Home |
Current Issue |
Past Issues |
In the Clinic |
ACP Journal Club |
CME |
Collections |
Audio/Video |
Mobile |
Subscribe |
Tools |
Help |
ACP Online
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||
1 November 1993 | Volume 119 Issue 9 | Pages 952-953
I agree with the conclusions of Raufman and colleagues [1] that drugs such as cimetidine and ranitidine that are used to suppress the production of gastric acid do not influence the serum ethanol concentrations reached after moderate alcohol consumption. This is true when alcohol is consumed on an empty stomach as well as after a meal [2]. Accordingly, this drug-alcohol interaction, the subject of unprecedented news media attention, lacks any clinical or medicolegal relevance [3].
However, their inclusion of breath alcohol measurements raised concerns about their analysis. As shown in Table 1, peak serum ethanol concentrations reported by Raufman and colleagues are approximately 7% to 17% lower than the values estimated by breath analysis. Breath ethanol levels are always approximately 2000 times lower than the coexisting concentration in an equal volume of blood [4]. LETTER
Histamine-2-Receptor Antagonists and Serum Ethanol Levels
TO THE EDITOR:
|
Furthermore, breath alcohol devices such as the Lion Alcolmeter S-D2 (MPD, Inc., Owensboro, Kentucky) are calibrated with NALCO (MPD, Inc.) alcohol-gas standards to give an estimate of the alcohol concentration in venous whole blood and not in serum. It is widely known that the ethanol concentrations in plasma or serum are about 10% to 20% higher than those in an equal volume of whole blood because of the different amounts of water in these biofluids [5]. I believe this discrepancy may be explained by inaccurate calibration of the breath alcohol analyzer or an arithmetic error in translating the instrument readings into serum ethanol levels (mmol/L).
Nonetheless, because the same breath-alcohol analyzer was used to test patients receiving all treatments, this bias in the reported readings Table 1 would not negate their conclusions.
References
|
|---|
|
|
|---|
1. Raufman JP, Notar-Francesco V, Raffaniello RD, Straus EW. Histamine-2 receptor antagonists do not alter serum ethanol levels in fed, nonalcoholic men. Ann Intern Med. 1993; 118:488-94.
2. Jonsson KAngstrom, Jones AW, Bostrom H, Andersson T. Lack of effect of omeprazole, cimetidine, and ranitidine on the pharmacokinetics of ethanol in fasting male volunteers. Eur J Clin Pharmacol. 1992; 42: 209-12.[Medline]
3. Levitt MD. Lack of clinical significance of the interaction between H2-receptor antagonists and ethanol. Aliment Pharmacol Ther. 1993; 7:131-8.
4. Jones AW. Physiological aspects of breath-alcohol measurements. Alcohol, Drugs & Driving. 1990;6:1-25.
5. Jones AW, Hahn RG, Stalberg HP. Distribution of ethanol and water between plasma and whole blood: Inter- and intra-individual variations after administration of ethanol by intravenous infusion. Scand J Clin Lab Invest. 1990; 50:775-80.
About Letters
|
|
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.
| ||||||||||||||||||||||||||||||||||||||||||||||||||||