Citation

Powers RH, Dean DE. J. Anal. Toxicol. 2009; 33(8): 561-563.

Affiliation

Connecticut Department of Public Safety, Controlled Substances/Toxicolog Laboratory, Hartford, Connecticut 06424, USA. robert.powers@po.state.ct.us

Copyright

(Copyright © 2009, Preston Publications)

DOI

unavailable

PMID

19874670

Abstract

The Connecticut Department of Public Safety laboratory recently addressed a legal challenge to a hospital alcohol dehydrogenase (ADH)-based serum ethanol determination based on the suggestion of interference by lactate dehydrogenase (LDH)-catalyzed oxidation of lactate. Both ADH- and LDH-oxidations require NAD(+) (present in excess in the assay). NADH produced by LDH-catalyzed lactate oxidation in the assay is interpreted as derived from ethanol. Hepatic trauma was suggested as the basis for elevated levels of lactate and LDH. Clinical laboratory results were evaluated, specifically serum hepatic enzymes, ions, and anion gap. Aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) were 229 and 144 U/L, respectively (approximately 8x and 4x reference range midpoint values). Na(+), K(+), Cl(-), and CO(2) levels were 143, 3.0, 112, and 20 meq/L, respectively, yielding an anion gap of 8 meq/L (ref. range 8-15). Serum lactate contributes to "unmeasured anions"; hence, the anion gap was inconsistent with a significant lactate elevation. Based on the slight elevation of ASAT and ALAT, LDH levels were estimated to be elevated to no more than 10-fold. Calculation of the amount of LDH and ADH present in the ethanol assay suggest an ADH/LDH ratio of 200:1. Hence, contribution by lactate oxidation to the serum ethanol concentration in this case would have been negligible.

Language: en