Nardone G, d'Armiento F, Corso G, Coscione P, Esposito M, Budillon G
Cattedra di Gastroenterologia, Università Federico II, Naples, Italy.
Gastroenterology. 1994 Aug;107(2):362-8. doi: 10.1016/0016-5085(94)90160-0.
BACKGROUND/AIMS: Gastric mucosa phospholipids play an important protective role against exogenous and endogenous toxic agents. Recently, we described a significant alteration of phospholipid profile in patients with chronic atrophic gastritis without Helicobacter pylori infection. The aim of the present study was to assess the phospholipid composition of gastric biopsy specimens in 41 subjects with chronic gastritis in relation to H. pylori infection (no. 26) and nonalcoholic cirrhosis (no. 18).
Phospholipids were extracted from homogenate mucosal samples using Folch's method, purified, and separated by thin-layer chromatography, while bound fatty acids were analyzed by gas liquid chromatography.
The amounts of five gastric phospholipid classes, their rank order, and percent distribution of the principal ones (phosphatidylcholine [PC] 58%, phosphatidylethanolamine [PE] 26%, and phosphatidylinositol 11% vs. values of 49, 19, and 14, respectively, in the earlier study) were confirmed in chronic gastritis without H. pylori infection. H. pylori infection induced a dramatic reduction (about 30%) in the absolute amount of total phospholipids (24.2 micrograms/mg protein versus 35.1 of the H. pylori-negative group; P < 0.01), PC and PE being the most affected (-36% and -26%, respectively), while bound fatty acids remained unchanged. There was no difference in cirrhotic vs. noncirrhotic subjects.
(1) The development of gastritis is characterized by an alteration of the lipid mucosal pattern that can change with the different etiologies, the most dramatic variations being observed in the presence of H. pylori infection; and (2) cirrhosis does not affect further the alteration in the phospholipid profile of the antral mucosa caused by chronic gastritis.
背景/目的：胃黏膜磷脂对外源性和内源性毒性因子具有重要的保护作用。最近，我们描述了在无幽门螺杆菌感染的慢性萎缩性胃炎患者中磷脂谱的显著改变。本研究的目的是评估41例慢性胃炎患者胃活检标本的磷脂组成，这些患者与幽门螺杆菌感染（26例）和非酒精性肝硬化（18例）相关。
使用Folch法从匀浆的黏膜样本中提取磷脂，进行纯化，并通过薄层色谱法分离，同时通过气相色谱法分析结合脂肪酸。
在无幽门螺杆菌感染的慢性胃炎中，确认了五种胃磷脂类别的含量、其排列顺序以及主要磷脂（磷脂酰胆碱[PC]58%、磷脂酰乙醇胺[PE]26%和磷脂酰肌醇11%，而在早期研究中分别为49%、19%和14%）的百分比分布。幽门螺杆菌感染导致总磷脂绝对量显著降低（约30%）（幽门螺杆菌阴性组为35.1μg/mg蛋白质，幽门螺杆菌阳性组为24.2μg/mg蛋白质；P<0.01），PC和PE受影响最大（分别降低36%和26%），而结合脂肪酸保持不变。肝硬化患者与非肝硬化患者之间无差异。
（1）胃炎的发展特征是脂质黏膜模式的改变，这种改变会因不同病因而变化，在幽门螺杆菌感染时观察到最显著的变化；（2）肝硬化不会进一步影响由慢性胃炎引起的胃窦黏膜磷脂谱的改变。
