To the Editor:
We read with interest the recent article by Zehtabchi et al. entitled “Does ethanol explain the acidosis commonly seen in ethanol-intoxicated patients?” (Citation1). As a result of this study, the authors rejected their research hypothesis that a dose-response curve could be produced to predict the expected acidosis for any given level of ethanol.
This hypothesis was generated with the assumption that ethanol intoxication results in acidosis. In on our experience, acidosis is not commonly seen in ethanol-intoxicated patients. Although ethanol is metabolized to acetic acid, this is well handled by the body's buffering systems. Ethanol metabolism may facilitate the production of lactic acid from pyruvic acid due to an elevated level of NADH. However, no new acids are generated in this process. In addition, this study has not demonstrated any correlation between lactate and ethanol levels.
We are also concerned about the widespread use of the term “ethanol-intoxicated”. It must be emphasized that ethanol intoxication is a clinical syndrome dependent to a large degree on the patient's ethanol tolerance. The patients included in the “ethanol-intoxicated” group fulfilled the inclusion criterion of having an ethanol level above the legal limit of 80 mg/dL. We are not provided with any clinical data providing an accurate assessment of intoxication.
REFERENCES
- Zehtabchi S, Sinert R, Baron BJ, Paladino L, Yadav K. Does ethanol explain the acidosis commonly seen in ethanol-intoxicated patients?. Clin Tox 2005; 43: 161–166