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脊柱关节病中肠道炎症的病程及治疗后果。

Course of gut inflammation in spondylarthropathies and therapeutic consequences.

作者信息

Mielants H, Veys E M, Cuvelier C, De Vos M

机构信息

Department of Rheumatology, University Hospital, Ghent, Belgium.

出版信息

Baillieres Clin Rheumatol. 1996 Feb;10(1):147-64. doi: 10.1016/s0950-3579(96)80010-0.

Abstract

Gut inflammation plays a crucial role in the pathogenesis of spondylarthropathies (SpA) since ileocolonoscopic studies have demonstrated the presence of gut inflammation in different forms of this concept: in ankylosing spondylitis (AS) (60%), in enterogenic (90%) and urogenital reactive arthritis (20%), in undifferentiated SpA (65%), in the pauciarticular and axial forms of psoriatic arthritis (16%), in late onset pauciarticular juvenile chronic arthritis (80%) and in acute anterior uveitis (66%). The strong relationship between gut and joint inflammation was demonstrated by performing a second ileocolonoscopy: remission of the joint inflammation was always connected with a disappearance of gut inflammation, whereas persistence of locomotor inflammation was mostly associated with the persistence of gut inflammation. During further evolution 20% of the non-ankylosing spondylitis SpA patients can develop AS. About 6% of the total group SpA patients, in whom inflammatory bowel disease (IBD) was excluded, developed Crohn's disease 5 to 9 years later. All these patients initially presented with gut inflammation, which indicates that this finding has prognostic value. The high prevalence of evolution to IBD in SpA patients confirms the thesis that both disease entities bear common pathogenic mechanisms, and confirms the place of IBD in the concept of SPA. Sulphasalazine (SASP), a successful drug in the treatment of IBD, has demonstrated its effectiveness in the treatment of SpA. The beneficial effect of the drug in this disease entity could be due to its anti-inflammatory effect on the gut wall, by normalizing its permeability and by preventing the entrance of antigens through the defective gut wall. However, SASP could not prevent the evolution to IBD.

摘要

肠道炎症在脊柱关节病(SpA)的发病机制中起着关键作用,因为回结肠镜检查研究已证实在该概念的不同形式中均存在肠道炎症:强直性脊柱炎(AS)(60%)、肠道源性(90%)和泌尿生殖系统反应性关节炎(20%)、未分化SpA(65%)、银屑病关节炎的少关节型和轴向型(16%)、晚发型少关节型青少年慢性关节炎(80%)以及急性前葡萄膜炎(66%)。通过再次进行回结肠镜检查证实了肠道与关节炎症之间的密切关系:关节炎症的缓解总是与肠道炎症消失相关,而运动性炎症的持续大多与肠道炎症的持续相关。在疾病进一步发展过程中,20%的非强直性脊柱炎SpA患者可发展为AS。在排除炎症性肠病(IBD)的SpA患者总数中,约6%在5至9年后发展为克罗恩病。所有这些患者最初均表现为肠道炎症,这表明该发现具有预后价值。SpA患者发展为IBD的高发生率证实了这两种疾病实体具有共同致病机制的论点,并证实了IBD在SpA概念中的地位。柳氮磺胺吡啶(SASP)是治疗IBD的一种成功药物,已证明其在治疗SpA方面的有效性。该药物对这种疾病实体的有益作用可能归因于其对肠壁的抗炎作用,即通过使其通透性正常化以及防止抗原通过有缺陷的肠壁进入。然而,SASP无法阻止发展为IBD。

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