{"id":14327,"date":"2023-04-24T15:12:17","date_gmt":"2023-04-24T14:12:17","guid":{"rendered":"https:\/\/touchimmunology.com\/?p=14327"},"modified":"2023-07-18T19:44:24","modified_gmt":"2023-07-18T18:44:24","slug":"managing-inflammatory-bowel-disease-in-spondyloarthritis","status":"publish","type":"post","link":"https:\/\/touchimmunology.com\/axial-spondyloarthritis\/journal-articles\/managing-inflammatory-bowel-disease-in-spondyloarthritis\/","title":{"rendered":"Managing Inflammatory Bowel Disease in Spondyloarthritis"},"content":{"rendered":"

Spondyloarthritides are chronic rheumatic diseases associated with diverse extra-articular manifestations, such as psoriasis, uveitis and\u00a0inflammatory bowel diseases<\/span>\u00a0(IBDs<\/span><\/span>), namely\u00a0Crohn\u2019s disease<\/span>\u00a0(CD<\/span>) and\u00a0ulcerative colitis<\/span>\u00a0(UC<\/span>). Historically,\u00a0spondyloarthritis (SpA)<\/span>\u00a0was divided into several subcategories, namely,\u00a0ankylosing spondylitis<\/span>\u00a0(AS<\/span>), 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.<\/p>\n

Epidemiology<\/h1>\n

Clinical SpA occurs in up to\u00a013<\/span>%<\/span>\u00a0of patients with IBD, and CD in particular.1<\/sup><\/span>\u00a0However, in a Canadian cohort, subclinical sacroiliitis was found in\u00a016<\/span>%<\/span>\u00a0of cases, with no difference in prevalence between CD and UC.2<\/sup><\/span>\u00a0On the contrary, up to\u00a060<\/span>%<\/span>\u00a0of patients with SpA have subclinical, histological<\/span>, gastrointestinal inflammation.3<\/sup><\/span>\u00a0IBD seems to be more associated with AS than\u00a0with\u00a0<\/span>psoriatic arthritis<\/span>.4<\/sup><\/span>\u00a0In a large British AS cohort, the prevalence of IBD at diagnosis was 3.7%, which\u00a0was\u00a0<\/span>lower than\u00a0the rate of\u00a0<\/span>acute anterior uveitis\u00a0or<\/span>\u00a0<\/span>psoriasis.5<\/sup><\/span> The incidence rate was 2.4 per 1,<\/span>000<\/span>\u00a0person-years, giving a cumulative incidence at\u00a020<\/span>\u00a0years<\/span>\u00a0of 7.5%, with a higher risk in the first year after diagnosis. High Bath\u00a0Ankylosing Spondylitis<\/span>\u00a0Disease Activity Index\u00a0(<\/span>BASDAI<\/span>)<\/span>\u00a0or Bath\u00a0Ankylosing Spondylitis<\/span>\u00a0Disease Functional Index\u00a0(BASFI)<\/span>\u00a0scores were associated with microscopic gut inflammation, without necessarily having a clinical impact.6<\/sup><\/span>\u00a0<\/span>Interestingly,\u00a0a study of the<\/span>\u00a0British BSRBR-AS cohort\u00a0revealed that, overall,<\/span>\u00a0exposure to anti-tumour necrosis factor (<\/span>TNF)<\/span> therapy was associated with an increased risk of developing IBD compared with unexposed patients;<\/span><\/span>\u00a0<\/span>however,\u00a0<\/span>t<\/span>his\u00a0finding\u00a0<\/span>was\u00a0only replicated in the observational studies and\u00a0<\/span>not in\u00a0the\u00a0<\/span>randomized controlled trials included in the meta-analysis, possibly dye to<\/span>\u00a0u<\/span>nadjusted confounding factors<\/span>.7<\/sup><\/span><\/span><\/p>\n

Pathophysiology<\/h1>\n

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,\u00a0human leukocyte antigen B27<\/span>\u00a0(<\/span>HLA-B27)<\/span>\u00a0is 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<\/sup><\/span>\u00a0which 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\u00a0<\/span>patients<\/span>.9<\/sup><\/span>\u00a0Conversely, HLA-B27\u00a0wa<\/span>s also associated with gut dysbiosis in patients\u00a0with SpA,\u00a0<\/span>and these effects\u00a0<\/span>were<\/span>\u00a0highly dependent on host genetic background and environment.9<\/sup><\/span>\u00a0On the contrary,\u00a0g<\/span>enome–<\/span>wide association studies have shown common genetic factors between SpA and IBD. The largest\u00a0genome-wide association study<\/span>\u00a0explains\u00a027.8<\/span>%<\/span>\u00a0of the heritability of SpA, which is mostly related to\u00a0m<\/span>ajor\u00a0h<\/span>istocompatibility\u00a0c<\/span>omplex\u00a0<\/span>loci.10<\/sup><\/span>\u00a0Others, such as genes related to type\u00a0<\/span>3<\/span>\u00a0immunity 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<\/sup><\/span><\/p>\n

<\/span>Immunologically<\/span>, type\u00a0<\/span>3<\/span>\u00a0immunity, which is involved in the integrity of the intestinal endothelial barrier, seems to play a major<\/span>\u00a0<\/span>role\u00a0in the development of both SpA and IBD<\/span><\/span><\/span>.11<\/sup><\/span>\u00a0Apart from TNF–<\/span>\u03b1<\/span>, the key cytokine in the pathophysiology of IBD is\u00a0interleukin (<\/span>IL)<\/span>-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 T–<\/span>helper lymphocytes type 17, which in turn produce TNF–<\/span>\u03b1<\/span>\u00a0and IL-17A. There is,<\/span>\u00a0therefore,<\/span>\u00a0an IL-23\/IL-17A axis of inflammation,<\/span>\u00a0but it is not inflexible: treatments directed against IL-23 work well in\u00a0both\u00a0<\/span>IBD and SpA, whereas treatments directed against\u00a0<\/span>IL-17A<\/span><\/span>\u00a0are effective in SpA but not in IBD. This could be explained by different interaction networks and cytokine effects depending on the tissue studied.11<\/sup><\/span><\/p>\n

Serum IL–<\/span>17A\u00a0<\/span>is also higher in patients\u00a0with AS\u00a0compared with\u00a0both healthy controls and patients with IBD<\/span><\/span><\/span>,<\/span><\/span>12<\/sup><\/span>\u00a0and small–<\/span>intestine IL–<\/span>23 concentrations\u00a0a<\/span>re\u00a0<\/span>higher in patients with AS and\u00a0<\/span><\/span>CD\u00a0than in healthy controls<\/span><\/span>.13<\/sup><\/span><\/p>\n

The gut microbiome\u00a0has been<\/span>\u00a0<\/span>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<\/sup><\/span>\u00a0In particular, an imbalance in the ratio of Firmicutes\/Bacteroidetes could cause AS.16<\/sup><\/span><\/p>\n

These three mechanisms\u00a0\u2212\u00a0<\/span><\/span><\/span>genetic, immunological and microbiome\u00a0\u2212<\/span><\/span>\u00a0are strongly linked,\u00a0altering\u00a0<\/span>the epithelial barrier,\u00a0<\/span>causing\u00a0<\/span><\/span>subclinical inflammation,\u00a0and\u00a0<\/span>leading to recruitment of pro-inflammatory cells and cytokines in the axial and peripheral skeleton. It is therefore a real\u00a0<\/span>‘<\/span>gut\u2212<\/span>joint axis‘<\/span><\/span>.3<\/sup><\/span><\/p>\n

Recognizing\u00a0inflammatory bowel disease\u00a0<\/span>in the context of\u00a0spondylo<\/span>arthritis<\/span><\/h1>\n

<\/span>It is important for clinicans, including rheumatologists, to have\u00a0<\/span>good knowledge of the clinical signs and diagnosis of IBD,<\/span>\u00a0to ensure\u00a0<\/span>it is promptly diagnosed and treated<\/span><\/span>. An Italian team proposed a set of criteria\u00a0for<\/span>\u00a0referral to a gastroenterologist: chronic diarrho<\/span>ea, rectal bleeding, perianal abscess\/fistula, chronic abdominal pain and nocturnal symptoms were major criteria (one is sufficient for referral), while oral aphthosis, fever, ana<\/span>emia, a family history of IBD, and weight loss were minor criteria (at least two criteria are necessary for referral).17 <\/sup>T<\/span>hese signs s<\/span>hould be\u00a0assessed\u00a0<\/span>at each follow-up visit.<\/p>\n

The diagnostic strategy for IBD in a patient with a history of SpA does not change from\u00a0that for\u00a0<\/span>the general population. As mentioned in the\u00a0European Crohn’s and Colitis Organisation (ECCO)<\/span>\/European Society of Gastrointestinal and Abdominal Radiology<\/span><\/span><\/span>\u00a0recommendations,18<\/sup><\/span>\u00a0no single test is diagnostic of IBD. Instead, diagnosis\u00a0<\/span>is based on a combination of clinical and paraclinical evidence. Fa<\/span>ecal 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<\/sup><\/span>\u00a0This marker could also define\u00a0patients\u00a0<\/span>at risk of developing IBD.20<\/sup><\/span>\u00a0An ileocolonoscopy remains mandatory to\u00a0diagnose IBD<\/span>, 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<\/sup><\/span>\u00a0There are only\u00a0a\u00a0<\/span>few endoscopic studies in SpA. In a Korean series of\u00a0108<\/span>\u00a0patients<\/span>, lesions were found in\u00a040<\/span>\u00a0cases\u00a0<\/span>(37%)<\/span><\/span>.21<\/sup><\/span>\u00a0Ulceration was the most frequently found lesion, and the terminal ileum was the most frequently affected site.21<\/sup><\/span>\u00a0Small-bowel capsule endoscopy<\/span>\u00a0can also be used. Two studies have evaluated its\u00a0use\u00a0<\/span>in SpA, in comparison with ileocolonoscopy.<\/span>\u00a0Eliakim\u00a0et al<\/span>.\u00a0<\/span><\/span>showed in\u00a02005<\/span>\u00a0that, in 20 patients,<\/span>\u00a0small-bowel capsule endoscopy\u00a0<\/span>uncovered more lesions than ileocolonoscopy\u00a0(30%<\/span>\u00a0versu<\/span>s<\/span>\u00a0<\/span>5%, respectively<\/span>)<\/span>.22<\/sup><\/span>\u00a0Similar results\u00a0(42.2%<\/span>\u00a0versu<\/span>s\u00a0<\/span>10.9%, respectively)\u00a0<\/span><\/span>were found in a prospective study\u00a0of 64 patients<\/span>\u00a0in\u00a02018<\/span><\/span><\/span><\/span><\/span><\/span><\/span>.23<\/sup><\/span><\/p>\n

Managing\u00a0inflammatory bowel disease\u00a0<\/span>in the context of\u00a0spondyloarthritis<\/span><\/h1>\n

Consideration of IBD is important for the therapeutic management of patients with SpA. Indeed, some treatments are not effective,<\/span>\u00a0or\u00a0are\u00a0<\/span>even contraindicated,<\/span>\u00a0in the presence of this extra-articular manifestation.\u00a0Disease activity\u00a0<\/span>at the articular and digestive levels is also an element to be taken into account.<\/p>\n

Non-steroidal anti-inflammatory drugs (NSAIDs)<\/span>, 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,<\/span>24<\/sup><\/span>\u00a0and 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\u00a0patient’s<\/span>\u00a0gastroenterologist. A selective\u00a0c<\/span>yclooxygenase<\/span><\/span>-2 inhibitor may be preferred because of the absence of\u00a0<\/span>short-term exacerbation<\/span>\u00a0of IBD\u00a0<\/span>in two studies included in a Cochrane review.25<\/sup><\/span><\/p>\n

Systemic corticosteroids should not be used long\u00a0<\/span>term in pure axial involvement, and may be used with caution in psoriatic arthritis.26<\/sup><\/span>\u00a0Studies are rare, and\u00a0<\/span>have small sample sizes\u00a0<\/span>and\u00a0<\/span>short follow-up periods<\/span>.27,28<\/sup><\/span>\u00a0ECCO guidelines suggest the use of systemic corticosteroids for\u00a0inducing\u00a0<\/span>clinical response and remission in\u00a0<\/span>CD<\/span>, but long-term use does not prevent relapse.29<\/sup><\/span><\/p>\n

Regarding conventional,<\/span>\u00a0synthetic,\u00a0<\/span>disease-modifying\u00a0anti-rheumatic drugs<\/span>, the latest\u00a0European League Against Rheumatism (<\/span>EULAR)<\/span>\u00a0recommendations suggest that they can be tried in cases of peripheral involvement, with preference given to sulfasalazine, which has demonstrated efficacy, unlike methotrexate.30<\/sup><\/span>\u00a0The ECCO guidelines are against the use of\u00a0aminosalicylic acid<\/span>\u00a0(<\/span>5-ASA)<\/span>\u00a0compounds due to lack of efficacy in CD.29<\/sup><\/span>\u00a0On the contrary, in UC, there is a strong recommendation to use 5-ASA orally and\/or rectally for\u00a0inducing\u00a0<\/span>remission, and a weak recommendation for\u00a0maintaining\u00a0<\/span>remission.31<\/sup><\/span>\u00a0No agreement\u00a0was<\/span>\u00a0reached regarding methotrexate in CD,<\/span>\u00a0but the authors state that this treatment can be considered in cases of moderate-to-severe disease when alternative options cannot be use<\/span>d.29<\/sup><\/span>\u00a0<\/span>No study suggests its use in UC.<\/p>\n

If disease activity persists despite conventional therapy, TNF\u00a0inhibitors<\/span><\/span>, IL–<\/span>17\u00a0inhibitors<\/span>\u00a0<\/span><\/span><\/span>and Janus kinase (JAK) i<\/span>nhibitors a<\/span>re indicated in axial disease, with the usual practice of starting with TNF\u00a0<\/span>inhibitors<\/span>\u00a0or IL–<\/span>17\u00a0<\/span>inhibitors<\/span>. In peripheral SpA, IL–<\/span>23\u00a0<\/span>inhibitors<\/span>\u00a0can also be considered. The\u00a0Assessment of SpondyloArthritis\u00a0I<\/span>nternational Society (ASAS)<\/span><\/span>-EULAR guidelines also state that,<\/span>\u00a0in active IBD, a monoclonal antibody to TNF should be\u00a0<\/span>preferred.30<\/sup><\/span>\u00a0<\/span>Indeed, various studies have shown the efficacy of anti-TNF antibodies in CD and UC, and the lack of efficacy of etanercept and\u00a0<\/span>secukinumab<\/span>.32\u201335<\/sup><\/span><\/p>\n

Furthermore, the\u00a0<\/span>ASAS-EULAR guidelines\u00a0<\/span><\/span>do not suggest one anti-TNF\u00a0<\/span>antibody over another,\u00a0<\/span>but it should be noted that certolizumab is not approved for UC and golimumab is not approved for CD.30<\/sup><\/span>\u00a0In addition, a network meta-analysis showed superiority of infliximab plus azathioprine and\u00a0of\u00a0<\/span>adalimumab monotherapy over certolizumab in inducing remission in patients with CD.36<\/sup><\/span><\/p>\n

The ineffectiveness of IL–<\/span>17\u00a0<\/span>inhibitors<\/span>\u00a0in IBD,\u00a0and their association<\/span>\u00a0with disease worsening,\u00a0despite<\/span>\u00a0the IL–<\/span>23\/IL–<\/span>17 pathway\u00a0being\u00a0<\/span>involved in its occurrence and these treatments working<\/span>\u00a0in SpA, illustrates the complex links between type\u00a0<\/span>3<\/span>\u00a0immunity and the pathophysiology of IBD and SpA. Although no excess risk of developing\u00a0de novo<\/em><\/span>\u00a0IBD has been definitively demonstrated, patients on anti-IL–<\/span>17\u00a0therapy\u00a0<\/span>should be carefully monitored for the occurrence of digestive signs.37<\/sup><\/span><\/p>\n

<\/span>Ustekinumab<\/span>, an anti-IL–<\/span>12\/–<\/span>23 monoclonal antibody, has demonstrated efficacy38,39<\/sup><\/span>\u00a0and is recommended for the induction and maintenance of remission in both CD and UC.29,31<\/sup><\/span> It is also effective i<\/span>n p<\/span>eripheral<\/span> spondyloarthritis40<\/sup> b<\/span>ut not effective in axial involvement.41<\/sup><\/span><\/p>\n

Regarding JAK\u00a0<\/span><\/span>inhibitors<\/span>, two are approved by the\u00a0US Food and Drug Administration (<\/span>FDA)<\/span>\u00a0for AS and\u00a0psoriatic arthritis<\/span>: tofacitinib\u00a0(<\/span>non-selective)<\/span>\u00a0and upadacitinib\u00a0(<\/span>JAK1-selective<\/span>)<\/span>.42\u201345<\/sup><\/span>\u00a0<\/span>Tofacitinib is approved for UC and <\/span>recommended by ECCO<\/span>.31<\/sup><\/span>\u00a0Upadacitinib is also approved for UC. However, evidence of an increased risk of major cardiovascular events in selected patients treated with JAK\u00a0<\/span>inhibitors<\/span>\u00a0versu<\/span>s TNF\u00a0<\/span>inhibitors<\/span>\u00a0for rheumatoid arthritis (age\u00a0\u2265<\/span><\/span>50<\/span>\u00a0years<\/span>, and at least one additional cardiovascular risk factor)46<\/sup><\/span>\u00a0prompted the FDA and\u00a0European Medicines Agency\u00a0<\/span>to issue a warning about the use of this treatment for all approved indications.<\/span>\u00a0Additional data are needed to clarify the safety and place of this therapeutic class in the management of SpA and IBD.<\/p>\n

Finally, some treatments are recommended in IBD but not in SpA.47,48<\/sup><\/span>\u00a0<\/span>In particular, vedolizumab, a monoclonal antibody directed against \u03b14\u03b27 integrin\u00a0is<\/span>\u00a0effective in\u00a0inducing and maintaining\u00a0<\/span>remission in CD and UC, thanks to gut-selective anti-inflammatory activity.<\/span>\u00a0The ECCO\u00a0guidelines<\/span><\/span>\u00a0suggest the use of vedolizumab rather than adalimumab for\u00a0inducing and maintaining\u00a0<\/span>remission in patients with moderately-to-severely active UC based on the results of a randomized controlled\u00a0<\/span>trial.<\/span><\/span>31,49<\/sup><\/span>\u00a0Several authors have reported the occurrence of severe\u00a0de novo<\/em><\/span>\u00a0<\/em>SpA50<\/sup><\/span>\u00a0and isolated enthesitis51<\/sup><\/span>\u00a0following vedolizumab treatment.<\/p>\n

<\/span>Thiopurines\u00a0<\/span>such as azathioprine are also recommended for\u00a0m<\/span>aintaining<\/span>\u00a0<\/span>remission in patients with steroid-dependent CD or UC.29,31<\/sup><\/span>\u00a0However, 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.<\/p>\n

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\u00a0introducing\u00a0<\/span>immunosuppressive therapy, as well as regular monitoring of infection\u00a0risk<\/span>, should be performed, as in the case of SpA without associated IBD.<\/p>\n

Conclusions<\/span><\/h1>\n

In conclusion, recognizing IBD in a patient with SpA is important. Indeed, IBD with clinical manifestations\u00a0is\u00a0<\/span>not rare in patients\u00a0with SpA,\u00a0<\/span>and some treatments are not effective on one or other of these pathologies. Collaboration with the gastroenterologist remains important for optimal patient management.<\/p>\n","protected":false},"excerpt":{"rendered":"

Spondyloarthritides are chronic rheumatic diseases associated with diverse extra-articular manifestations, such as psoriasis, uveitis and\u00a0inflammatory bowel diseases\u00a0(IBDs), namely\u00a0Crohn\u2019s disease\u00a0(CD) and\u00a0ulcerative colitis\u00a0(UC). Historically,\u00a0spondyloarthritis (SpA)\u00a0was divided into several subcategories, namely,\u00a0ankylosing spondylitis\u00a0(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, […]<\/p>\n","protected":false},"author":77788,"featured_media":8304,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_relevanssi_hide_post":"","_relevanssi_hide_content":"","_relevanssi_pin_for_all":"","_relevanssi_pin_keywords":"","_relevanssi_unpin_keywords":"","_relevanssi_related_keywords":"","_relevanssi_related_include_ids":"","_relevanssi_related_exclude_ids":"","_relevanssi_related_no_append":"","_relevanssi_related_not_related":"","_relevanssi_related_posts":"","_relevanssi_noindex_reason":"","rank_math_lock_modified_date":false,"footnotes":""},"categories":[1],"tags":[],"class_list":["post-14327","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-uncategorised","vocabulary_1-axial-spondyloarthritis","journal-touchreviews-in-immunology"],"acf":{"wpcf-article_introduction":"","wpcf-article_abstract":"Spondyloarthritis is a chronic inflammatory rheumatism associated with a variety of extra-articular manifestations, including chronic inflammatory bowel disease (Crohn\u2019s disease<\/span>\u00a0and\u00a0ulcerative colitis<\/span>). Subclinical gastrointestinal<\/span>\u00a0manifestations in patients with\u00a0spondyloarthritis<\/span>\u00a0are common, and clinical involvement exists in a number of patients. The pathophysiology remains poorly understood and involves genetic and immunological factors,<\/span>\u00a0as well as the gut microbiome. Screening for inflammatory bowel disease in\u00a0patients with\u00a0<\/span>spondyloarthritis is important because its occurence modifies the therapeutic management of these patients.","wpcf-article_keywords":"Spondyloarthritis, ankylosing spondylitis, inflammatory bowel disease, Crohn\u2019s disease, ulcerative colitis, biological therapy","wpcf-article_citation_override":"touchREVIEWS in RMD.<\/i> 2023;2(1):7\u201310 DOI: https:\/\/doi.org\/10.17925\/RMD.2023.2.1.7<\/a>","wpcf-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.","wpcf-article_disclosure":"Olivier Fakih has no financial or non-financial relationships or activities to declare in relation to this article.","wpcf-review_process":"Double-blind peer review.","wpcf-authorship":"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.","wpcf-article_correspondence":"Dr Olivier Fakih, CHU de Besan\u00e7on, 3 boulevard Fleming, 25030 Besan\u00e7on Cedex, France. E: ofakih@chu-besancon.fr","wpcf-article_support":"No funding was received in the publication of this article.","wpcf-open_access":"This article is freely accessible at touchIMMUNOLOGY.com \u00a9 Touch Medical Media 2023","wpcf-article_pdf":"https:\/\/touchimmunology.com\/wp-content\/uploads\/sites\/18\/2023\/07\/touchIMMUNO_RMD_pp7-10.pdf","wpcf-article_pdf-gated":false,"wpcf-article_doi":"","wpcf-old_nid":"","wpcf-article_image":"","wpcf-editor_choice":false,"wpcf-old_author_ids":"","wpcf-article_references":"

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2.<\/span>\u00a0Kelly<\/span>\u00a0OB<\/span><\/span>,\u00a0Li<\/span>\u00a0N<\/span><\/span>,\u00a0Smith<\/span>\u00a0M<\/span><\/span>,\u00a0et al<\/span>.\u00a0The prevalence and clinical associations of subclinical sacroiliitis in inflammatory bowel disease<\/span>.\u00a0Inflamm Bowel Dis<\/em><\/span>.\u00a02019<\/span>;25<\/span><\/span>:1066<\/span>\u201371<\/span>.\u00a0DOI<\/span>:\u00a010.1093\/ibd\/izy339<\/span><\/p>\r\n

3.<\/span>\u00a0Gracey<\/span>\u00a0E<\/span><\/span>,\u00a0Vereecke<\/span>\u00a0L<\/span><\/span>,\u00a0McGovern<\/span>\u00a0D<\/span><\/span>,\u00a0et al<\/span>.\u00a0Revisiting the gut-joint axis:\u00a0Ll<\/span><\/span>inks between gut inflammation and spondyloarthritis<\/span>.\u00a0Nat Rev Rheumatol<\/em><\/span>.\u00a02020<\/span>;16<\/span><\/span>:415<\/span>\u201333<\/span>.\u00a0DOI<\/span>:\u00a010.1038\/s41584-020-0454-9<\/span><\/p>\r\n

4.<\/span>\u00a0Bengtsson<\/span>\u00a0K<\/span><\/span>,\u00a0Forsblad-d\u2019Elia<\/span>\u00a0H<\/span><\/span>,\u00a0Deminger<\/span>\u00a0A<\/span><\/span>,\u00a0et al<\/span>.\u00a0Incidence of extra-articular manifestations in ankylosing spondylitis, psoriatic arthritis and undifferentiated spondyloarthritis:\u00a0Rr<\/span><\/span>esults from a national register-based cohort study<\/span>.\u00a0Rheumatology (Oxford<\/em>)<\/span>.\u00a02021<\/span>;60<\/span><\/span>:2725<\/span>\u201334<\/span>.\u00a0DOI<\/span>:\u00a010.1093\/rheumatology\/keaa692<\/span><\/p>\r\n

5.<\/span>\u00a0Stolwijk<\/span>\u00a0C<\/span><\/span>,\u00a0Essers<\/span>\u00a0I<\/span><\/span>,\u00a0van Tubergen<\/span>\u00a0A<\/span><\/span>,\u00a0et al<\/span>.\u00a0The epidemiology of extra-articular manifestations in ankylosing spondylitis:\u00a0Aa<\/span><\/span>\u00a0population-based matched cohort study<\/span>.\u00a0Ann Rheum Dis<\/em><\/span>.\u00a02015<\/span>;74<\/span><\/span>:1373<\/span><\/span>\u20138<\/span>.\u00a0DOI<\/span>:\u00a010.1136\/annrheumdis-2014-205253<\/span><\/p>\r\n

6.<\/span>\u00a0Van Praet<\/span>\u00a0L<\/span><\/span>,\u00a0Van den Bosch<\/span>\u00a0FE<\/span><\/span>,\u00a0Jacques<\/span>\u00a0P<\/span><\/span>,\u00a0et al<\/span>.\u00a0Microscopic gut inflammation in axial spondyloarthritis:\u00a0Aa<\/span><\/span>\u00a0multiparametric predictive model<\/span>.\u00a0Ann Rheum Dis<\/em><\/span>.\u00a02013<\/span>;72<\/span><\/span>:414<\/span><\/span>\u20137<\/span>.\u00a0DOI<\/span>:\u00a010.1136\/annrheumdis-2012-202135<\/span><\/p>\r\n

7.<\/span>\u00a0Macfarlane<\/span>\u00a0GJ<\/span><\/span>,\u00a0Biallas<\/span>\u00a0R<\/span><\/span>,\u00a0Dean<\/span>\u00a0LE<\/span><\/span>,\u00a0et al<\/span>.\u00a0Inflammatory bowel disease risk in patients with axial spondyloarthritis treated with biologic agents determined using the BSRBR-AS and a metaanalysis<\/span>.\u00a0J Rheumatol<\/em><\/span>.\u00a02023<\/span>;50<\/span>:175<\/span>\u201384<\/span>.\u00a0DOI<\/span>:\u00a010.3899\/jrheum.211034<\/span><\/p>\r\n

8.<\/span>\u00a0Goyette<\/span>\u00a0P<\/span><\/span>,\u00a0Boucher<\/span>\u00a0G<\/span><\/span>,\u00a0Mallon<\/span>\u00a0D<\/span><\/span>,\u00a0et al<\/span>.\u00a0High-density mapping of the MHC identifies a shared role for HLA-DRB1*01:03 in inflammatory bowel diseases and heterozygous advantage in ulcerative colitis<\/span>.\u00a0Nat Genet<\/em><\/span>.\u00a02015<\/span>;47<\/span>:172<\/span>\u20139<\/span>.\u00a0DOI<\/span>:\u00a010.1038\/ng.3176<\/span><\/p>\r\n

9.<\/span>\u00a0Xu<\/span>\u00a0H<\/span><\/span>,\u00a0Yin<\/span>\u00a0J<\/span><\/span>.\u00a0HLA risk alleles and gut microbiome in ankylosing spondylitis and rheumatoid arthritis<\/span>.\u00a0Best Pract Res Clin Rheumatol<\/em><\/span>.\u00a02019<\/span>;33<\/span>:101499<\/span>.\u00a0DOI<\/span>:\u00a010.1016\/j.berh.2020.101499<\/span><\/p>\r\n

10.<\/span>\u00a0Ellinghaus<\/span>\u00a0D<\/span><\/span>,\u00a0Jostins<\/span>\u00a0L<\/span><\/span>,\u00a0Spain<\/span>\u00a0SL<\/span><\/span>,\u00a0et al<\/span>.\u00a0Analysis of five chronic inflammatory diseases identifies 27 new associations and highlights disease-specific patterns at shared loci<\/span>.\u00a0Nat Genet<\/em><\/span>.\u00a02016<\/span>;48<\/span>:510<\/span>\u20138<\/span>.\u00a0DOI<\/span>:\u00a010.1038\/ng.3528<\/span><\/p>\r\n

11.<\/span>\u00a0Schett<\/span>\u00a0G<\/span><\/span>,\u00a0McInnes<\/span>\u00a0IB<\/span><\/span>,\u00a0Neurath<\/span>\u00a0MF<\/span><\/span>.\u00a0Reframing immune-mediated inflammatory diseases through signature cytokine hubs<\/span>.\u00a0N Engl J Med<\/em><\/span>.\u00a02021<\/span>;385<\/span><\/span>:628<\/span>\u201339<\/span>.\u00a0DOI<\/span>:\u00a010.1056\/NEJMra1909094<\/span><\/p>\r\n

12.<\/span>\u00a0Ciccia<\/span>\u00a0F<\/span><\/span>,\u00a0Bombardieri<\/span>\u00a0M<\/span><\/span>,\u00a0Principato<\/span>\u00a0A<\/span><\/span>,\u00a0et al<\/span>.\u00a0Overexpression of interleukin-23, but not interleukin-17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis<\/span>.\u00a0Arthritis Rheum<\/em><\/span>.\u00a02009<\/span>;60<\/span><\/span>:955<\/span>\u201365<\/span>.\u00a0DOI<\/span>:\u00a010.1002\/art.24389<\/span><\/p>\r\n

13.<\/span>\u00a0Gracey<\/span>\u00a0E<\/span><\/span>,\u00a0Yao<\/span>\u00a0Y<\/span><\/span>,\u00a0Green<\/span>\u00a0B<\/span><\/span>,\u00a0et al<\/span>.\u00a0Sexual dimorphism in the Th17 signature of ankylosing spondylitis<\/span>.\u00a0Arthritis Rheumatol<\/em><\/span><\/span>.\u00a02016<\/span>;68<\/span><\/span>:679<\/span>\u201389<\/span>.\u00a0DOI<\/span>:\u00a010.1002\/art.39464<\/span><\/p>\r\n

14.<\/span>\u00a0Zhou<\/span>\u00a0C<\/span><\/span>,\u00a0Zhao<\/span>\u00a0H<\/span><\/span>,\u00a0Xiao<\/span>\u00a0XY<\/span><\/span>,\u00a0et al<\/span>.\u00a0Metagenomic profiling of the pro-inflammatory gut microbiota in ankylosing spondylitis<\/span>.\u00a0J Autoimmun<\/em><\/span>.\u00a02020<\/span>;107<\/span>:102360<\/span>.\u00a0DOI<\/span>:\u00a010.1016\/j.jaut.2019.102360<\/span><\/p>\r\n

15.<\/span>\u00a0Manasson<\/span>\u00a0J<\/span><\/span>,\u00a0Shen<\/span>\u00a0N<\/span><\/span>,\u00a0Garcia Ferrer<\/span>\u00a0HR<\/span><\/span>,\u00a0et al<\/span>.\u00a0Gut microbiota perturbations in reactive arthritis and postinfectious spondyloarthritis<\/span>.\u00a0Arthritis Rheumatol<\/em><\/span><\/span>.\u00a02018<\/span>;70<\/span><\/span>:242<\/span>\u201354<\/span>.\u00a0DOI<\/span>:\u00a010.1002\/art.40359<\/span><\/p>\r\n

16.<\/span>\u00a0Liu<\/span>\u00a0G<\/span><\/span>,\u00a0Hao<\/span>\u00a0Y<\/span><\/span>,\u00a0Yang<\/span>\u00a0Q<\/span><\/span>,\u00a0Deng<\/span>\u00a0S<\/span><\/span>.\u00a0The association of fecal microbiota in ankylosing spondylitis cases with C-reactive protein and erythrocyte sedimentation rate<\/span>.\u00a0Mediators Inflamm<\/em><\/span>.\u00a02020<\/span>;2020<\/span>:8884324<\/span>.\u00a0DOI<\/span>:\u00a010.1155\/2020\/8884324<\/span><\/p>\r\n

17.<\/span>\u00a0Felice<\/span>\u00a0C<\/span><\/span>,\u00a0Leccese<\/span>\u00a0P<\/span><\/span>,\u00a0Scudeller<\/span>\u00a0L<\/span><\/span>,\u00a0et al<\/span>.\u00a0Red flags for appropriate referral to the gastroenterologist and the rheumatologist of patients with inflammatory bowel disease and spondyloarthritis<\/span>.\u00a0Clin Exp Immunol<\/em><\/span>.\u00a02019<\/span>;196<\/span><\/span>:123<\/span>\u201338<\/span>.\u00a0DOI<\/span>:\u00a010.1111\/cei.13246<\/span><\/p>\r\n

18.<\/span>\u00a0Maaser<\/span>\u00a0C<\/span><\/span>,\u00a0Sturm<\/span>\u00a0A<\/span><\/span>,\u00a0Vavricka<\/span>\u00a0SR<\/span><\/span>,\u00a0et al<\/span>.\u00a0ECCO-ESGAR guideline for diagnostic assessment in IBD Part 1:\u00a0Ii<\/span><\/span>nitial diagnosis, monitoring of known IBD, detection of complications<\/span>.\u00a0J Crohns Colitis<\/em><\/span><\/span>.\u00a02019<\/span>;13<\/span><\/span>:144<\/span><\/span>\u201364<\/span>.\u00a0DOI<\/span>:\u00a010.1093\/ecco-jcc\/jjy113<\/span><\/p>\r\n

19.<\/span>\u00a0Campos<\/span>\u00a0JF<\/span><\/span>,\u00a0Resende<\/span>\u00a0GG<\/span><\/span>,\u00a0Barbosa<\/span>\u00a0AJA<\/span><\/span>,\u00a0et al<\/span>.\u00a0Fecal calprotectin as a biomarker of microscopic bowel inflammation in patients with spondyloarthritis<\/span>.\u00a0Int J Rheum Dis<\/em><\/span>.\u00a02022<\/span>;25<\/span><\/span>:1078<\/span>\u201386<\/span>.\u00a0DOI<\/span>:\u00a010.1111\/1756-185X.14388<\/span><\/p>\r\n

20.<\/span>\u00a0Klingberg<\/span>\u00a0E<\/span><\/span>,\u00a0Strid<\/span>\u00a0H<\/span><\/span>,\u00a0St\u00e5hl<\/span>\u00a0A<\/span><\/span>,\u00a0et al<\/span>.\u00a0A longitudinal study of fecal calprotectin and the development of inflammatory bowel disease in ankylosing spondylitis<\/span>.\u00a0Arthritis Res Ther<\/em><\/span><\/span>.\u00a02017<\/span>;19<\/span>:21<\/span>.\u00a0DOI<\/span>:\u00a010.1186\/s13075-017-1223-2<\/span><\/span><\/p>\r\n

21.<\/span>\u00a0Ahn<\/span>\u00a0SM<\/span><\/span>,\u00a0Kim<\/span>\u00a0YG<\/span><\/span>,\u00a0Bae<\/span>\u00a0SH<\/span><\/span>,\u00a0et al<\/span>.\u00a0Ileocolonoscopic findings in patients with ankylosing spondylitis: A single center retrospective study<\/span>.\u00a0Korean J Intern Med<\/em><\/span>.\u00a02017<\/span>;32<\/span>:916<\/span>\u201322<\/span>.\u00a0DOI<\/span>:\u00a010.3904\/kjim.2015.313<\/span><\/p>\r\n

22.<\/span>\u00a0Eliakim<\/span>\u00a0R<\/span><\/span>,\u00a0Karban<\/span>\u00a0A<\/span><\/span>,\u00a0Markovits<\/span>\u00a0D<\/span><\/span>,\u00a0et al<\/span>.\u00a0Comparison of capsule endoscopy with ileocolonoscopy for detecting small-bowel lesions in patients with seronegative spondyloarthropathies<\/span>.\u00a0Endoscopy<\/em><\/span>.\u00a02005<\/span>;37<\/span><\/span>:1165<\/span>\u20139<\/span>.\u00a0DOI<\/span>:\u00a010.1055\/s-2005-870559<\/span><\/p>\r\n

23.<\/span>\u00a0Kopylov<\/span>\u00a0U<\/span><\/span>,\u00a0Starr<\/span>\u00a0M<\/span><\/span>,\u00a0Watts<\/span>\u00a0C<\/span><\/span>,\u00a0et al<\/span>.\u00a0Detection of Crohn disease in patients with spondyloarthropathy:\u00a0Tt<\/span><\/span>he space capsule study<\/span>.\u00a0J Rheumatol<\/em><\/span>.\u00a02018<\/span>;45<\/span><\/span>:498<\/span>\u2013505<\/span>.\u00a0DOI<\/span>:\u00a010.3899\/jrheum.161216<\/span><\/p>\r\n

24.<\/span>\u00a0Cohen-Mekelburg<\/span>\u00a0S<\/span><\/span>,\u00a0Van<\/span>\u00a0T<\/span><\/span>,\u00a0Wallace<\/span>\u00a0B<\/span><\/span>,\u00a0et al<\/span>.\u00a0The association between nonsteroidal anti-inflammatory drug use and inflammatory bowel disease exacerbations:\u00a0Aa<\/span><\/span>\u00a0true association or residual bias?<\/span>\u00a0Am J Gastroenterol<\/em><\/span>.\u00a02022<\/span>;117<\/span><\/span>:1851<\/span>\u20137<\/span>.\u00a0DOI<\/span>:\u00a010.14309\/ajg.0000000000001932<\/span><\/p>\r\n

25.<\/span>\u00a0Miao<\/span>\u00a0XP<\/span><\/span>,\u00a0Li<\/span>\u00a0JS<\/span><\/span>,\u00a0Ouyang<\/span>\u00a0Q<\/span><\/span>,\u00a0et al<\/span>.\u00a0Tolerability of selective cyclooxygenase 2 inhibitors used for the treatment of rheumatological manifestations of inflammatory bowel disease<\/span>.\u00a0Cochrane Database Syst Rev<\/em><\/span>.\u00a02014<\/span>:CD007744<\/span>.\u00a0DOI<\/span>:\u00a010.1002\/14651858.CD007744.pub2<\/span><\/p>\r\n

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27.<\/span>\u00a0Dhir<\/span>\u00a0V<\/span><\/span>,\u00a0Mishra<\/span>\u00a0D<\/span><\/span>,\u00a0Samanta<\/span>\u00a0J<\/span><\/span>.\u00a0Glucocorticoids in spondyloarthritis \u2013 systematic review and real-world analysis<\/span>.\u00a0Rheumatology (Oxford<\/em>)<\/span>.\u00a02021<\/span>;60<\/span>:4463<\/span>\u201375<\/span>.\u00a0DOI<\/span>:\u00a010.1093\/rheumatology\/keab275<\/span><\/p>\r\n

28.<\/span>\u00a0Haroon<\/span>\u00a0M<\/span><\/span>,\u00a0Ahmad<\/span>\u00a0M<\/span><\/span>,\u00a0Baig<\/span>\u00a0MN<\/span><\/span>,\u00a0et al<\/span>.\u00a0Inflammatory back pain in psoriatic arthritis is significantly more responsive to corticosteroids compared to back pain in ankylosing spondylitis:\u00a0Aa<\/span><\/span>\u00a0prospective, open-labelled, controlled pilot study<\/span>.\u00a0Arthritis Res Ther<\/em><\/span><\/span>.\u00a02018<\/span>;20<\/span>:73<\/span>.\u00a0DOI<\/span>:\u00a010.1186\/s13075-018-1565-4<\/span><\/span><\/p>\r\n

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38.<\/span>\u00a0Khanna<\/span>\u00a0R<\/span><\/span>,\u00a0Preiss<\/span>\u00a0JC<\/span><\/span>,\u00a0MacDonald<\/span>\u00a0JK<\/span><\/span>,\u00a0Timmer<\/span>\u00a0A<\/span><\/span>.\u00a0Anti-IL-12\/23p40 antibodies for induction of remission in Crohn\u2019s disease<\/span>.\u00a0Cochrane Database Syst Rev<\/em><\/span>.\u00a02015<\/span>;CD007572<\/span>:CD007572<\/span>.\u00a0DOI<\/span>:\u00a010.1002\/14651858.CD007572.pub2<\/span><\/p>\r\n

39.<\/span>\u00a0Sands<\/span>\u00a0BE<\/span><\/span>,\u00a0Sandborn<\/span>\u00a0WJ<\/span><\/span>,\u00a0Panaccione<\/span>\u00a0R<\/span><\/span>,\u00a0et al<\/span>.\u00a0Ustekinumab as induction and maintenance therapy for ulcerative colitis<\/span>.\u00a0N Engl J Med<\/em><\/span>.\u00a02019<\/span>;381<\/span>:1201<\/span>\u201314<\/span>.\u00a0DOI<\/span>:\u00a010.1056\/NEJMoa1900750<\/span><\/p>\r\n

40.<\/span>\u00a0Matsumoto<\/span>\u00a0S<\/span><\/span>,\u00a0Mashima<\/span>\u00a0H<\/span><\/span>.\u00a0Efficacy of ustekinumab against infliximab-induced psoriasis and arthritis associated with Crohn\u2019s disease<\/span>.\u00a0Biologics<\/em><\/span>.\u00a02018<\/span>;12<\/span>:69<\/span>\u201373<\/span>.\u00a0DOI<\/span>:\u00a010.2147\/BTT.S169326<\/span><\/p>\r\n

41.<\/span>\u00a0Deodhar<\/span>\u00a0A<\/span><\/span>,\u00a0Gensler<\/span>\u00a0LS<\/span><\/span>,\u00a0Sieper<\/span>\u00a0J<\/span><\/span>,\u00a0et al<\/span>.\u00a0Three multicenter, randomized, double-blind, placebo-controlled studies evaluating the efficacy and safety of ustekinumab in axial spondyloarthritis<\/span>.\u00a0Arthritis Rheumatol<\/em><\/span>.\u00a02019<\/span>;71<\/span>:258<\/span>\u201370<\/span>.\u00a0DOI<\/span>:\u00a010.1002\/art.40728<\/span><\/p>\r\n

<\/span><\/span>42.<\/span>\u00a0Pfizer<\/span>.\u00a0Pfizer Announces FDA Approval of XELJANZ\u00ae (tofacitinib) and XELJANZ\u00ae XR for the Treatment of Active Psoriatic Arthritis<\/span>.\u00a0Available at<\/span>:\u00a0www.pfizer.com\/news\/press-release\/press-release-detail\/us-fda-approves-pfizers-xeljanzr-tofacitinib-treatment-0<\/a><\/span>\u00a0(Date last accessed<\/span>:\u00a06<\/span>\u00a0April<\/span>\u00a02023<\/span>)<\/p>\r\n

<\/span>43.<\/span>\u00a0Pfizer<\/span>.\u00a0FDA Approves Pfizer\u2019s XELJANZ\u00ae (tofacitinib) for the Treatment of Active Ankylosing Spondylitis<\/span>.\u00a0Available at<\/span>:\u00a0www.pfizer.com\/news\/press-release\/press-release-detail\/pfizer_announces_fda_approval_of_xeljanz_tofacitinib_and_xeljanz_xr_for_the_treatment_of_active_psoriatic_arthritis<\/a><\/span>\u00a0(Date last accessed<\/span>:\u00a06<\/span>\u00a0April<\/span>\u00a02023<\/span>)<\/p>\r\n

<\/span>44.<\/span>\u00a0AbbVie<\/span>.\u00a0RINVOQ\u00ae (upadacitinib) Receives U.S. FDA Approval for Active Psoriatic Arthritis<\/span>.\u00a0Available at<\/span>:\u00a0https:\/\/news.abbvie.com\/news\/press-releases\/rinvoq-upadacitinib-receives-us-fda-approval-for-active-psoriatic-arthritis.htm<\/a><\/span>\u00a0(Date last accessed<\/span>:\u00a06<\/span>\u00a0April<\/span>\u00a02023<\/span>)<\/p>\r\n

<\/span>45.<\/span>\u00a0AbbVie<\/span>.\u00a0RINVOQ\u00ae (upadacitinib) Approved by U.S. FDA as an Oral Treatment for Adults with Active Ankylosing Spondylitis<\/span>.\u00a0Available at<\/span>:\u00a0https:\/\/news.abbvie.com\/news\/press-releases\/rinvoq-upadacitinib-approved-by-us-fda-as-an-oral-treatment-for-adults-with-active-ankylosing-spondylitis.htm<\/a><\/span>\u00a0(Date last accessed<\/span>:\u00a06<\/span>\u00a0April<\/span>\u00a02023<\/span>)<\/p>\r\n

46.<\/span>\u00a0Ytterberg<\/span>\u00a0SR<\/span><\/span>,\u00a0Bhatt<\/span>\u00a0DL<\/span><\/span>,\u00a0Mikuls<\/span>\u00a0TR<\/span><\/span>,\u00a0et al<\/span>.\u00a0Cardiovascular and cancer risk with tofacitinib in rheumatoid arthritis<\/span>.\u00a0N Engl J Med<\/em><\/span>.\u00a02022<\/span>;386<\/span><\/span>:316<\/span>\u201326<\/span>.\u00a0DOI<\/span>:\u00a010.1056\/NEJMoa2109927<\/span><\/p>\r\n

47.<\/span>\u00a0Sandborn<\/span>\u00a0WJ<\/span><\/span>,\u00a0Feagan<\/span>\u00a0BG<\/span><\/span>,\u00a0Rutgeerts<\/span>\u00a0P<\/span><\/span>,\u00a0et al<\/span>.\u00a0Vedolizumab as induction and maintenance therapy for Crohn\u2019s disease<\/span>.\u00a0New Engl J Med<\/em><\/span>.\u00a02013<\/span>;369<\/span>:711<\/span>\u201321<\/span>.\u00a0DOI<\/span>:\u00a010.1056\/NEJMoa1215739<\/span><\/p>\r\n

48.<\/span>\u00a0Feagan<\/span>\u00a0BG<\/span><\/span>,\u00a0Rutgeerts<\/span>\u00a0P<\/span><\/span>,\u00a0Sands<\/span>\u00a0BE<\/span><\/span>,\u00a0et al<\/span>.\u00a0Vedolizumab as induction and maintenance therapy for ulcerative colitis<\/span>.\u00a0N Engl J Med<\/em><\/span>.\u00a02013<\/span>;369<\/span>:699<\/span>\u2013710<\/span>.\u00a0DOI<\/span>:\u00a010.1056\/NEJMoa1215734<\/span><\/p>\r\n

<\/span>49.<\/span>\u00a0Sands<\/span>\u00a0BE<\/span><\/span>,\u00a0Peyrin-Biroulet<\/span>\u00a0L<\/span><\/span>,\u00a0Loftus<\/span>\u00a0EV<\/span>\u00a0Jr<\/span><\/span>,\u00a0et al<\/span>.\u00a0Vedolizumab versus adalimumab for moderate-to-severe ulcerative colitis<\/span>.\u00a0N Engl J Med<\/em><\/span>.\u00a02019<\/span>;381<\/span><\/span>:1215<\/span>\u201326<\/span>.\u00a0DOI<\/span>:\u00a010.1056\/NEJMoa1905725<\/span><\/p>\r\n

50.<\/span>\u00a0Felice<\/span>\u00a0C<\/span><\/span>,\u00a0Pugliese<\/span>\u00a0D<\/span><\/span>,\u00a0Papparella<\/span>\u00a0LG<\/span><\/span>,\u00a0et al<\/span>.\u00a0Clinical management of rheumatologic conditions co-occurring with inflammatory bowel diseases<\/span>.\u00a0Expert Rev Clin Immunol<\/em><\/span>.\u00a02018<\/span>;14<\/span><\/span>:751<\/span>\u20139<\/span>.\u00a0DOI<\/span>:\u00a010.1080\/1744666X.2018.1513329<\/span><\/p>\r\n

51.<\/span>\u00a0Ruscio<\/span>\u00a0MD<\/span><\/span>,\u00a0Tinazzi<\/span>\u00a0I<\/span><\/span>,\u00a0Variola<\/span>\u00a0A<\/span><\/span>,\u00a0et al<\/span>.\u00a0Prevalence and real-world management of vedolizumab-associated enthesitis in successfully treated IBD patients<\/span>.\u00a0Rheumatology<\/em><\/span>.\u00a02021<\/span>;60<\/span>:5809<\/span>\u201313<\/span>.\u00a0DOI<\/span>:\u00a010.1093\/rheumatology\/keab135<\/span><\/p>","wpcf-article_received_date":"20221214","wpcf-article_accepted_date":"20230315","wpcf-article_published_online":"20230424","wpcf-podcast":"","wpcf-ogg":"","wpcf-article_end_page":"","wpcf-article_start_page":"","wpcf-acknowledgements":"","wpcf-errata_pdf":"","wpcf-article_flipper_image":"","wpcf-corrected_online":null,"wpcf-supplementary_information":"","wpcf-article_highlight_pdf":"","data_availability":"Data sharing is not applicable to this article as no datasets were generated or analysed during the writing of this article.","digital_features":""},"_links":{"self":[{"href":"https:\/\/touchimmunology.com\/wp-json\/wp\/v2\/posts\/14327"}],"collection":[{"href":"https:\/\/touchimmunology.com\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/touchimmunology.com\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/touchimmunology.com\/wp-json\/wp\/v2\/users\/77788"}],"replies":[{"embeddable":true,"href":"https:\/\/touchimmunology.com\/wp-json\/wp\/v2\/comments?post=14327"}],"version-history":[{"count":13,"href":"https:\/\/touchimmunology.com\/wp-json\/wp\/v2\/posts\/14327\/revisions"}],"predecessor-version":[{"id":18677,"href":"https:\/\/touchimmunology.com\/wp-json\/wp\/v2\/posts\/14327\/revisions\/18677"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/touchimmunology.com\/wp-json\/wp\/v2\/media\/8304"}],"wp:attachment":[{"href":"https:\/\/touchimmunology.com\/wp-json\/wp\/v2\/media?parent=14327"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/touchimmunology.com\/wp-json\/wp\/v2\/categories?post=14327"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/touchimmunology.com\/wp-json\/wp\/v2\/tags?post=14327"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}