Department of Immunology and Rheumatology, National Institute of Medical Sciences and Nutrition Salvador Zubirán, Vasco de Quiroga 15, Col Sección XVI, Del, Tlalpan, Mexico City, Mexico.
World J Gastroenterol. 2009 Nov 28;15(44):5517-24. doi: 10.3748/wjg.15.5517.
This article reviews the literature concerning rheumatic manifestations of inflammatory bowel disease (IBD), including common immune-mediated pathways, frequency, clinical course and therapy. Musculoskeletal complications are frequent and well-recognized manifestations in IBD, and affect up to 33% of patients with IBD. The strong link between the bowel and the osteo-articular system is suggested by many clinical and experimental observations, notably in HLA-B27 transgenic rats. The autoimmune pathogenic mechanisms shared by IBD and spondyloarthropathies include genetic susceptibility to abnormal antigen presentation, aberrant recognition of self, the presence of autoantibodies against specific antigens shared by the colon and other extra-colonic tissues, and increased intestinal permeability. The response against microorganisms may have an important role through molecular mimicry and other mechanisms. Rheumatic manifestations of IBD have been divided into peripheral arthritis, and axial involvement, including sacroiliitis, with or without spondylitis, similar to idiopathic ankylosing spondylitis. Other periarticular features can occur, including enthesopathy, tendonitis, clubbing, periostitis, and granulomatous lesions of joints and bones. Osteoporosis and osteomalacia secondary to IBD and iatrogenic complications can also occur. The management of the rheumatic manifestations of IBD consists of physical therapy in combination with local injection of corticosteroids and nonsteroidal anti-inflammatory drugs; caution is in order however, because of their possible harmful effects on intestinal integrity, permeability, and even on gut inflammation. Sulfasalazine, methotrexate, azathioprine, cyclosporine and leflunomide should be used for selected indications. In some cases, tumor necrosis factor-alpha blocking agents should be considered as first-line therapy.
这篇文章回顾了炎症性肠病(IBD)的风湿表现的文献,包括常见的免疫介导途径、频率、临床过程和治疗。肌肉骨骼并发症是 IBD 的常见且公认的表现,影响多达 33%的 IBD 患者。许多临床和实验观察表明,肠道和骨关节系统之间存在紧密联系,尤其是在 HLA-B27 转基因大鼠中。IBD 和脊柱关节炎之间共同的自身免疫发病机制包括对异常抗原呈递的遗传易感性、对自身的异常识别、针对结肠和其他结肠外组织共同的特定抗原的自身抗体的存在,以及肠道通透性的增加。通过分子模拟和其他机制,针对微生物的反应可能具有重要作用。IBD 的风湿表现可分为外周关节炎和轴性受累,包括伴有或不伴有脊柱炎的骶髂关节炎,类似于特发性强直性脊柱炎。其他关节周围特征也可能发生,包括附着病、肌腱炎、指(趾)末节增粗、骨膜炎和关节及骨骼的肉芽肿性病变。IBD 和医源性并发症引起的骨质疏松症和骨软化症也可能发生。IBD 风湿表现的治疗包括物理治疗结合局部注射皮质类固醇和非甾体抗炎药;然而,需要谨慎,因为它们可能对肠道完整性、通透性甚至肠道炎症产生有害影响。柳氮磺胺吡啶、甲氨蝶呤、硫唑嘌呤、环孢素和来氟米特应根据具体适应证使用。在某些情况下,应考虑使用肿瘤坏死因子-α 阻断剂作为一线治疗。