Bettenworth Dominik, Rieder Florian
Department of Medicine B, University Hospital of Münster, Münster, Germany.
Department of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
Fibrogenesis Tissue Repair. 2014 Mar 29;7(1):5. doi: 10.1186/1755-1536-7-5.
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.
克罗恩病(CD)是一种慢性缓解和复发性疾病。肠道狭窄、缩窄及最终梗阻等纤维狭窄性并发症是其一些最常见的长期并发症。尽管近期对CD的病理生理学认识取得了进展,抗炎治疗也有了显著改善,但针对狭窄性CD的药物治疗仍然不足。目前尚无特异性抗纤维化疗法,狭窄的发生率基本保持不变。因此,目前对已形成的纤维狭窄的治疗主要包括内镜扩张以及手术方法。然而,这些治疗选择会带来严重并发症以及高复发率。因此,迫切需要针对CD的特异性抗纤维化疗法。重要的是,现在有越来越多的证据表明,对于皮肤、肺、肾和肝等其他器官的纤维化疾病可以进行预防以及有效药物治疗。鉴于这些器官纤维化形成的分子机制具有相似性,将其他纤维化疾病的治疗方法应用于肠道似乎是一种有前景的治疗策略。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-血管紧张素系统成分阻断、IL-13抑制剂和雷帕霉素靶蛋白(mTOR)抑制剂已成为抗纤维化治疗的潜在候选药物,可能会延缓疾病进展,甚至逆转已形成的肠道纤维化。然而,将新型抗纤维化药物转化为肠道纤维化治疗面临着重大挑战,比如需要开发合适的生物标志物来预测疾病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最佳时机、阐明最佳给药途径以及评估候选药物实现最终目标(即预防或逆转CD患者已形成的纤维化和狭窄)潜力的前提条件。