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利用胃特异性血浆生物标志物诊断和筛查萎缩性胃炎的原理

Rationale in diagnosis and screening of atrophic gastritis with stomach-specific plasma biomarkers.

作者信息

Agréus Lars, Kuipers Ernst J, Kupcinskas Limas, Malfertheiner Peter, Di Mario Francesco, Leja Marcis, Mahachai Varocha, Yaron Niv, van Oijen Martijn, Perez Perez Guillermo, Rugge Massimo, Ronkainen Jukka, Salaspuro Mikko, Sipponen Pentti, Sugano Kentaro, Sung Joseph

机构信息

Karolinska Institute, Center for Family and Community Medicine, Stockholm, Sweden.

出版信息

Scand J Gastroenterol. 2012 Feb;47(2):136-47. doi: 10.3109/00365521.2011.645501.

Abstract

BACKGROUND AND AIMS

Atrophic gastritis (AG) results most often from Helicobacter pylori (H. pylori) infection. AG is the most important single risk condition for gastric cancer that often leads to an acid-free or hypochlorhydric stomach. In the present paper, we suggest a rationale for noninvasive screening of AG with stomach-specific biomarkers.

METHODS

The paper summarizes a set of data on application of the biomarkers and describes how the test results could be interpreted in practice.

RESULTS

In AG of the gastric corpus and fundus, the plasma levels of pepsinogen I and/or the pepsinogen I/pepsinogen II ratio are always low. The fasting level of gastrin-17 is high in AG limited to the corpus and fundus, but low or non-elevated if the AG occurs in both antrum and corpus. A low fasting level of G-17 is a sign of antral AG or indicates high intragastric acidity. Differentiation between antral AG and high intragastric acidity can be done by assaying the plasma G-17 before and after protein stimulation, or before and after administration of the proton pump inhibitors (PPI). Amidated G-17 will rise if the antral mucosa is normal in structure. H. pylori antibodies are a reliable indicator of helicobacter infection, even in patients with AG and hypochlorhydria.

CONCLUSIONS

Stomach-specific biomarkers provide information about the stomach health and about the function of stomach mucosa and are a noninvasive tool for diagnosis and screening of AG and acid-free stomach.

摘要

背景与目的

萎缩性胃炎(AG)大多由幽门螺杆菌(H. pylori)感染引起。AG是胃癌最重要的单一风险因素,常导致无酸或胃酸过少的胃部状态。在本文中,我们提出了一种使用胃特异性生物标志物对AG进行无创筛查的基本原理。

方法

本文总结了一系列关于生物标志物应用的数据,并描述了如何在实际中解读检测结果。

结果

在胃体和胃底的AG中,胃蛋白酶原I的血浆水平和/或胃蛋白酶原I/胃蛋白酶原II比值总是较低。局限于胃体和胃底的AG中,胃泌素-17的空腹水平较高,但如果AG同时发生在胃窦和胃体,则该水平较低或无升高。胃泌素-17空腹水平低是胃窦AG的标志或表明胃内酸度高。胃窦AG和胃内高酸度之间的鉴别可通过检测蛋白质刺激前后或质子泵抑制剂(PPI)给药前后的血浆胃泌素-17来进行。如果胃窦黏膜结构正常,酰胺化胃泌素-17会升高。幽门螺杆菌抗体是幽门螺杆菌感染的可靠指标,即使在AG和胃酸过少的患者中也是如此。

结论

胃特异性生物标志物可提供有关胃部健康及胃黏膜功能的信息,是诊断和筛查AG及无酸胃的无创工具。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2bf/3279132/51d35d6e9dda/sgas47-136-f1.jpg

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