[Update: enterogenic spondylarthritis].
Update: enteropathische Spondyloarthritis.
Chronic inflammatory bowel disease
Crohn’s disease
Enterogenic reactive arthritis
Treatment
Ulcerative colitis
Journal
Zeitschrift fur Rheumatologie
ISSN: 1435-1250
Titre abrégé: Z Rheumatol
Pays: Germany
ID NLM: 0414162
Informations de publication
Date de publication:
Aug 2021
Aug 2021
Historique:
accepted:
16
04
2021
pubmed:
29
5
2021
medline:
7
8
2021
entrez:
28
5
2021
Statut:
ppublish
Résumé
Spondylarthritis (SpA) is one of the most frequent extraintestinal manifestations of chronic inflammatory bowel disease (IBD). Several arthritogenic enterobacterial infections can induce sequelae such as reactive SpA. Studies on the gut-synovium axis in view of genetic, immunological, clinical and therapeutic aspects has made enterogenic SpA a model disease of all forms of SpA. The same applies for investigating IBD, as subclinical gut inflammation seen in SpA patients has provided significant evidence for a better understanding of mucosa-associated early immune events in Crohn's disease (CD). This article summarizes the pathognomonic clinical features, diagnostic steps, differential diagnosis and current pathogenetic models of enterogenic SpA. Knowledge of pathogenetic contexts leads to concrete treatment recommendations. These vary individually depending on the underlying IBD, on the inflammatory intestinal or rheumatic activity and on the rheumatological manifestation pattern. Spondyloarthritiden (SpA) gehören zu den häufigsten extraintestinalen Manifestationen der chronisch entzündlichen Darmerkrankungen (CED). Auch bestimmte arthritogene Enterobakterien können als Folgeerkrankung der Gastroenteritis eine reaktive enteropathische SpA auslösen. Die Erforschung der „Darm-Synovium-Achse“ unter genetischen, immunologischen, klinischen und therapeutischen Gesichtspunkten hat die enteropathische SpA zu einer Modellerkrankung der SpAs gemacht. Ähnliches gilt für die Erforschung der CED, da die subklinischen Darmentzündungen bei Patienten mit SpA dazu beigetragen haben, die Mukosa-assoziierten frühen Immunphänomene des Morbus Crohn (CD) besser zu verstehen. Dieser Beitrag stellt neben den pathognomonischen klinischen Bildern, der Diagnostik und Differenzialdiagnostik die aktuellen pathogenetischen Modelle der enteropathischen SpAs vor. Aus dem Wissen um pathogenetische Zusammenhänge ergeben sich konkrete Empfehlungen zur Therapie, wobei individuell nach der zugrunde liegenden Darmerkrankung, nach der entzündlichen intestinalen oder rheumatischen Aktivität und nach dem rheumatologischen Befallsmuster unterschieden wird.
Autres résumés
Type: Publisher
(ger)
Spondyloarthritiden (SpA) gehören zu den häufigsten extraintestinalen Manifestationen der chronisch entzündlichen Darmerkrankungen (CED). Auch bestimmte arthritogene Enterobakterien können als Folgeerkrankung der Gastroenteritis eine reaktive enteropathische SpA auslösen. Die Erforschung der „Darm-Synovium-Achse“ unter genetischen, immunologischen, klinischen und therapeutischen Gesichtspunkten hat die enteropathische SpA zu einer Modellerkrankung der SpAs gemacht. Ähnliches gilt für die Erforschung der CED, da die subklinischen Darmentzündungen bei Patienten mit SpA dazu beigetragen haben, die Mukosa-assoziierten frühen Immunphänomene des Morbus Crohn (CD) besser zu verstehen. Dieser Beitrag stellt neben den pathognomonischen klinischen Bildern, der Diagnostik und Differenzialdiagnostik die aktuellen pathogenetischen Modelle der enteropathischen SpAs vor. Aus dem Wissen um pathogenetische Zusammenhänge ergeben sich konkrete Empfehlungen zur Therapie, wobei individuell nach der zugrunde liegenden Darmerkrankung, nach der entzündlichen intestinalen oder rheumatischen Aktivität und nach dem rheumatologischen Befallsmuster unterschieden wird.
Identifiants
pubmed: 34046687
doi: 10.1007/s00393-021-01014-2
pii: 10.1007/s00393-021-01014-2
doi:
Types de publication
Journal Article
Langues
ger
Sous-ensembles de citation
IM
Pagination
539-551Informations de copyright
© 2021. Springer Medizin Verlag GmbH, ein Teil von Springer Nature.
Références
Rudwaleit M, Baeten D (2006) Ankylosing spondylitis and bowel disease. Best Pract Res Clin Rheumatol 20:451
pubmed: 16777576
doi: 10.1016/j.berh.2006.03.010
Shivashankar R, Loftus EV Jr, Tremaine WJ, Bongartz T, Harmsen WS, Zinsmeister AR (2012) Matteson EL Incidence of spondyloarthropathy in patients with Crohn’s disease: a population-based study. J Rheumatol 39:2148–2152
pubmed: 22984277
pmcid: 3496378
doi: 10.3899/jrheum.120321
Shivashankar R, Loftus EV Jr, Tremaine WJ, Harmsen WS, Zinsmeister AR, Matteson EL (2013) Incidence of Spondyloarthropathy in patients with ulcerative colitis: a population-based study. J Rheumatol 40:1153–1157
pubmed: 23678160
doi: 10.3899/jrheum.121029
Vavricka SR, Brun L, Ballabeni P et al (2011) Frequency and risk factors for extraintestinal manifestations in the Swiss inflammatory bowel disease cohort. Am J Gastroenterol 106:110–119
pubmed: 20808297
doi: 10.1038/ajg.2010.343
Karreman MC, Luime JJ, Hazes JM, Weel AE (2017) The prevalence and incidence of axial and peripheral spondyloarthritis in inflammatory bowel disease: a systematic review and meta-analysis. J Crohns Colitis 11:631–642
pubmed: 28453761
Orchard TR, Thiyagaraja S, Welsh KI, Wordsworth BP, Hill Gaston JS, Jewell DP (2000) Clinical phenotype is related to HLA genotype in the peripheral arthropathies of inflammatory bowel disease. Gastroenterology 118:274–278
pubmed: 10648455
doi: 10.1016/S0016-5085(00)70209-5
Peeters H, Vander Cruyssen B, Laukens D et al (2004) Radiological sacroiliitis, a hallmark of spondylitis, is linked with CARD15 gene polymorphisms in patients with Crohn’s disease. Ann Rheum Dis 63:1131–1134
pubmed: 15308523
pmcid: 1755138
doi: 10.1136/ard.2004.021774
Zeitz J, Vavricka SR (2013) Therapie der extraintestinalen CED-Manifestationen : Eine schwierige Herausforderung. Gastroenterologe 8:217–225
doi: 10.1007/s11377-012-0726-2
Travis S (1997) Sweet’s syndrome: an unusual cutaneous feature of Crohn’s disease or ulcerative colitis. The south west gastroenterology group. Eur J Gastroenterol Hepatol 9:15–720
doi: 10.1097/00042737-199707000-00013
Märker-Hermann E (2020) Reaktive Arthritis – eine vergessene Erkrankung? Dtsch Med Wochenschr 145:1786–1790
pubmed: 33254255
doi: 10.1055/a-1036-9359
Ajene AN, Fischer Walker CL, Black RE (2013) Enteric pathogens and reactive arthritis: a systematic review of campylobacter, salmonella and shigella-associated reactive arthritis. J Health Popul Nutr 31:299
pubmed: 24288942
pmcid: 3805878
doi: 10.3329/jhpn.v31i3.16515
Vasala M, Hallanvuo S, Ruuska P et al (2014) High frequency of reactive arthritis in adults after Yersinia pseudotuberculosis O:1 outbreak caused by contaminated grated carrots. Ann Rheum Dis 73:1793–1796
pubmed: 23852698
doi: 10.1136/annrheumdis-2013-203431
Tuompo R, Lääveri T, Hannu T et al (2020) Reactive arthritis and other musculoskeletal symptoms associated with acquisition of diarrhoeagenic escherichia coli (DEC). Ann Rheum Dis 79:605–611
pubmed: 32179576
doi: 10.1136/annrheumdis-2019-216736
Mielants H, Veys EM, Cuvelier C et al (1995) The evolution of spondyloarthropathies in relation to gut histology. II. Histological aspects. J Rheumatol 22:2273–2278
pubmed: 8835561
Mielants H, Veys EM, Cuvelier C, De Vos M (1996) Course of gut inflammation in spondylarthropathies and therapeutic consequences. Baillieres Clin Rheumatol 10:147–164
pubmed: 8674145
doi: 10.1016/S0950-3579(96)80010-0
Van Praet L, Van den Bosch FE, Jacques P et al (2013) Microscopic gut inflammation in axial spondyloarthritis: a multiparametric predictive model. Ann Rheum Dis 72:414–417
pubmed: 23139267
doi: 10.1136/annrheumdis-2012-202135
Klingberg E, Strid H, Ståhl A et al (2017) A longitudinal study of fecal calprotectin and the development of inflammatory bowel disease in ankylosing spondylitis. Arthritis Res Ther 19(1):21
pubmed: 28148281
pmcid: 5289027
doi: 10.1186/s13075-017-1223-2
Rudwaleit M, van der Heijde D, Landewe R et al (2011) The assessment of spondyloarthritis international society classification criteria for peripheral spondyloarthritis and for spondyloarthritis in general. Ann Rheum Dis 70:25–31
pubmed: 21109520
doi: 10.1136/ard.2010.133645
Rudwaleit M, van der Heijde D, Landewe R et al (2009) The development of assessment of spondyloarthritis international society classification criteria for axial spondyloarthritis (part II): validation and final selection. Ann Rheum Dis 68:777–783
pubmed: 19297344
doi: 10.1136/ard.2009.108233
Chan J, Sari I, Salonen D, Silverberg MS et al (2018) Prevalence of sacroiliitis in inflammatory bowel disease using a standardized CT scoring system. Arthritis Care Res (Hoboken) 70:807–810
doi: 10.1002/acr.23323
Kiltz U, Braun J, DGRh et al (2019) Langfassung zur S3-Leitlinie Axiale Spondyloarthritis inklusive Morbus Bechterew und Frühformen, Update 2019. Z Rheumatol 78:3–64
pubmed: 31784900
doi: 10.1007/s00393-019-0670-3
Leclerc-Jacob S, Lux G, Rat AC et al (2014) The prevalence of inflammatory sacroiliitis assessed on magnetic resonance imaging of inflammatory bowel disease: a retrospective study performed on 186 patients. Aliment Pharmacol Ther 39:957–962
pubmed: 24593050
doi: 10.1111/apt.12680
de Miguel E, Cobo T, Muñoz-Fernández S et al (2009) Validity of enthesis ultrasound assessment in spondyloarthropathy. Ann Rheum Dis 68:169–174
pubmed: 18390909
doi: 10.1136/ard.2007.084251
Silverberg MS, Mirea L, Bull SB et al (2003) A population- and family-based study of Canadian families reveals association of HLA DRB1*0103 with colonic involvement in inflammatory bowel disease. Inflamm Bowel Dis 9:1–9
pubmed: 12656131
doi: 10.1097/00054725-200301000-00001
Ossum AM, Palm Ø, Lunder AK et al (2018) Ankylosing spondylitis and axial spondyloarthritis in patients with long-term inflammatory bowel disease: results from 20 years of follow-up in the IBSEN study. J Crohns Colitis 12:96–104
pubmed: 28961700
doi: 10.1093/ecco-jcc/jjx126
De Vos M, Hindryckx P, Laukens D (2011) Novel development in extraintestinal manifestations and spondylarthropathy. Best Pract Res Clin Gastroenterol 25(1):S19–S26
pubmed: 21640926
doi: 10.1016/S1521-6918(11)70006-3
van der Paardt M, Crusius JBA, de Koning MHMT et al (2003) CARD15 gene mutations are not associated with ankylosing spondylitis. Genes Immun 4:77–78
pubmed: 12595906
doi: 10.1038/sj.gene.6363914
D’Amato M, Sorrentino R, Pettersson S (2014) The Crohn’s associated NOD2 3020InsC frameshift mutation does not confer susceptibility to ankylosing spondylitis. J Rheumatol 41:187
Laukens D, Peeters H, Marichal D et al (2005) CARD15 gene polymorphisms in patients with spondyloarthropathies identify a specific phenotype previously related to Crohn’s disease. Ann Rheum Dis 64:930–935
pubmed: 15539413
doi: 10.1136/ard.2004.028837
Danoy P, Pryce K, Hadler J et al (2010) Association of variants at 1q32 and STAT3 with ankylosing spondylitis suggests genetic overlap with Crohn’s disease. PLoS Genet 6:e1001195
pubmed: 21152001
pmcid: 2996314
doi: 10.1371/journal.pgen.1001195
Laukens D, Georges M, Libioulle C et al (2010) Evidence for significant overlap between common risk variants for Crohn’s disease and ankylosing spondylitis. PLoS One 5:e13795
pubmed: 21072187
pmcid: 2970560
doi: 10.1371/journal.pone.0013795
Pointon JJ, Harvey D, Karaderi T et al (2010) Elucidating the chromosome 9 association with AS; CARD9 is a candidate gene. Genes Immun 11:490–496
pubmed: 20463747
pmcid: 2933507
doi: 10.1038/gene.2010.17
Duerr RH, Taylor KD, Brant SR et al (2006) A genome-wide association study identifies IL23R as an inflammatory bowel disease gene. Science 314:1461–1463
pubmed: 17068223
pmcid: 4410764
doi: 10.1126/science.1135245
The Australo-Anglo-American Spondyloarthritis Consortium (TASC) (2010) Genome-wide association study of ankylosing spondylitis identifies non-MHC susceptibility loci. Nat Genet 42:123–127
doi: 10.1038/ng.513
Van Deventer SJ (1997) Tumour necrosis factor and crohn’s disease. Gut 40:443–448
pubmed: 9176068
pmcid: 1027115
doi: 10.1136/gut.40.4.443
Leppkes M, Roulis M, Neurath MF et al (2014) Pleiotropic functions of TNF‑α in the regulation of the intestinal epithelial response to inflammation. Int Immunol 26:509–515
pubmed: 24821262
doi: 10.1093/intimm/dxu051
Mei Y, Pan F, Gao J et al (2011) Increased serum IL-17 and IL-23 in the patient with ankylosing spondylitis. Clin Rheumatol 30:269–273
pubmed: 21161669
doi: 10.1007/s10067-010-1647-4
Appel H, Maier R, Wu P et al (2011) Analysis of IL-17(+) cells in facet joints of patients with spondyloarthritis suggests that the innate immune pathway might be of greater relevance than the Th17-mediated adaptive immune response. Arthritis Res Ther 13:R95
pubmed: 21689402
pmcid: 3218910
doi: 10.1186/ar3370
Ciccia F, Bombardieri M, Principato A et al (2009) Overexpression of interleukin-23, but not interleukin-17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis. Arthritis Rheum 60:955–965
pubmed: 19333939
doi: 10.1002/art.24389
Sherlock JP, Joyce-Shaikh B, Turner SP et al (2012) IL-23 induces spondyloarthropathy by acting on ROR-γt+ CD3+CD4-CD8- entheseal resident T cells. Nat Med 18:1069–1076
pubmed: 22772566
doi: 10.1038/nm.2817
Benham H, Rehaume LM, Hasnain SZ et al (2014) Interleukin-23 mediates the intestinal response to microbial β‑1,3‑glucan and the development of spondyloarthritis pathology in SKG mice. Arthritis Rheumatol 66:1755–1767
pubmed: 24664521
doi: 10.1002/art.38638
Taurog JD, Richardson JA, Croft JT et al (1994) The germfree state prevents development of gut and joint inflammatory disease in HLA-B27 transgenic rats. J Exp Med 180:2359–2364
pubmed: 7964509
doi: 10.1084/jem.180.6.2359
Breban M, Tap J, Leboime A et al (2017) Faecal microbiota study reveals specific dysbiosis in spondyloarthritis. Ann Rheum Dis 76:1614–1622
pubmed: 28606969
doi: 10.1136/annrheumdis-2016-211064
Tito RY, Cypers H, Joossens M et al (2017) Brief report: dialister as a microbial marker of disease activity in spondyloarthritis. Arthritis Rheumatol 69:114–121
pubmed: 27390077
doi: 10.1002/art.39802
Gracey E, Qaiyum Z, Almaghlouth I et al (2016) IL‑7 primes IL-17 in mucosal-associated invariant T (MAIT) cells, which contribute to the Th17-axis in ankylosing spondylitis. Ann Rheum Dis 75:2124–2132
pubmed: 27165176
doi: 10.1136/annrheumdis-2015-208902
Qaiyum Z, Gracey E, Yao Y, Inman RD (2019) Integrin and transcriptomic profiles identify a distinctive synovial CD8+ T cell subpopulation in spondyloarthritis. Ann Rheum Dis 78:1566
pubmed: 31471299
doi: 10.1136/annrheumdis-2019-215349
May E, Märker-Hermann E, Wittig BM et al (2000) Identical T‑cell expansions in the colon mucosa and the synovium of a patient with enterogenic spondyloarthropathy. Gastroenterology 119:1745–1755
pubmed: 11113096
doi: 10.1053/gast.2000.20173
Severs M, van Erp SJ, van der Valk ME, Dutch Initiative on Crohn and Colitis et al (2016) Smoking is associated with extra-intestinal manifestations in inflammatory bowel disease. J Crohns Colitis 10:455–461
pubmed: 26721937
doi: 10.1093/ecco-jcc/jjv238
Preiß JC, Bokemeyer B, Buhr HJ et al (2014) Aktualisierte S3-Leitlinie – „Diagnostik und Therapie des Morbus Crohn“ 2014. AWMF-Registrierungsnummer: 021-004. Z Gastroenterol 52:1431–1484
pubmed: 25474283
doi: 10.1055/s-0034-1385199
Kucharzik T, Dignass AU, Atreya R et al (2020) Aktualisierte S3-Leitlinie Colitis ulcerosa—Living Guideline August 2020—AWMF-Registriernummer: 021-009. Z Gastroenterol 58:e241–e345
pubmed: 33260237
doi: 10.1055/a-1296-3444
Tadbiri S, Peyrin-Biroulet L, Serrero M, Getaid Observ-IBD study group et al (2018) Impact of vedolizumab therapy on extra-intestinal manifestations in patients with inflammatory bowel disease: a multicentre cohort study nested in the Observ-IBD cohort. Aliment Pharmacol Ther 47:485–493
pubmed: 29250803
doi: 10.1111/apt.14419
Clegg DO, Reda DJ, Abdellatif M (1999) Comparison of sulfasalazine and placebo for the treatment of axial and peripheral articular manifestations of the seronegative spondylarthropathies: a department of veterans affairs cooperative study. Arthritis Rheum 42:2325–2329
pubmed: 10555027
doi: 10.1002/1529-0131(199911)42:11<2325::AID-ANR10>3.0.CO;2-C
Van den Bosch F, Kruithof E, De Vos M et al (2000) Crohn’s disease associated with spondyloarthropathy: effect of TNF-alpha blockade with infliximab on articular symptoms. Lancet 356:1821–1822
pubmed: 11117919
doi: 10.1016/S0140-6736(00)03239-6
Generini S, Giacomelli R, Fedi R et al (2004) Infliximab in spondyloarthropathy associated with Crohn’s disease: an open study on the efficacy of inducing and maintaining remission of musculoskeletal and gut manifestations. Ann Rheum Dis 63:1664–1669
pubmed: 15297279
pmcid: 1754868
doi: 10.1136/ard.2003.012450
Luchetti MM, Benfaremo D, Ciccia F et al (2017) Adalimumab efficacy in enteropathic spondyloarthritis: a 12-mo observational multidisciplinary study. World J Gastroenterol 23:7139–7149
pubmed: 29093622
pmcid: 5656461
doi: 10.3748/wjg.v23.i39.7139
Sandborn WJ, Hanauer SB, Katz S et al (2001) Etanercept for active Crohn’s disease: a randomized, double-blind, placebo-controlled trial. Gastroenterology 121:1088–1094
pubmed: 11677200
doi: 10.1053/gast.2001.28674
Marzo-Ortega H, McGonagle D, O’Connor P et al (2003) Efficacy of etanercept for treatment of Crohn’s related spondyloarthritis but not colitis. Ann Rheum Dis 62:74–76
pubmed: 12480676
pmcid: 1754306
doi: 10.1136/ard.62.1.74
Sandborn WJ, Gasink C, Gao LL et al (2012) Ustekinumab induction and maintenance therapy in refractory Crohn’s disease. N Engl J Med 367:1519–1528
pubmed: 23075178
doi: 10.1056/NEJMoa1203572
Sands BE, Sandborn WJ, Panaccione R et al (2019) Ustekinumab as induction and maintenance therapy for ulcerative colitis. N Engl J Med 381:1201–1214
pubmed: 31553833
doi: 10.1056/NEJMoa1900750
Deodhar A, Gensler LS, Sieper J et al (2019) Three multicenter, randomized, double-blind, placebo-controlled studies evaluating the efficacy and safety of ustekinumab in axial spondyloarthritis. Arthritis Rheumatol 71:258–270
pubmed: 30225992
doi: 10.1002/art.40728
Song X, Dai D, He X, Zhu S, Yao Y, Gao H, Wang J, Qu F, Qiu J, Wang H et al (2015) Growth factor FGF2 cooperates with Interleukin-17 to repair intestinal epithelial damage. Immunity 43:488–501
pubmed: 26320657
doi: 10.1016/j.immuni.2015.06.024
Burisch J, Eigner W, Schreiber S et al (2020) Risk for development of inflammatory bowel disease under inhibition of interleukin 17: a systematic review and meta-analysis. PLoS ONE 15(5):e233781
pubmed: 32459816
pmcid: 7252630
doi: 10.1371/journal.pone.0233781