Payen J L, Cales P, Pienkowski P, Sozzani P, Kervran A, Frexinos J, Pascal J P
Service d'Hepato-Gastroenterologie, CHU Purpan, Toulouse, France.
J Hepatol. 1995 Dec;23(6):689-96. doi: 10.1016/0168-8278(95)80035-2.
BACKGROUND/AIMS: It has been suggested that the vulnerability of gastric mucosa is increased in patients with cirrhosis as a result of a PGE2 deficiency. Therefore, we evaluated whether PGE2 mucosal generation, and gastric potential difference - a reflection of the gastric mucosal barrier - were correlated to endoscopic features and whether these alterations could be alleviated.
The potential difference was measured before (basal) and after a stimulation test by aspirin. The serum levels of gastrin and glucagon were also determined. Finally, the effects of a 1-week administration of propranolol or enprostil were tested on potential difference. The endoscopic grade of portal hypertensive gastropathy was assessed according to McCormack et al. The results are presented respectively for controls, patients with mild gastropathy, and patients with severe gastropathy. Comparisons were made using variance or covariance analysis after adjustment with age.
Basal potential difference was significantly different between the three groups: -30.6, -28.8, -24.9 mV, p <0.05, respectively. The effects of aspirin administration on potential difference parameters were significantly different between the three groups (irritability index: 35 +/- 25, 92 +/- 98, 114 +/- 74 mV2.min, p <0.05, respectively) when non-responders to aspirin were excluded. PGE2 mucosal generation was significantly increased in both the antrum (9.8, 19.5, 19.7 ng/mg proteins, p<0.05, respectively) and in the corpus (8.1, 14.0, 20.2 ng/mg proteins, p<0.05, respectively). PGE2 generation was not related to potential difference. Glucagon serum levels were related to the grade of gastropathy. A 1-week administration of 160 mg/d long-acting propranolol, 35 micro g/d enprostil or placebo did not significantly modify basal potential difference.
Portal hypertensive gastropathy is characterized by a decreased potential difference proportional to the endoscopic severity. The gastric mucosa of patients with cirrhosis seems to be more susceptible to aspirin than that of healthy subjects. It appears that the role of PGE2 is controversial in portal hypertensive gastropathy. Propranolol and enprostil do not improve this decreased potential difference.
背景/目的：有研究表明，肝硬化患者因前列腺素E2（PGE2）缺乏，胃黏膜的脆弱性增加。因此，我们评估了PGE2的黏膜生成以及胃黏膜屏障的反映指标——胃电位差，是否与内镜特征相关，以及这些改变是否能够得到缓解。
在阿司匹林刺激试验前后测量电位差。同时测定血清胃泌素和胰高血糖素水平。最后，测试给予普萘洛尔或恩前列素1周对电位差的影响。根据McCormack等人的方法评估门脉高压性胃病的内镜分级。分别给出对照组、轻度胃病患者和重度胃病患者的结果。经年龄校正后，采用方差分析或协方差分析进行比较。
三组的基础电位差有显著差异：分别为-30.6、-28.8、-24.9 mV，p<0.05。排除对阿司匹林无反应者后，三组之间阿司匹林给药对电位差参数的影响有显著差异（应激指数：分别为35±25、92±98、114±74 mV2·min，p<0.05）。胃窦（分别为9.8、19.5、19.7 ng/mg蛋白质，p<0.05）和胃体（分别为8.1、14.0、20.2 ng/mg蛋白质，p<0.05）中PGE2的黏膜生成均显著增加。PGE2的生成与电位差无关。血清胰高血糖素水平与胃病分级相关。给予160 mg/d长效普萘洛尔、35 μg/d恩前列素或安慰剂1周，对基础电位差无显著影响。
门脉高压性胃病的特征是电位差降低，且与内镜严重程度成正比。肝硬化患者的胃黏膜似乎比健康受试者更容易受到阿司匹林的影响。PGE2在门脉高压性胃病中的作用似乎存在争议。普萘洛尔和恩前列素不能改善这种降低的电位差。
