Rogler Gerhard, Hausmann Martin
Department of Gastroenterology and Hepatology, University Hospital, University of Zurich, Zurich, Switzerland.
Zurich Center for Integrative Human Physiology (ZIHP), University of Zurich, Zurich, Switzerland.
Front Med (Lausanne). 2017 Jul 7;4:96. doi: 10.3389/fmed.2017.00096. eCollection 2017.
The concepts on the pathophysiology of intestinal fibrosis in Crohn's disease (CD) have changed in recent years. Some years ago fibrosis was regarded to be a consequence of long-standing inflammation with subsequent destruction of the gut wall matrix followed by scar formation and collagen deposition. Fibrosis in CD patients appeared to be an irreversible process that could hardly be influenced. Therefore, the main target in CD therapy was to control inflammation to avoid fibrosis development. Many of these assumptions seem to be only partially true. Inflammation may be a necessary prerequisite for the initiation of fibrosis. However, when the pathophysiologic processes that lead to fibrosis in CD patients have been initiated fibrosis development may be independent of inflammation and may continue even when inflammation is under good medical control. Fibrosis in CD also may be reversible. After strictureplasty local collagen deposits decrease or even disappear. With new animal models for intestinal fibrosis on the horizon, we need to spend more efforts on understanding the factors influencing fibrosis in CD patients to finally find specific therapies. In this context, it will be as important to find markers and quantitative imaging tools to have reliable endpoints for clinical trials in fibrosing CD.
近年来，克罗恩病（CD）肠道纤维化的病理生理学概念发生了变化。几年前，纤维化被认为是长期炎症的结果，随后肠壁基质遭到破坏，继而形成瘢痕并沉积胶原蛋白。CD患者的纤维化似乎是一个不可逆转的过程，几乎无法受到影响。因此，CD治疗的主要目标是控制炎症以避免纤维化发展。其中许多假设似乎只是部分正确。炎症可能是纤维化起始的必要前提。然而，当导致CD患者纤维化的病理生理过程启动后，纤维化的发展可能独立于炎症，甚至在炎症得到良好医学控制时仍会继续。CD中的纤维化也可能是可逆的。狭窄成形术后局部胶原蛋白沉积减少甚至消失。随着新的肠道纤维化动物模型即将出现，我们需要更加努力地了解影响CD患者纤维化的因素，以便最终找到特异性治疗方法。在这种情况下，找到标志物和定量成像工具以获得纤维化CD临床试验的可靠终点同样重要。
