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患有肌病型慢性特发性肠假性梗阻患者中c-kit+细胞的缺乏。

Deficiency of c-kit+ cells in patients with a myopathic form of chronic idiopathic intestinal pseudo-obstruction.

作者信息

Isozaki K, Hirota S, Miyagawa J, Taniguchi M, Shinomura Y, Matsuzawa Y

机构信息

Second Department of Internal Medicine, Osaka University Medical School, Japan.

出版信息

Am J Gastroenterol. 1997 Feb;92(2):332-4.

PMID:9040218
Abstract

OBJECTIVES

Chronic idiopathic intestinal pseudo-obstruction (CIIP) is a syndrome characterized by a failure of intestinal movement, but the cause of dysmotility remains unknown. Because interstitial cells of Cajal (ICCs) are believed to initiate basic contractile activity of the gastrointestinal tract, there is a possibility that changes in ICCs are involved in the development of CIIP. ICCs express c-kit in mice, and it has been reported that the c-kit+ cells, the location and shape of which resemble those in mice, are detected in the human gastrointestinal muscular layer using immunohistochemistry. In the present study, we counted the number of c-kit+ cells in the affected intestine of two patients with myopathic form of CIIP and compared this number with the number of c-kit+ cells in the normal intestine.

METHODS

The c-kit+ cells in the external muscle layer were detected by immunohistochemistry, and the number of them was counted under the microscope. Mast cells, which are known to express c-kit, were detected by staining with Alcian blue, and the number of them was also counted.

RESULTS

Immunohistochemistry revealed that the distribution pattern of c-kit+ cells resembles that of ICCs in the external muscle layer of normal control subjects. The numbers of c-kit+ cells apart from mast cells in two patients with myopathic form of CIIP decreased to about 3% of those in normal subjects.

CONCLUSIONS

The failure of intestinal movement in patients with CIIP, at least in a subpopulation, might be related to a deficiency of c-kit+ cells, probably ICCs.

摘要

目的

慢性特发性肠道假性梗阻(CIIP)是一种以肠道运动功能障碍为特征的综合征,但其运动功能障碍的原因尚不清楚。由于人们认为 Cajal 间质细胞(ICCs)启动胃肠道的基本收缩活动,因此 ICCs 的变化有可能参与了 CIIP 的发生发展。ICCs 在小鼠中表达 c-kit,并且有报道称,使用免疫组织化学方法在人类胃肠道肌层中检测到了 c-kit+细胞,其位置和形态与小鼠中的相似。在本研究中,我们对两名肌病型 CIIP 患者病变肠道中的 c-kit+细胞数量进行了计数,并将该数量与正常肠道中的 c-kit+细胞数量进行了比较。

方法

通过免疫组织化学检测外肌层中的 c-kit+细胞,并在显微镜下对其数量进行计数。已知表达 c-kit 的肥大细胞通过阿尔辛蓝染色进行检测,其数量也进行了计数。

结果

免疫组织化学显示,c-kit+细胞的分布模式与正常对照受试者外肌层中 ICCs 的分布模式相似。两名肌病型 CIIP 患者中除肥大细胞外的 c-kit+细胞数量降至正常受试者的约 3%。

结论

CIIP 患者的肠道运动功能障碍,至少在一部分患者中,可能与 c-kit+细胞(可能是 ICCs)的缺乏有关。

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