Simanowski U A, Egerer G, Oneta C, Keil T, Parés X, Conradt C, Arce L, Waldherr R, Stickel F, Russell R M, Aderjan R, Klee F, Seitz H K
Laboratory of Alcohol Research, Liver Disease and Nutrition, Department of Medicine, Salem Medical Center, Heidelberg, Germany.
Digestion. 1998 Jul-Aug;59(4):314-20. doi: 10.1159/000007508.
BACKGROUND/AIMS: Ethanol is metabolized by alcohol dehydrogenase in the human stomach. This metabolism contributes to the so-called first-pass metabolism of ethanol which is affected by gender, medication, and morphological alterations of the gastric mucosa. Recently, it has been shown that Helicobacter pylori is capable to oxidize ethanol to acetaldehyde in vitro. Since H. pylori also injures gastric mucosa, the present study examines the effect of this bacterium on gastric alcohol dehydrogenase activity and systemic availability of ethanol in vivo.
Thirteen volunteers (7 men and 6 women, aged 18-52 years) with gastric H. pylori infection diagnosed by a positive CLO test and positive gastric histology received ethanol (0.225 g/kg) either orally or intravenously before and after H. pylori elimination to determine systemic availability of ethanol. In addition, gastric biopsy specimens were taken from all subjects before and after H. pylori elimination for histological assessment of mucosal alterations and determinations of gastric alcohol dehydrogenase activity and phenotype of the enzyme.
In the presence of H. pylori the first-pass metabolism of ethanol was found to be significantly reduced (625 +/- 234 vs. 1,155 +/- 114 mg/dl/min, p = 0.046). This reduction of first-pass metabolism of ethanol was associated with a significant decrease in alcohol dehydrogenase activity (4.8 +/- 1.5 vs. 12.1 +/- 2.3 nmol/mg protein x min, p < 0.05) and an increase in the severity of mucosal damage as determined by a histological score (p < 0.05).
H. pylori infection leads to gastric mucosal injury which is associated with a decrease in gastric alcohol dehydrogenase activity and first-pass metabolism of ethanol. Ethanol metabolism by H. pylori does not play an important role in vivo. However, gastric morphology is one important factor determining systemic availability of ethanol in man.
背景/目的：乙醇在人体胃内通过乙醇脱氢酶进行代谢。这种代谢促成了乙醇所谓的首过代谢，而首过代谢会受到性别、药物以及胃黏膜形态改变的影响。最近有研究表明，幽门螺杆菌在体外能够将乙醇氧化为乙醛。由于幽门螺杆菌也会损伤胃黏膜，因此本研究探讨了该细菌对胃乙醇脱氢酶活性以及乙醇体内全身利用率的影响。
13名志愿者（7名男性和6名女性，年龄18 - 52岁）经CLO试验阳性和胃组织学检查确诊为胃幽门螺杆菌感染，在根除幽门螺杆菌前后分别口服或静脉注射乙醇（0.225 g/kg），以确定乙醇的全身利用率。此外，在根除幽门螺杆菌前后从所有受试者获取胃活检标本，用于黏膜改变的组织学评估以及胃乙醇脱氢酶活性和酶表型的测定。
在存在幽门螺杆菌的情况下，发现乙醇的首过代谢显著降低（625 ± 234 vs. 1,155 ± 114 mg/dl/min，p = 0.046）。乙醇首过代谢的这种降低与乙醇脱氢酶活性的显著降低（4.8 ± 1.5 vs. 12.1 ± 2.3 nmol/mg蛋白质×分钟，p < 0.05）以及组织学评分确定的黏膜损伤严重程度增加相关（p < 0.05）。
幽门螺杆菌感染导致胃黏膜损伤，这与胃乙醇脱氢酶活性降低以及乙醇首过代谢减少有关。幽门螺杆菌对乙醇的代谢在体内并不起重要作用。然而，胃形态是决定人体乙醇全身利用率的一个重要因素。
