Bode C, Maute G, Bode J C
Department of Physiology of Nutrition, Hohenheim University, Stuttgart, Germany.
Gut. 1996 Sep;39(3):348-52. doi: 10.1136/gut.39.3.348.
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.
Fifty six alcoholic patients and 66 subjects without alcohol misuse were included in the study.
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.
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.
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.
实验研究结果支持以下假说,即前列腺素生成减少可能在酒精所致胃黏膜损伤中起作用。本研究旨在调查酒精滥用是否会损害胃黏膜中前列腺素E2(PGE2)和前列腺素F2α(PGF2α)的合成。
本研究纳入了56例酒精性患者和66例无酒精滥用的受试者。
从胃窦和胃体获取黏膜活检标本。在活检标本的微粒体部分测定PGE2和PGF2α的最大合成率。
胃窦活检标本中两种前列腺素的合成率与胃体活检标本中的合成率无显著差异。与黏膜正常的非酒精性组相比,戒酒少于5天的酒精性患者中两种前列腺素的合成均显著降低(PGE2分别降低40%,PGF2α降低42%)。在患有严重胃炎的非酒精性患者中,PGE2合成增加(+30%,p < 0.05),PGF2α合成降低(-42.5%,p < 0.025)。与患有严重胃炎的非酒精性组相比,患有严重胃炎的酒精性患者中PGE2合成降低近60%(p < 0.001)。幽门螺杆菌定植和吸烟对前列腺素合成均无显著影响。
长期酒精滥用与胃黏膜中前列腺素合成能力显著降低有关,且这种酒精诱导的前列腺素合成减少受胃炎的存在和程度调节。