幽门螺杆菌
医学
胃肠病学
内科学
胃窦
胃炎
螺旋藻科
磷脂
亚油酸
花生四烯酸
胃
活检
脂肪酸
胃粘膜
胃酸
萎缩性胃炎
胃内容物
生物
生物化学
膜
酶
作者
Tadahiro Orihara,Hiroyuki Wakabayashi,Atsuko Nakaya,Kanako Fukuta,Shinya Makimoto,Kotaro Naganuma,Akio Entani,Akiharu Watanabe
标识
DOI:10.1046/j.1440-1746.2001.02440.x
摘要
Abstract Background and Aims: Whether Helicobacter pylori eradication alters gastric mucosal phospholipid contents and their fatty acid composition remains unclear. The aim of the present study was to clarify the effect of H. pylori eradication on gastric mucosal phosphatidylcholine (PC) content and its fatty acid composition. Methods: Endoscopic biopsy specimens were taken from the antrum and body of each of 19 asymtomatic male volunteers for detection of H. pylori , histopathological assessment of gastritis, phospholipid determination and fatty acid analysis. All the subjects with H. pylori infection were treated with eradication therapy. Endoscopy and tissue sampling were repeated again 1 and 6 months after all treatment. Results: In eight subjects, H. pylori infection was evident and was successfully eradicated. Pretreatment degrees of lymphocytes and plasma cells (inflammation) and polymorphonuclear neutrophils (activity) were greater in H. pylori ‐positive subjects compared with H. pylori ‐negative subjects ( P < 0.001), whereas the degree of inflammation decreased ( P < 0.001), and neutrophils had completely disappeared at 6 months after eradication. Moreover, the gastric mucosal PC contents at the antrum and body were unchanged within 1 month after cessation of treatment, but increased at 6 months after eradication ( P < 0.05). At 6 months after cessation of treatment, H. pylori ‐eradicated subjects had an increase (+ 30% at antrum, + 18% at body) in linoleic acid composition and a decrease (− 37%, − 43%) in arachidonic acid composition of PC at the antrum and body, respectively. Conclusions: These findings suggest that H. pylori eradication reduces the production of various eicosanoids, resulting in the normalization of gastric mucosal PC content and its fatty acid composition, which may consequently cause the gastric mucosal hydrophobicity to be normalized.
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