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克罗恩病中小肠黏膜下层的闭塞性肌化:小肠梗阻的一种可能机制。

Obliterative muscularization of the small bowel submucosa in Crohn disease: a possible mechanism of small bowel obstruction.

作者信息

Koukoulis G, Ke Y, Henley J D, Cummings O W

机构信息

Department of Pathology, School of Medicine, Indiana University, Indianapolis, USA.

出版信息

Arch Pathol Lab Med. 2001 Oct;125(10):1331-4. doi: 10.5858/2001-125-1331-OMOTSB.

Abstract

CONTEXT

The pathology of small bowel obstruction in Crohn disease has not been studied extensively. Stricture formation has been attributed mainly to fibrosis, although muscularization of the submucosa has been discussed previously.

OBJECTIVE

To identify additional pathologic changes in Crohn disease that could be involved in the formation of strictures.

DESIGN

We reviewed 50 ileal resections from patients with Crohn disease. The histopathologic slides were reviewed initially without knowledge of the macroscopic or clinical findings. We identified an unusual muscular proliferation that we refer to as obliterative muscularization of the submucosa, defined as a thick and continuous muscle layer from the mucosal base to the muscularis propria that is at least 1 cm in length. Subsequently, histopathologic findings were correlated with macroscopic and clinical findings.

RESULTS

Obliterative muscularization of the submucosa was present in 14 specimens, and in 11 of these 14 it was topographically restricted to strictures. Submucosal fibrosis was observed in sections from adjacent regions. Obliterative muscularization of the submucosa, including thick-walled vessels and hyperplastic nerves but not prominent scarring, was more common in specimens with strictures; the difference was statistically significant (P <.001).

CONCLUSIONS

Obliterative muscularization of the submucosa may be pathogenetically involved in the formation of strictures either directly by causing a sustained spasm, or indirectly by minimizing the vasoprotective role of the submucosa, impairing repair and enhancing scarring.

摘要

背景

克罗恩病中小肠梗阻的病理学尚未得到广泛研究。狭窄形成主要归因于纤维化,尽管此前已讨论过黏膜下层的肌化。

目的

确定克罗恩病中可能参与狭窄形成的其他病理变化。

设计

我们回顾了50例克罗恩病患者的回肠切除术。最初在不了解宏观或临床发现的情况下对组织病理学切片进行回顾。我们发现了一种不寻常的肌肉增生,我们将其称为黏膜下层闭塞性肌化,定义为从黏膜基部到固有肌层的一层厚实且连续的肌肉层,长度至少为1厘米。随后,将组织病理学发现与宏观和临床发现进行关联。

结果

14个标本中存在黏膜下层闭塞性肌化,在这14个标本中的11个中,其在地形上局限于狭窄部位。在相邻区域的切片中观察到黏膜下纤维化。黏膜下层闭塞性肌化,包括厚壁血管和增生性神经,但无明显瘢痕形成,在有狭窄的标本中更常见;差异具有统计学意义(P <.001)。

结论

黏膜下层闭塞性肌化可能在发病机制上通过直接引起持续性痉挛或间接通过最小化黏膜下层的血管保护作用、损害修复并增强瘢痕形成而参与狭窄的形成。

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