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[梗阻性黄疸患者胃十二指肠黏膜的急性消化性病变]

[Acute peptic lesions of the gastroduodenal mucosa in patients with obstructive jaundice].

作者信息

Upyrev A V, Gusev E Iu, Il'ichev V A, Gorchakov V K, Muratova O A

出版信息

Khirurgiia (Mosk). 1989 Jan(1):42-6.

PMID:2704159
Abstract

Complex study of the gastric acid-producing activity, the condition of the gastroduodenal mucosa, and the serum gastrin concentration in 80 patients with obstructive jaundice showed that the appearance of acute erosive-ulcerative injuries of the mucosa of the gastroduodenal zone depended on the increase of activity of the peptic factor of the gastric medium. Peptic complications occurred in 27.1% of patients with initial normo and hyperacidity and a high level of blood gastrin. The absence of bile in the duodenum (obstructive jaundice, by-pass biliodigestive anastomoses) stimulated the peptic factor. This is evidently linked with secretin deficiency (absence of the effect of bile on the secretin producing S-cells) leading to weakened inhibiting effect of secretin on the serum gastrin content, which results in hypergastrinemia and hyperacidity.

摘要

对80例梗阻性黄疸患者胃酸分泌活性、胃十二指肠黏膜状况及血清胃泌素浓度进行的综合研究表明,胃十二指肠区黏膜急性糜烂性溃疡损伤的出现取决于胃内消化因子活性的增加。在初始胃酸分泌正常和胃酸过多且血胃泌素水平较高的患者中,消化性并发症发生率为27.1%。十二指肠内胆汁缺乏(梗阻性黄疸、胆肠吻合旁路)会刺激消化因子。这显然与促胰液素缺乏有关(胆汁对产生促胰液素的S细胞无作用),导致促胰液素对血清胃泌素含量的抑制作用减弱,从而引起高胃泌素血症和胃酸过多。

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