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胃泌素对促胰液素激发的反应是胃窦G细胞数量的一种功能吗?结果导致胃酸分泌不足引起的高胃泌素血症。

Is the gastrin response to secretin provocation a function of antral G-cell mass? Results in the hypergastrinemia of acid hyposecretion.

作者信息

Brady C E, Hyatt J R, Utts S J

机构信息

Gastroenterology Service, Wilford Hall USAF Medical Center, San Antonio, Texas.

出版信息

J Clin Gastroenterol. 1989 Feb;11(1):27-32. doi: 10.1097/00004836-198902000-00007.

DOI:10.1097/00004836-198902000-00007
PMID:2921489
Abstract

Some patients with hypergastrinemic achlorhydria may have false-positive secretin provocation as an exaggeration of the normal gastrin response to secretin, presumably related to an increased, or more responsive, antral G-cell mass. To test this hypothesis, we reviewed our experience with secretin provocation in normogastrinemic subjects with presumed normal antral G-cell mass (normal--17, duodenal ulcer--13) and in patients with hypergastrinemia related to changes in antral G-cells (vagotomy--5, hypochlorhydria--7, achlorhydria--10). Basal serum gastrin (mean +/- SEM) was progressively higher for each group; normal (42 +/- 3 pg/ml), duodenal ulcer (53 +/- 4 pg/ml), vagotomy (226 +/- 54 pg/ml), hypochlorhydria (346 +/- 92 pg/ml), achlorhydria (844 +/- 100 pg/ml). On selective analysis of only those with gastrin rises, significant differences (p less than 0.05) in peak gastrin change were found between achlorhydria (93 +/- 21 pg/ml) compared with all other groups and between hypochlorhydria (40 +/- 12 pg/ml) versus normal (6 +/- 1 pg/ml). Linear regression in these responders showed a significant correlation (p less than 0.001) between basal gastrin and peak gastrin change after secretin. There were no false-positive secretin provocation tests, but four achlorhydric patients had gastrin rises greater than 100 pg/ml, whereas no patient in the other categories had rises above 90 pg/ml. Our results support the concept that patients with hypergastrinemic achlorhydria tend to have greater G-cell responsiveness to secretin provocation, which may account for the false-positive results in some such patients.

摘要

一些高胃泌素血症伴胃酸缺乏的患者可能会出现促胰液素激发试验假阳性,这是由于正常胃泌素对促胰液素的反应被夸大,推测与胃窦G细胞数量增加或反应性增强有关。为验证这一假设,我们回顾了在假定胃窦G细胞数量正常的正常胃泌素血症受试者(正常人17例,十二指肠溃疡患者13例)以及因胃窦G细胞变化导致高胃泌素血症的患者(迷走神经切断术患者5例,胃酸过少患者7例,胃酸缺乏患者10例)中进行促胰液素激发试验的经验。每组的基础血清胃泌素(均值±标准误)逐渐升高;正常人(42±3 pg/ml),十二指肠溃疡患者(53±4 pg/ml),迷走神经切断术患者(226±54 pg/ml),胃酸过少患者(346±92 pg/ml),胃酸缺乏患者(844±100 pg/ml)。仅对胃泌素升高的患者进行选择性分析时,发现胃酸缺乏患者(93±21 pg/ml)与所有其他组之间以及胃酸过少患者(40±12 pg/ml)与正常人(6±1 pg/ml)之间的胃泌素峰值变化存在显著差异(p<0.05)。这些反应者的线性回归显示基础胃泌素与促胰液素后胃泌素峰值变化之间存在显著相关性(p<0.001)。没有促胰液素激发试验假阳性,但有4例胃酸缺乏患者胃泌素升高超过100 pg/ml,而其他类别患者中没有胃泌素升高超过90 pg/ml的。我们的结果支持这样的概念,即高胃泌素血症伴胃酸缺乏的患者对促胰液素激发试验往往具有更高的G细胞反应性,这可能解释了一些此类患者的假阳性结果。

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Is the gastrin response to secretin provocation a function of antral G-cell mass? Results in the hypergastrinemia of acid hyposecretion.胃泌素对促胰液素激发的反应是胃窦G细胞数量的一种功能吗?结果导致胃酸分泌不足引起的高胃泌素血症。
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引用本文的文献

1
Hypochlorhydria and achlorhydria are associated with false-positive secretin stimulation testing for Zollinger-Ellison syndrome.胃酸过少和胃酸缺乏与 Zollinger-Ellison 综合征的促胰液素刺激试验假阳性有关。
Pancreas. 2013 Aug;42(6):932-6. doi: 10.1097/MPA.0b013e3182847b2e.
2
Serum gastrin in Zollinger-Ellison syndrome: II. Prospective study of gastrin provocative testing in 293 patients from the National Institutes of Health and comparison with 537 cases from the literature. evaluation of diagnostic criteria, proposal of new criteria, and correlations with clinical and tumoral features.佐林格-埃利森综合征中的血清胃泌素:II. 对美国国立卫生研究院293例患者进行胃泌素激发试验的前瞻性研究,并与文献中的537例病例进行比较。评估诊断标准,提出新标准,并与临床和肿瘤特征进行相关性分析。
Medicine (Baltimore). 2006 Nov;85(6):331-364. doi: 10.1097/MD.0b013e31802b518c.