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Prostaglandin E2 and prostaglandin F2 alpha biosynthesis in human gastric mucosa: effect of chronic alcohol misuse.

机译:人胃粘膜中前列腺素E2和前列腺素F2α的生物合成:慢性酒精滥用的影响。

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摘要

BACKGROUND AND AIMS: The results of experimental studies support the hypothesis that decreased prostaglandin production might play a part in the gastric mucosal injury induced by alcohol. In this study, it was investigated whether alcohol misuse impairs the synthesis of prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha) in gastric mucosa. PATIENTS: Fifty six alcoholic patients and 66 subjects without alcohol misuse were included in the study. METHODS: Mucosal biopsy specimens were obtained from the antrum and body of the stomach. Maximal synthesis rates of PGE2 and PGF2 alpha were determined in the microsomal fraction of the biopsy specimens. RESULTS: The rates of synthesis of both prostaglandins in biopsy specimens from the antrum were not significantly different from those obtained in the body. Synthesis of both prostaglandins was significantly reduced in alcoholic patients who abstained less than five days compared with the non-alcoholic group with normal mucosa (PGE2-40%, PGF2 alpha-42% respectively). In non-alcoholic patients with severe gastritis PGE2 synthesis was increased (+30%, p < 0.05) and PGF2 alpha synthesis was decreased (-42.5%, p < 0.025). In alcoholic patients with severe gastritis PGE2 synthesis was depressed by almost 60% (p < 0.001) compared with the non-alcoholic group with severe gastritis. Neither colonisation of Helicobacter pylori nor smoking had a significant influence on the prostaglandin synthesis. CONCLUSIONS: Chronic alcohol misuse is associated with significantly reduced capacity for prostaglandin synthesis in gastric mucosa and this alcohol induced decrease in prostaglandin synthesis is modulated by the presence and degree of gastritis.
机译:背景与目的:实验研究的结果支持以下假设:前列腺素生成减少可能是酒精引起的胃粘膜损伤的一部分。在这项研究中,调查了酒精滥用是否会损害胃粘膜中前列腺素E2(PGE2)和前列腺素F2 alpha(PGF2 alpha)的合成。患者:56名酒精中毒患者和66名无酒精滥用的受试者被纳入研究。方法:从胃窦和胃部获取粘膜活检标本。在活检标本的微粒体部分中确定了PGE2和PGF2α的最大合成率。结果:来自胃窦的活检标本中两种前列腺素的合成速率与体内获得的速率没有显着差异。与正常黏膜正常的非酒精饮料组相比,戒酒时间少于五天的酒精患者的两种前列腺素的合成均显着降低(分别为PGE2-40%,PGF2α-42%)。在非酒精性重症胃炎患者中,PGE2合成增加(+ 30%,p <0.05),PGF2α合成减少(-42.5%,p <0.025)。与非酒精性重症胃炎组相比,重症胃炎的酒精中毒患者的PGE2合成降低了近60%(p <0.001)。幽门螺杆菌的定植和吸烟都对前列腺素的合成没有显着影响。结论:慢性酒精滥用与胃粘膜中前列腺素合成的能力显着降低有关,并且这种酒精诱导的前列腺素合成的减少受胃炎的存在和程度的调节。

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