NIHR Birmingham Biomedical Research Centre, University Hospitals Birmingham NHS Foundation Trust and University of Birmingham.
Institute of Immunology and Immunotherapy, University of Birmingham.
Eur J Gastroenterol Hepatol. 2020 Nov;32(11):1432-1439. doi: 10.1097/MEG.0000000000001796.
Strictures related to Crohn's disease due to fibrosis are a result of an exaggerated tissue remodelling response to inflammation, characterized by accumulation of collagen-rich extracellular matrix produced by mesenchymal cells.
The objective of this study was to characterize histological changes seen in resected 'fibrotic' strictures to better understand individual components of intestinal stenosis.
We identified patients undergoing surgery for ileal Crohn's disease secondary to symptomatic stricturing disease (Montreal B2) using the histopathology database at Queen Elizabeth Hospital in Birmingham, UK, between 2012 and 2017. Phenotypic data were recorded and resection specimens reviewed. Two independent pathologists applied the semiquantitative scoring system previously developed by us to the microscopic images. Data were analyzed using the possible maximum total score (%PMTS).
Forty-eight patients (M = 25) were included. with median disease duration of 7 years (range 0.25-39 years); nearly two-thirds had ileocolonic distribution (L3). In this cohort, despite presurgery diagnosis of noninflamed fibrosis, chronic inflammation was noted to be a prominent component of all strictures. The histological scoring showed presence of several other prominent findings such as muscular hyperplasia and volume expansion.There was statistically significant positive correlation between chronic inflammation and fibrosis and muscular hyperplasia.
The histological features of Crohn's disease-related strictures show multiple changes in multiple layers and not simply fibrosis. In our cohort, despite the observation prior to surgery that strictures were clinically considered fibrotic, the finding of chronic inflammation as a dominant component at a histological level in the resection is important. The findings might suggest that one of the main drivers of progressive fibrosis is the inflammatory component, which probably is never fully resolved.
纤维化导致的克罗恩病狭窄是炎症引起的组织重塑反应过度的结果，其特征是间质细胞产生富含胶原蛋白的细胞外基质积聚。
本研究旨在描述切除的“纤维化”狭窄组织的组织学变化，以更好地了解肠狭窄的各个组成部分。
我们在英国伯明翰伊丽莎白女王医院的组织病理学数据库中，确定了 2012 年至 2017 年间因症状性狭窄病（蒙特利尔 B2 型）而行手术的回肠克罗恩病患者。记录表型数据并复查切除标本。两名独立的病理学家应用我们之前开发的半定量评分系统对显微镜图像进行评分。使用可能的最大总分（%PMTS）进行数据分析。
共纳入 48 例患者（M=25），中位疾病持续时间为 7 年（范围 0.25-39 年）；近三分之二为回结肠分布（L3）。在本队列中，尽管术前诊断为非炎症性纤维化，但所有狭窄处均可见明显的慢性炎症。组织学评分显示还存在其他几个突出的发现，如肌肉增生和体积扩张。慢性炎症与纤维化和肌肉增生之间存在统计学上显著的正相关。
克罗恩病相关狭窄的组织学特征显示出多个层次的多种变化，而不仅仅是纤维化。在我们的队列中，尽管术前观察到狭窄被临床认为是纤维化的，但在切除标本的组织学水平上发现慢性炎症是主要成分这一发现很重要。这一发现可能表明，进行性纤维化的主要驱动因素之一是炎症成分，而炎症可能从未完全得到解决。
