急性和长期溃疡性结肠炎纤维化的发展。

Development of Fibrosis in Acute and Longstanding Ulcerative Colitis.

机构信息

Department of Gastroenterology and Hepatology, Academic Medical Center, Amsterdam, The Netherlands Tytgat Institute for Liver and Intestinal Research, Academic Medical Center, Amsterdam, The Netherlands.

Department of Pathology, Academic Medical Center, Amsterdam, The Netherlands.

出版信息

J Crohns Colitis. 2015 Nov;9(11):966-72. doi: 10.1093/ecco-jcc/jjv133. Epub 2015 Aug 5.

DOI:10.1093/ecco-jcc/jjv133

PMID:26245217

Abstract

BACKGROUND

Intestinal fibrosis is a process driven by chronic inflammation leading to increased presence of myofibroblasts and collagen deposition. Although strictures are rarely seen in ulcerative colitis [UC], longstanding disease is believed to cause fibrosis resulting in altered bowel function.

METHODS

The presence of fibrosis was studied in colectomy specimens from patients with recent-onset UC refractory to medical treatment [n = 13] and longstanding UC [n = 16], and colon cancer patients without UC [n = 7] as controls. Severity of inflammation was scored according to the Geboes score on haematoxylin and eosin stainings. Immunohistochemistry was performed to detect α-smooth muscle actin, fibronectin and collagen I and III.

RESULTS

Colectomy specimens from patients with acute UC showed significantly more inflammation than those with longstanding disease [19 vs 9 points, p = 0.01]. Both acute and longstanding UC showed a thicker muscularis mucosa than controls [0.10 vs 0.10 vs 0.05 mm, respectively, p = 0.019]. An increase in collagen I and III deposition in the mucosa was observed in UC compared with controls (40% [30-75] vs 25% [10-25], p = 0.033), but this did not differ significantly among acute and longstanding UC patients.

CONCLUSIONS

Collagen deposition is enhanced in UC compared with controls. However, UC collagen deposition does not increase significantly over time and does not seem to aggravate the entire fibrotic process.

摘要

背景

肠纤维化是一种由慢性炎症驱动的过程，导致肌成纤维细胞增多和胶原沉积。尽管溃疡性结肠炎[UC]很少出现狭窄，但长期疾病被认为会导致纤维化，从而改变肠道功能。

方法

研究了最近发病的对药物治疗难治性 UC [n = 13]和长期 UC [n = 16]患者的结肠切除术标本以及无 UC 的结肠癌患者[n = 7]的纤维化存在情况。根据苏木精和伊红染色的 Geboes 评分对炎症严重程度进行评分。进行免疫组织化学检测以检测α-平滑肌肌动蛋白、纤维连接蛋白和胶原 I 和 III。

结果

急性 UC 患者的结肠切除术标本显示出比长期疾病患者更严重的炎症[19 分比 9 分，p = 0.01]。急性和长期 UC 患者的黏膜肌层均比对照组厚[分别为 0.10 比 0.10 比 0.05 毫米，p = 0.019]。与对照组相比，UC 中观察到黏膜中胶原 I 和 III 沉积增加（40%[30-75]比 25%[10-25]，p = 0.033），但急性和长期 UC 患者之间无显著差异。