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幽门螺杆菌相关的高胃泌素血症并非由胃窦表面pH值升高所致。胃窦碱化研究。

Helicobacter pylori-related hypergastrinaemia is not due to elevated antral surface pH. Studies with antral alkalinisation.

作者信息

Chittajallu R S, Neithercut W D, Ardill J E, McColl K E

机构信息

University Dept. of Medicine and Therapeutics, Western Infirmary, Glasgow, Scotland, U.K.

出版信息

Scand J Gastroenterol. 1992;27(3):218-22. doi: 10.3109/00365529208999952.

DOI:10.3109/00365529208999952
PMID:1502485
Abstract

It has been postulated that Helicobacter pylori-related hypergastrinaemia is due to bacterial ammonia raising antral surface pH and thus preventing acid inhibition of gastrin release. If true, the infection should not alter gastrin release at neutral intragastric pH. To test this, we have studied basal and meal-stimulated gastrin at uncontrolled pH and at pH greater than 6 in duodenal ulcer patients before and after eradication of H. pylori. The median integrated gastrin response to the meal alone was 2525 ng/l.min (range, 550-8725) before and 725 ng/l.min (range, 250-2925) after eradication of H. pylori (p less than 0.01). The corresponding values when intragastric pH was maintained above 6 were 3700 ng/l.min (range, 1900-14,100) and 1400 ng/l.min (range, 400-3400) (p less than 0.01). The median reduction in gastrin after eradication of H. pylori was thus similar when the meal was taken at uncontrolled pH (61%; range, 0-97%) and at pH greater than 6 (69%; range, 36-89%). Likewise, 5 h of gastric alkalinisation did not cause the basal gastrin values when H. pylori was eradicated to increase to those observed when H. pylori was present. These findings indicate that the hypergastrinaemia is not due to elevated antral surface pH.

摘要

据推测,幽门螺杆菌相关的高胃泌素血症是由于细菌产生的氨使胃窦表面pH值升高,从而阻止了胃酸对胃泌素释放的抑制作用。如果这一推测正确,那么在胃内pH值为中性时,感染不应改变胃泌素的释放。为了验证这一点,我们研究了十二指肠溃疡患者在根除幽门螺杆菌前后,在未控制的pH值和pH值大于6的情况下,基础状态和进食刺激后的胃泌素水平。根除幽门螺杆菌前,单独进食时胃泌素的中位积分反应为2525 ng/l·min(范围为550 - 8725),根除后为725 ng/l·min(范围为250 - 2925)(p < 0.01)。当胃内pH值维持在6以上时,相应的值分别为3700 ng/l·min(范围为1900 - 14100)和1400 ng/l·min(范围为400 - 3400)(p < 0.01)。因此,在未控制的pH值(61%;范围为0 - 97%)和pH值大于6(69%;范围为36 - 89%)的情况下进食时,根除幽门螺杆菌后胃泌素的中位降低幅度相似。同样,在根除幽门螺杆菌后,5小时的胃碱化也未使基础胃泌素值升高到幽门螺杆菌存在时所观察到的水平。这些发现表明,高胃泌素血症并非由于胃窦表面pH值升高所致。

相似文献

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引用本文的文献

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J Clin Pathol. 1993 Jan;46(1):75-8. doi: 10.1136/jcp.46.1.75.
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Helicobacter pylori related hypergastrinaemia is the result of a selective increase in gastrin 17.幽门螺杆菌相关的高胃泌素血症是胃泌素17选择性增加的结果。
Gut. 1993 Jun;34(6):757-61. doi: 10.1136/gut.34.6.757.
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Gastrin and somatostatin in Helicobacter pylori infected antral mucosa.幽门螺杆菌感染的胃窦黏膜中的胃泌素和生长抑素
Gut. 1994 May;35(5):615-8. doi: 10.1136/gut.35.5.615.
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Dig Dis Sci. 1995 Feb;40(2 Suppl):24S-49S. doi: 10.1007/BF02214870.
5
Inflammation, acid and ulcers.炎症、胃酸与溃疡。
Yale J Biol Med. 1994 May-Aug;67(3-4):135-44.
6
Role of ammonia in the pathogenesis of the gastritis, hypergastrinaemia, and hyperpepsinogenaemia I caused by Helicobacter pylori infection.氨在幽门螺杆菌感染所致胃炎、高胃泌素血症及高胃蛋白酶原血症发病机制中的作用。
Gut. 1992 Dec;33(12):1612-6. doi: 10.1136/gut.33.12.1612.