In Vivo Interactions Between H2-Receptor Antagonists and Ethanol Metabolism in Man and in Rats

Seitz, Helmut K.; Veith, S.; Czygan, P.; Bösche, J; Simon, Bernd; Gugler, R; Kommerell, B

doi:10.1002/hep.1840040623

Cited by 70 publications

(32 citation statements)

References 24 publications

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“…The differences in the dose of cimetidine might also be a factor. Thus, the dose used by Feely & Wood (1982) was 1.25 times, and that used by Seitz et al (1983Seitz et al ( , 1984) was 1.5 times higher than the dose used in the present study. In addition, the type of ethanol beverage and food intake may have affected the rate and the extent of ethanol absorption by changing gastric emptying rate.…”

Section: Discussioncontrasting

confidence: 58%

“…They suggested that this increase was due to inhibition of ethanol metabolism by cimetidine. Seitz et al (1983Seitz et al ( , 1984 also found increased plasma ethanol concentrations and AUC values after cimetidine but not after ranitidine. Tan et al (1983) speculated that cimetidine may increase the absorption rate of ethanol by increasing gastric emptying.…”

Section: Discussionmentioning

confidence: 89%

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Effects of H2‐receptor antagonists on ethanol metabolism in Japanese volunteers.

Tanaka

Nakamura

1988

Brit J Clinical Pharma

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The effects of H2‐receptor antagonists (cimetidine, ranitidine, and famotidine) on ethanol metabolism were investigated. Neither in aldehyde dehydrogenase (ALDH)‐1 deficient subjects nor in those with normal ALDH‐1, did the three H2‐receptor antagonists and placebo differ in their effects on the pharmacokinetic parameters of ethanol (i.e. peak time (tmax), metabolic rate (k0), peak serum concentration (Cmax), volume of distribution (V) and area under the concentration‐time curve (AUC). The AUC of acetaldehyde was slightly but significantly (P less than 0.05) larger only after treatment with cimetidine. Cmax and tmax of acetaldehyde were unchanged.

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Section: Discussioncontrasting

confidence: 58%

Section: Discussionmentioning

confidence: 89%

Effects of H2‐receptor antagonists on ethanol metabolism in Japanese volunteers.

Tanaka

Nakamura

1988

Brit J Clinical Pharma

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“…The existence of FPM may explain the fact that following an oral dose of ethanol, blood ethanol concentrations are significantly lower than blood levels following intravenous administration of the same dose of ethanol [6,7]. Gastric ADH activity and FPM of ethanol are affected by various factors including gender [2,4], ethnology [8][9][10], age [4,11,12], medication [3,13,14], gastric morphology [15,16], and the concentration of ethanol in the alcoholic beverage [17,18]. Furthermore, FPM of ethanol is also influenced by the gastric emptying time [16,18].…”

Section: Introductionmentioning

confidence: 99%

<i>Helicobacter pylori</i> Infection Decreases Gastric Alcohol Dehydrogenase Activity and First-Pass Metabolism of Ethanol in Man

et al. 1998

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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. Methods: 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. Results: 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 × min, p < 0.05) and an increase in the severity of mucosal damage as determined by a histological score (p < 0.05). Conclusions: 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.

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“…This analysis does not include one study, 25 because the fed or fasted status was not described. Regardless of food intake, cimetidine and ranitidine resulted in modestly higher serum 28 C,R 10 Fasted 0.5 DiPadova et al 2 C,R,F 6 Fed 0.3 Dobrilla et al 24 C 6 C,R,F 12 Fed 0.3 Fraser et al 4 C,R,F 23 Fed 0.8 Fraser et al 18 R 20 Fed 0.3 Guram et al 3 C,R,F,N 6 Fed 0.75 Hernandez-Munoz et al 14 C,F 5 Fed 0.15 Jonsson et al 27 C,R 12 Fasted 0.8 Kendall et al 20 C,R,F 24 Fed 0.5-0.8 Mallat et al 15 C,R,F 12 Fed 0.3 Palmer et al 17 C 23 Fed 0.15 Palmer et al 17 C,R,N 23 Fed 0.15 Papke et al 26 C 10 Fasted 0.8 Raufman et al 5 C,R,F,N 23 Fed 0.3 Seitz et al 13 C,R 8 Fed 0.8 Sharma et al 16 C 11 Fed 0.3 Tanaka & Nakamura 22 C,R,F 6 Fasted 0.8 Toon et al 29 R 18 Fed/Fasted 0.5 Webster et al 25 C,R 7 Not 0.7 * C indicates cimetidine; R, ranitidine; F, famotidine; N, nizatidine. alcohol levels, while famotidine had no effect.…”

Section: Resultsmentioning

confidence: 99%

“…[7][8][9][10] Twenty-four trials were eligible for this meta-analysis. [1][2][3][4][5][6][12][13][14][15][16][17][18][19][20][24][25][26][27][28][29][30] Several studies administered more than one drug. These trials are listed in Table 1.…”

Section: Resultsmentioning

confidence: 99%

Effect of histamine-2 receptor antagonists on blood alcohol levels

Weinberg

Burnham²,

Berlin

1998

J Gen Intern Med

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OBJECTIVE:To determine the effect, if any, of histamine type 2 receptor antagonists (H 2 RAs) on serum alcohol levels under various conditions including type of H 2 RA receptor antagonist, alcohol dose, and fed status of the subject. STUDY DESIGN:Meta-analysis of the published literature.DATA SOURCES: Studies were identified by MEDLINE (January 1982 through December 1997) using the key words H 2 receptor antagonists and alcohol. Other studies were identified by reviewing bibliographies of retrieved articles and by discussion with colleagues. STUDY SELECTION:Studies were selected if they involved the coadministration of H 2 RAs and alcohol in healthy, human volunteers. Studies that may have addressed this goal but were performed in another context, for instance the measurement of ulcer healing, were excluded. DATA EXTRACTION:Data were extracted on the design, number of participants, participant characteristics, type and dose of H 2 RA administered, serum alcohol levels (measured as C max ) along with standard deviations, dose of alcohol received, and fed or fasted status of participants. Alcohol dose was arbitrarily divided into low dose ( Յ 0.5 g/kg body weight) versus high dose ( Ͼ 0.5 g/kg body weight). In addition, studies involving ranitidine and cimetidine were stratified by sample size into small ( n Յ 10) versus not small ( n Ͼ 10). MEASUREMENTS AND MAIN RESULTS:

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In Vivo Interactions Between H2-Receptor Antagonists and Ethanol Metabolism in Man and in Rats

Cited by 70 publications

References 24 publications

Effects of H2‐receptor antagonists on ethanol metabolism in Japanese volunteers.

Effects of H2‐receptor antagonists on ethanol metabolism in Japanese volunteers.

<i>Helicobacter pylori</i> Infection Decreases Gastric Alcohol Dehydrogenase Activity and First-Pass Metabolism of Ethanol in Man

Effect of histamine-2 receptor antagonists on blood alcohol levels

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