM-Corp-Site-Icons-17TMM-Corp-Site-Icons-18TMM-Corp-Site-Icons-19TMM-Corp-Site-Icons-20TMM-Corp-Site-Icons-21TMM-Corp-Site-Icons-22TMM-Corp-Site-Icons-23TMM-Corp-Site-Icons-24TMM-Corp-Site-Icons-25TMM-Corp-Site-Icons-26TMM-Corp-Site-Icons-27TMM-Corp-Site-Icons-28TMM-Corp-Site-Icons-29TMM-Corp-Site-Icons-30TMM-Corp-Site-Icons-31TMM-Corp-Site-Icons-32TMM-Corp-Site-Icons-33TMM-Corp-Site-Icons-34TMM-Corp-Site-Icons-35TMM-Corp-Site-Icons-36TMM-Corp-Site-Icons-37TMM-Corp-Site-Icons-38TMM-Corp-Site-Icons-39TMM-Corp-Site-Icons-40TMM-Corp-Site-Icons-41TMM-Corp-Site-Icons-42TMM-Corp-Site-Icons-43TMM-Corp-Site-Icons-44TMM-Corp-Site-Icons-45TMM-Corp-Site-Icons-46TMM-Corp-Site-Icons-47TMM-Corp-Site-Icons-48TMM-Corp-Site-Icons-49TMM-Corp-Site-Icons-50TMM-Corp-Site-Icons-51TMM-Corp-Site-Icons-52TMM-Corp-Site-Icons-53TMM-Corp-Site-Icons-54TMM-Corp-Site-Icons-55TMM-Corp-Site-Icons-56TMM-Corp-Site-Icons-57TMM-Corp-Site-Icons-58TMM-Corp-Site-Icons-59TMM-Corp-Site-Icons-60TMM-Corp-Site-Icons-61TMM-Corp-Site-Icons-62TMM-Corp-Site-Icons-63TMM-Corp-Site-Icons-64TMM-Corp-Site-Icons-65TMM-Corp-Site-Icons-66TMM-Corp-Site-Icons-67TMM-Corp-Site-Icons-68TMM-Corp-Site-Icons-69TMM-Corp-Site-Icons-70TMM-Corp-Site-Icons-71TMM-Corp-Site-Icons-72