狭窄性克罗恩病的医学治疗:肠道可以从其他器官学习什么-系统回顾。

Dominik Bettenworth, Florian Rieder
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引用次数: 71

摘要

克罗恩病(CD)是一种慢性缓解和复发的疾病。纤维狭窄并发症如肠狭窄、狭窄和最终梗阻是其最常见的长期并发症。尽管最近在对乳糜泻的病理生理理解和抗炎治疗方面取得了重大进展,但对狭窄性乳糜泻的药物治疗仍然不足。没有特异性的抗纤维化治疗存在,狭窄的发生率基本保持不变。因此,目前对已建立的纤维化狭窄的治疗主要包括内镜扩张和手术途径。然而,这些治疗方案与主要并发症和高复发率有关。因此,迫切需要一种针对CD的特异性抗纤维化治疗方法。重要的是,现在有越来越多的证据表明,对皮肤、肺、肾和肝等其他器官的纤维化疾病进行预防和有效的医学治疗。鉴于这些器官中纤维形成的分子机制的相似性,将其他纤维化疾病的治疗方法转化为肠道似乎是一种很有前途的治疗策略。特别是转化生长因子β (TGF-β)中和、选择性酪氨酸激酶抑制剂、肾素-血管紧张素系统组分的阻断、IL-13抑制剂和哺乳动物雷帕霉素靶点(mTOR)抑制剂已成为抗纤维化治疗的潜在候选药物,并可能延缓进展甚至逆转已建立的肠道纤维化。然而,在将新型抗纤维化药物转化为肠纤维化治疗的过程中,还需要克服一些重大挑战,例如开发合适的生物标志物来预测发展并准确监测治疗反应。未来的临床研究是评估抗纤维化治疗方法的最佳时机、阐明最佳应用途径和评估候选药物的潜力的先决条件,以达到最终目标:预防或逆转CD患者已建立的纤维化和狭窄。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Medical therapy of stricturing Crohn's disease: what the gut can learn from other organs - a systematic review.

Crohn's disease (CD) is a chronic remitting and relapsing disease. Fibrostenosing complications such as intestinal strictures, stenosis and ultimately obstruction are some of its most common long-term complications. Despite recent advances in the pathophysiological understanding of CD and a significant improvement of anti-inflammatory therapeutics, medical therapy for stricturing CD is still inadequate. No specific anti-fibrotic therapy exists and the incidence rate of strictures has essentially remained unchanged. Therefore, the current therapy of established fibrotic strictures comprises mainly endoscopic dilation as well as surgical approaches. However, these treatment options are associated with major complications as well as high recurrence rates. Thus, a specific anti-fibrotic therapy for CD is urgently needed. Importantly, there is now a growing body of evidence for prevention as well as effective medical treatment of fibrotic diseases of other organs such as the skin, lung, kidney and liver. In face of the similarity of molecular mechanisms of fibrogenesis across these organs, translation of therapeutic approaches from other fibrotic diseases to the intestine appears to be a promising treatment strategy. In particular transforming growth factor beta (TGF-β) neutralization, selective tyrosine kinase inhibitors, blockade of components of the renin-angiotensin system, IL-13 inhibitors and mammalian target of rapamycin (mTOR) inhibitors have emerged as potential drug candidates for anti-fibrotic therapy and may retard progression or even reverse established intestinal fibrosis. However, major challenges have to be overcome in the translation of novel anti-fibrotics into intestinal fibrosis therapy, such as the development of appropriate biomarkers that predict the development and accurately monitor therapeutic responses. Future clinical studies are a prerequisite to evaluate the optimal timing for anti-fibrotic treatment approaches, to elucidate the best routes of application, and to evaluate the potential of drug candidates to reach the ultimate goal: the prevention or reversal of established fibrosis and strictures in CD patients.

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