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胃癌继发贲门失弛缓症患者食管神经的严重破坏。嗜酸性粒细胞神经毒性蛋白的可能作用。

Severe destruction of esophageal nerves in a patient with achalasia secondary to gastric cancer. A possible role of eosinophil neurotoxic proteins.

作者信息

Fredens K, Tøttrup A, Kristensen I B, Dahl R, Jacobsen N O, Funch-Jensen P, Thommesen P

机构信息

Department of Neurobiology, University of Aarhus, Denmark.

出版信息

Dig Dis Sci. 1989 Feb;34(2):297-303. doi: 10.1007/BF01536066.

Abstract

We present a case of secondary achalasia due to an adenocarcinoma of the stomach with no tumor infiltration of the esophagus. Immunohistochemical staining revealed a massive infiltration of activated eosinophils in the muscularis of the esophagus with secretion of the highly cytotoxic and neurotoxic eosinophil cationic protein (ECP). Immunohistochemical staining for the neuropeptides VIP and substance P, as well as the histochemical demonstration of AChE, revealed a nearly total absence of all three neurotransmitters/modulators compared to control. The hypothesis is advanced that eosinophil neurotoxicity is the cause of secondary achalasia.

摘要

我们报告一例因胃腺癌导致的继发性贲门失弛缓症,食管无肿瘤浸润。免疫组织化学染色显示食管肌层有大量活化嗜酸性粒细胞浸润,并分泌高细胞毒性和神经毒性的嗜酸性粒细胞阳离子蛋白(ECP)。对神经肽VIP和P物质进行免疫组织化学染色,以及对乙酰胆碱酯酶进行组织化学检测,结果显示与对照组相比,这三种神经递质/调节剂几乎完全缺失。我们提出假说,嗜酸性粒细胞神经毒性是继发性贲门失弛缓症的病因。

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