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乳糜泻患者空肠黏膜中载脂蛋白A-I合成缺陷。

Defective synthesis of apolipoprotein A-I in jejunal mucosa in coeliac disease.

作者信息

Florén C H, Alm P

机构信息

Dept. of Medicine, University Hospital, Lund, Sweden.

出版信息

Scand J Gastroenterol. 1988 Sep;23(7):856-60. doi: 10.3109/00365528809090773.

Abstract

Apolipoprotein A-I was studied in biopsy specimens from the duodenojejunal junction by means of an indirect immunoperoxidase technique. In normal control subjects apolipoprotein A-I was immunohistochemically detected only in the absorptive cells at the tips of villi and was mainly localized supranuclearly. In 14 patients with coeliac disease apolipoprotein A-I was virtually undetectable. This implies that the inflammatory lesion in coeliac disease decreases the intestinal mass of apolipoprotein A-I, because it destroys the villous absorptive cells. Apolipoprotein A-I concentrations in plasma were also decreased (by 40%) in patients with coeliac disease, suggesting that the intestine has a role in maintaining plasma apolipoprotein A-I levels.

摘要

采用间接免疫过氧化物酶技术,对十二指肠空肠交界处活检标本中的载脂蛋白A-I进行了研究。在正常对照受试者中,载脂蛋白A-I仅在绒毛顶端的吸收细胞中通过免疫组织化学方法检测到,且主要定位于核上。在14例乳糜泻患者中,几乎检测不到载脂蛋白A-I。这意味着乳糜泻中的炎性病变会降低肠道中载脂蛋白A-I的含量,因为它破坏了绒毛吸收细胞。乳糜泻患者血浆中载脂蛋白A-I的浓度也降低了(40%),这表明肠道在维持血浆载脂蛋白A-I水平方面发挥着作用。

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