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Blood Alcohol Levels after Prolonged Histamine-2-Receptor Antagonist Treatment
- Alessandro Cassini, MD;
- Franceso Mari, PhD; and
- Calogero Surrenti, MD
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TO THE EDITOR:
Recent studies indicate that cimetidine and ranitidine, but not famotidine, may inhibit gastric alcohol-dehydrogenase activity, thus impairing the gastric first-pass metabolism of ethanol [1-4]. Those studies, however, were done in “artificial” conditions (healthy patients; 1 week of treatment; last dose at breakfast, 1 hour before alcohol ingestion). We studied whether prolonged treatment with ranitidine or famotidine affected blood alcohol concentrations in 16 men with duodenal ulcers. Patients with Helicobacter pylori-associated duodenal ulcers were not enrolled [5]. Patients were randomly assigned to receive either 300 mg of ranitidine (n = 8) or 40 mg of famotidine (n = 8) at bedtime for 2 months. The rate of gastric first-pass metabolism was checked in all patients before study entry and was found to be 53% by comparing the area under the curve (AUC) of blood alcohol concentration after either intravenous or oral administration of 0.3 g/kg of ethanol (AUC [intravenous] = 11.6 ±1.6 mM/h; AUC [oral] = 5.4 ±0.6 mM/h). Patients had a standard lunch (at 1:00 p.m.), and 0.3 g/kg of alcohol was consumed 15 minutes after the meal. Blood alcohol concentrations were measured by a gas-chromatographic procedure up to 150 minutes after drinking alcohol. Ranitidine did not significantly modify either the mean oral AUC (5.8 ±1.8 mM/h before treatment compared with 6.2 ±1.4 mM/h after treatment) or the peak blood alcohol concentration (4.6 ±1.1 mM compared with 5.3 ±1.7 mM) after 2 months of treatment. Famotidine failed to affect blood alcohol concentration in the second group of patients (AUC [oral] = 5.0 ±1.4 mM/h compared with 5.6 mM/h ±1.7 mM/h, peak blood alcohol concentration = 4.0 mM ±1.7 mM compared with 4.3 mM ±1.8 mM; before and after treatment, respectively). No significant differences in alcohol-dehydrogenase activity were found in the gastric mucosal biopsy specimens of patients after treatment with either drug. Although ranitidine and some other histamine-2-receptor antagonists have been clearly shown to inhibit gastric alcohol-dehydrogenase activity in vitro, our results suggest that these studies may not be clinically relevant.
Alessandro Casini, MD
Francesco Mari, PhD
Calogero Surrenti, MD
Universita di Firenze; Firenze, Italy
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
