Histamine-2-Receptor Antagonists and Serum Ethanol Levels

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TO THE EDITOR:

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].

Table 1. Peak Serum Ethanol Concentrations and Peak Breath Ethanol Concentrations as Reported by Raufman and Colleagues*

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.

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References

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