Clinical and genetic factors associated with sacroiliitis in Crohn's disease

Peeters, Harald; Cruyssen, Bert Vander; Mielants, Herman; Vlam, Kurt de; Vermeire, Séverine; Louis, Édouard; Rutgeerts, Paul; Bélaïche, Jacques; Vos, Martine De

doi:10.1111/j.1440-1746.2007.05108.x

Cited by 63 publications

(43 citation statements)

References 32 publications

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“…Pure asymptomatic SI in CD is not strongly associated with HLA-B27 and a very recent study indicates a prevalence of 7% (comparable to prevalence in the healthy population) [43] , and it seems that evolution to AS is more likely to occur in HLAB27-positive patients [59] . This suggests that SI and AS in IBD patients are different entities.…”

Section: Hla-b27mentioning

confidence: 99%

“…Souza et al [49] , in a mixed Brazilian IBD population found a prevalence of 14.4%, with no difference between CD and UC. Al-Shamali et al [50] reported [43] 2008…”

Section: Epidemiologymentioning

confidence: 99%

“…Studies on IBD populations after the introduction of the ESSG criteria or Amor criteria are summarized in Table 6 [1, [34][35][36][37][38][39][40][41][42][43][44][45] . A discrete number of papers reporting on IBD-associated joint disease were not included.…”

Section: Epidemiologymentioning

confidence: 99%

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Clinical features and epidemiology of spondyloarthritides associated with inflammatory bowel disease

Salvarani

Fries

2009

WJG

109

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Inflammation of axial and/or peripheral joints is one of the most frequent extra-intestinal manifestations complicating the clinical course and therapeutic approach in inflammatory bowel diseases (IBD). The frequency of these complications seems to be similar for both diseases, Crohn's disease and ulcerative colitis. Arthritis associated with IBD belongs to the category of spondyloarthropathies. Axial involvement ranges from isolated inflammatory back pain to ankylosing spondylitis, whereas peripheral arthritis is noted in pauciarticular and in polyarticular disease. Asymptomatic radiological involvement of the sacroiliac joints is reported to occur in up to 50% of patients. Other musculoskeletal manifestations such as buttock pain, dactylitis, calcaneal enthesitis, and thoracic pain are frequently underdiagnosed and, consequently, are not treated appropriately. Several diagnostic approaches and criteria have been proposed over the past 40 years in an attempt to correctly classify and diagnose such manifestations. The correct recognition of spondylarthropathies needs an integrated multidisciplinary approach in order to identify common therapeutic strategies, especially in the era of the new biologic therapies.

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Section: Hla-b27mentioning

confidence: 99%

“…Souza et al [49] , in a mixed Brazilian IBD population found a prevalence of 14.4%, with no difference between CD and UC. Al-Shamali et al [50] reported [43] 2008…”

Section: Epidemiologymentioning

confidence: 99%

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Clinical features and epidemiology of spondyloarthritides associated with inflammatory bowel disease

Salvarani

Fries

2009

WJG

109

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“…Seventy-eight percent of CD patients with sacroiliitis were carriers of at least one SNP in NOD2, compared to 48% of those who were wild type for NOD2. However, in a second multi-center study, this observation could not be repeated [102]. The reason for this inconsistency is not clear.…”

Section: Nod2 (16q)mentioning

confidence: 86%

Genetics of Spondyloarthropathies and Inflammatory Bowel Disease: Searching for Common Susceptibility Factors

Laukens¹,

Vos

2008

CRR

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Ileocolonoscopic evidence for subclinical gut inflammation is found in a subpopulation of spondyloarthropathy (SpA) patients. The prevalence of microscopic intestinal lesions is even higher and can be classified as either an acute or a chronic type of inflammation. The latter condition is associated with an increased risk of developing overt inflammatory bowel disease (IBD), especially Crohn's disease (CD), over time. Evidence for genetic predisposition in both SpA and IBD is strong, and has resulted in the identification of several linked chromosomal loci and putative candidate genes. The regular co-existence of SpA and IBD within the same family suggests a common genetic component. Interestingly, comparison of genome-wide linkage and association data reveals thirteen disease-associated chromosomal regions that are shared between SpA and IBD. This should convince geneticists to examine genes within these regions as potential susceptibility genes for the development of both SpA and IBD. Significant association of such shared genetic determinants was established for NOD2 (16q), the major histocompatibility complex I allele HLA-B27 (6p) and recently also the interleukin 23 receptor (1p). Transgenic animals in which tumor necrosis factor alpha or HLA-B27 is overexpressed suffer both joint and gut abnormalities resembling human SpA/CD pathology, providing additional evidence for a common genetic predisposition for the onset of joint and gut inflammation. In view of a hypothetical pathway leading to intestinal and articular inflammation in SpA and IBD, we review and compare genome-wide linkage and genetic association data obtained for SpA and IBD.Keywords: Spondyloarthropathy, Crohn's disease, genetic susceptibility, NOD2, HLA-B27, IL23R.Spondyloarthropathy (SpA) and inflammatory bowel disease (IBD) are chronic inflammatory conditions in which the initiating events are complex. In SpA, the axial skeleton, the sacroiliac joints and, to a lesser degree, peripheral joints become inflamed, whereas in IBD involving Crohn's disease (CD) and ulcerative colitis (UC), the intestine is the primary site of inflammation. The estimated prevalence in Western countries is 0.3-2% for SpA and 0.1-0.3% for IBD. The unity between SpA and IBD is illustrated by a strong clinical as well as molecular overlap. The first symptoms present themselves in early adulthood, usually before the age of 30, but early childhood and late onset disease occur sporadically. Medical treatment is mainly based on diminishing the inflammation and maintaining the remission states. Spondyloarthropathy is a heterogeneous group generally divided into 5 disease categories: ankylosing spondylitis (AS), reactive arthritis (ReA), psoriatic arthritis (PsA), SpA associated with IBD (SpA-IBD) and undifferentiated SpA. In the SpA-IBD group, patients suffer from clinically overt CD or UC. However, the gut is also an important site of inflammation in patients belonging to the other SpA disease categories. In ileocolonoscopic studies of SpA patients, histological ...

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“…Enthesitis or inflammation of insertion of tendon to bone occurs in about 7% of patients. The axial arthropathy includes inflammatory back pain present in 20-30% of patients, radiologic evidence of sacroiliitis in 20-25% of patients and full diagnosis of ankylosing spondylitis (AS) according to Rome criteria in 2-10% of patients [1][2][3] . Sacroiliitis and AS are diagnosed on conventional rheumatological grounds supported by characteristic radiologic changes, magnetic resonance imaging being the most sensitive.…”

Section: Clinical Evidencementioning

confidence: 99%

Joint Involvement Associated with Inflammatory Bowel Disease

Vos

2009

Dig Dis

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Joint involvement associated with inflammatory bowel disease (IBD) belongs to the concept of spondyloarthritis (SpA) and includes two types of arthritis: a peripheral arthritis characterized by the presence of pauciarticular asymmetrical arthritis affecting preferentially joints of lower extremities and an axial arthropathy including inflammatory back pain, sacroiliitis and ankylosing spondylitis (AS). Treatment of arthritis includes a short-term use of NSAIDs associated with optimized treatment of gut inflammation. Safety concerns mean that long-term treatment with NSAIDs is best avoided if possible. Salazopyrine can be recommended for treatment of peripheral arthritis. Methotrexate and azathioprine are generally ineffective. Finally, efficacy of anti-TNF therapy (infliximab and adalimumab) is well established. However, use of etanercept is not recommended because of the increased risk for intestinal disease relapse. Pathogenesis of gut-joint iteropathy is not elucidated. Both inflammations are tightly related as suggested by human evidence of gut inflammation in patients with other forms of SpA and animal evidence of gut and joint inflammation in HLA-B27/human β₂-microglobulin transgenic rat model and TNF^Δ^ARE mice. Several clues for the linkage between gut and joint inflammation have been put forward including an altered recognition and handling of bacterial antigens, an aberrant trafficking of CD8+ T cells with an impaired T-helper type 1 cytokine profile and expression of aEb7 integrin, an altered trafficking of macrophages expressing CD163 and evidence of an increased angiogenesis. A transcriptome analysis of mucosal biopsies identified a set of 95 genes that are differentially expressed in both CD and SpA as compared with healthy controls suggesting common pathways. TNF plays a key role in the pathogenesis of various arthritic diseases and IBD. Mesenchymal/myofibroblast-like cells may represent the local primary targets of TNF in the induction of gut and joint pathology. Selective expression of TNFRI on these cells seems to be sufficient to orchestrate the complete development of SpA-related pathologies at least in TNF^Δ^ARE mice. Finally, genetic susceptibility is probably required to develop these pathologies. Genotyping of AS patients provided evidence for an important overlap between determinants of inherited predisposition to CD and AS. The best documented common association is with an IL-23R polymorphism, although the exact role remains unexplored. In addition, evidence suggests that a number of recently identified CD-susceptibility loci are associated with AS. Clinical, genetical, immunological and therapeutic evidence support the tight junction between gut and joint inflammation in two linked diseases, IBD and SpA, belonging to the ‘immune-mediated inflammatory diseases’.

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Clinical and genetic factors associated with sacroiliitis in Crohn's disease

Cited by 63 publications

References 32 publications

Clinical features and epidemiology of spondyloarthritides associated with inflammatory bowel disease

Clinical features and epidemiology of spondyloarthritides associated with inflammatory bowel disease

Genetics of Spondyloarthropathies and Inflammatory Bowel Disease: Searching for Common Susceptibility Factors

Joint Involvement Associated with Inflammatory Bowel Disease

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