De Vos M
Department of Gastroenterology, Ghent University Hospital, Belgium.
Aliment Pharmacol Ther. 2004 Oct;20 Suppl 4:36-42. doi: 10.1111/j.1365-2036.2004.02044.x.
Peripheral involvement of the joints, including pauciarticular, asymmetrical, transitory and migrating synovitis and enthesiopathy, is observed in 10-20% of affected inflammatory bowel disease patients. Recurrence is common and frequently coincides with a flare-up of intestinal disease. The true prevalence of axial involvement is less well established. Sacroiliitis is a hallmark of spondylitis, but is under-reported due to its insidious onset and sometimes asymptomatic nature. Radiographic evidence of sacroiliitis is present in about 20-25% of patients. Ankylosing spondylitis, as defined by the Rome criteria, is present in 3-10% of inflammatory bowel disease patients, and is thought to have a different genetic predisposition in these patients compared with 'classic' ankylosing spondylitis: whereas the human leucocyte antigen B27 phenotype is present in 90% of patients with 'classic' ankylosing spondylitis, the prevalence decreases to only 30% in patients with ankylosing spondylitis secondary to Crohn's disease. Polymorphisms involving CARD15 appear to be a possible genetic trigger: 78% of patients with Crohn's disease and symptomatic or asymptomatic sacroiliitis carry at least one mutation, compared with only 48% of control Crohn's disease patients. Moreover, in other forms of spondyloarthropathy, a similar association has been reported: 42% of patients with spondyloarthropathy and associated asymptomatic chronic gut inflammation, who are considered likely to develop Crohn's disease and ankylosing spondylitis, are carriers of at least one CARD15 mutation, compared with only 7% of patients with normal histology. In addition to genetic markers, clinical features support the relationship between gut and joint pathophysiology. In cases of spondyloarthropathy, a very rapid, substantial and sustained improvement in symptoms has been reported following treatment with infliximab, suggesting an essential role for tumour necrosis factor-alpha in spondyloarthropathy, similar to that observed in Crohn's disease.
10%-20%的炎性肠病患者会出现关节周围受累,包括少关节性、不对称性、短暂性和游走性滑膜炎及附着点病。复发很常见,且常与肠道疾病发作同时出现。轴向受累的真实患病率尚不太明确。骶髂关节炎是脊柱关节炎的标志,但由于其起病隐匿且有时无症状,报告的病例较少。约20%-25%的患者有骶髂关节炎的影像学证据。根据罗马标准定义的强直性脊柱炎在3%-10%的炎性肠病患者中存在,并且与“典型”强直性脊柱炎相比,这些患者被认为有不同的遗传易感性:90%的“典型”强直性脊柱炎患者存在人类白细胞抗原B27表型,而克罗恩病继发强直性脊柱炎患者的患病率仅降至30%。涉及CARD15的多态性似乎是一个可能的遗传触发因素:78%的克罗恩病伴症状性或无症状性骶髂关节炎患者至少携带一种突变,而对照克罗恩病患者中这一比例仅为48%。此外,在其他形式的脊柱关节病中也报道了类似的关联:42%的脊柱关节病伴无症状性慢性肠道炎症患者(这些患者被认为可能发展为克罗恩病和强直性脊柱炎)至少携带一种CARD15突变,而组织学正常的患者中这一比例仅为7%。除了遗传标记外,临床特征也支持肠道与关节病理生理学之间的关系。在脊柱关节病病例中,已报道英夫利昔单抗治疗后症状迅速、显著且持续改善,这表明肿瘤坏死因子-α在脊柱关节病中起重要作用,类似于在克罗恩病中观察到的情况。