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影响完整胃的C型胃炎中的细胞增殖。

Cell proliferation in type C gastritis affecting the intact stomach.

作者信息

Dowall J E, Willis P, Prescott R, Lamonby S, Lynch D A

机构信息

Department of Gastroenterology, Blackburn Royal Infirmary, UK.

出版信息

J Clin Pathol. 2000 Oct;53(10):784-7. doi: 10.1136/jcp.53.10.784.

Abstract

AIMS

Type C gastritis caused by bile reflux has a characteristic appearance, similar to that seen in other forms of chemical gastritis, such as those associated with NSAIDs or alcohol. An increase in mucosal cell proliferation increases the likelihood of a neoplastic clone of epithelial cells emerging, particularly where there is chronic epithelial injury associated with bile reflux. It has been shown previously that type C gastritis is associated with increased cell proliferation in the postsurgical stomach. The aim of this study was to determine cell proliferation in type C gastritis caused by bile reflux affecting the intact stomach.

METHODS

Specimens from 15 patients with a histological diagnosis of type C gastritis on antral biopsy were obtained from the pathology archives between 1994 and 1997. A control group of nine normal antral biopsies was also selected and all underwent MIB-1 immunostaining. The gastric glands were divided into three zones (zone 1, gastric pit; zone 2, isthmus; and zone 3, gland base) and the numbers of positively staining nuclei for 500 epithelial cell nuclei were counted in each zone to determine the percentage labelling index (LI%).

RESULTS

Cell proliferation was significantly higher in all three zones of the gastric glands with type C gastritis compared with controls as follows: zone 1, median LI% in type C gastritis 64.7 (range, 7.8-99.2), controls 4.7 (range, 2.0-11.3); zone 2, median LI% in type C gastritis 94.7 (range, 28.8-98.7), controls 40.2 (range, 23.1-70.3); and zone 3, median LI% in type C gastritis 20.0 (range, 1.3-96.0), controls 2.6 (range, 0.9-8.7).

CONCLUSIONS

Bile reflux is thought to act as a promoter of gastric carcinogenesis in the postsurgical stomach. The same may be true in the intact stomach.

摘要

目的

胆汁反流引起的C型胃炎具有特征性表现,类似于其他形式的化学性胃炎,如与非甾体抗炎药或酒精相关的胃炎。黏膜细胞增殖增加会增加上皮细胞肿瘤性克隆出现的可能性,特别是在存在与胆汁反流相关的慢性上皮损伤的情况下。先前已表明,C型胃炎与手术后胃中的细胞增殖增加有关。本研究的目的是确定胆汁反流影响完整胃所导致的C型胃炎中的细胞增殖情况。

方法

从1994年至1997年的病理档案中获取15例经组织学诊断为胃窦活检C型胃炎患者的标本。还选取了9例正常胃窦活检作为对照组,所有标本均进行MIB - 1免疫染色。胃腺分为三个区域(区域1,胃小凹;区域2,峡部;区域3,腺底部),并在每个区域中对500个上皮细胞核中阳性染色核的数量进行计数,以确定标记指数(LI%)百分比。

结果

与对照组相比,C型胃炎患者胃腺的所有三个区域中的细胞增殖均显著更高,如下所示:区域1,C型胃炎的LI%中位数为64.7(范围为7.8 - 99.2),对照组为4.7(范围为2.0 - 11.3);区域2,C型胃炎的LI%中位数为94.7(范围为28.8 - 98.7),对照组为40.2(范围为23.1 - 70.3);区域3,C型胃炎的LI%中位数为20.0(范围为1.3 - 96.0),对照组为2.6(范围为0.9 - 8.7)。

结论

胆汁反流被认为是手术后胃中胃癌发生的促进因素。在完整胃中可能也是如此。

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