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

Tanaka, Einosuke; Nakamura, Kōichi

doi:10.1111/j.1365-2125.1988.tb03370.x

Cited by 29 publications

(10 citation statements)

References 12 publications

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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%

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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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Section: Resultsmentioning

confidence: 99%

“…For famotidine, there was only one study of fasting subjects. 22 For nizatidine, the small number of studies (only three), did not permit stratification.…”

Section: Discussionmentioning

confidence: 99%

Effect of histamine-2 receptor antagonists on blood alcohol levels

Weinberg

Burnham²,

Berlin

1998

J Gen Intern Med

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“…While in some studies differences in the design may explain the discrepancy (Dobrilla et al 1984;Kleine & Ert11992;Tanaka & Nakamura 1988) the explanation is more difficult in other studies (Fraser et al 1991(Fraser et al , 1993Raufman et al 1993).…”

Section: H2-receptor Antagonistsmentioning

confidence: 94%

“…Again, part of the alcohol was consumed in the fasting state, and the remaining dose was taken in Drug Safety 10 (4) 1994 portions which would certainly produce a dilution of alcohol in the stomach. Tanaka and Nakamura (1988) tested Japanese volunteers, not taking into account that 1 specific ADH isoenzyme particularly important for alcohol oxidation in the gastric mucosa would have been missing in most of the participants . Fraser et al (1991) investigated the effect of cimetidine 800mg, ranitidine 300mg and famotidine 40mg on low dose (0.3 g/kg) postprandial (after dinner) alcohol absorption, but were unable to detect significant changes.…”

Section: H2-receptor Antagonistsmentioning

confidence: 98%

H2-Antagonists and Alcohol

Gugler

1994

Drug Safety

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There are conflicting data on the existence of significant first-pass metabolism of alcohol (ethanol) in the human stomach and its inhibition by histamine H2-receptor antagonists. Alcohol is predominantly metabolised in the liver by the microsomal alcohol oxidising system, alcohol dehydrogenase (ADH) and a catalase enzyme. Histochemical and kinetic studies have revealed several ADH isoenzymes in the gastric mucosa with different kinetic properties. After small oral doses of alcohol first-pass metabolism in the stomach occurs, as shown by reduced area under the plasma concentration-time curve (AUC) compared with intravenous or intraduodenal administration. The activity of gastric ADH is reduced in women, the elderly, Asian individuals, the fasting state, chronic alcoholism and after gastrectomy. The effect is only present with small (< or = 0.3 g/kg) alcohol doses and with a high alcohol concentration. In a number of studies, cimetidine in therapeutic doses over 7 days produced a significant increase in the AUC and in the peak plasma concentration after administration of alcohol 0.15 and 0.30 g/kg. This was related to an inhibition of gastric ADH activity, as shown by in vitro studies. Ranitidine inhibited gastric ADH to a similar extent on a molar basis, but its effect on alcohol levels in vivo was less constant in various studies. Nizatidine also reduced gastric alcohol first-pass metabolism, but famotidine and roxatidine did not show this effect. In other studies, H2-receptor antagonists did not change AUC and peak alcohol concentration. The controversy is not easy to resolve, since a number of the positive studies did not use a placebo-controlled, randomised, crossover design, while some of the negative studies did not exclude habitual alcohol consumers and included Oriental volunteers, although both groups have been shown to lack significant gastric ADH activity. In this case, when first-pass metabolism of alcohol does not exist, this by definition cannot be abolished by H2-antagonists. The inclusion of oral and intravenous dosage data of alcohol is mandatory to positively identify first-pass metabolism in any individuals. The significance of the effect of H2-antagonists on blood alcohol concentrations is minor. It only occurs in young, male, nonalcoholic, non-Asian individuals, and alcohol must be given in a small (social) dose, in a high concentration, and after meals. An increase in alcohol levels in predisposed patients during treatment with some H2-antagonists cannot be excluded, although the likelihood is small. Furthermore, carefully designed studies are needed to clarify fully the significance of this interaction.

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“…All patients were white. Thirteen subjects (six males, seven females) had been prescribed ranitidine 150 mg twice daily for at least three weeks (median six weeks, range 3-48) before 10.0 mg/100 ml and 16&5 v 7.5 mg/100 ml/h respectively) than in the control group (Fig 1, Table II). In contrast there were no significant differences between the groups in the median peak blood ethanol concentration and AUC after intravenous ethanol (Table III).…”

Section: Subjectsmentioning

confidence: 99%