What is the pathophysiology of ethylene glycol alcohol toxicity?

Updated: Jan 05, 2021
  • Author: Michael D Levine, MD; Chief Editor: Jeter (Jay) Pritchard Taylor, III, MD  more...
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Ethylene glycol (CH2 OH-CH2 OH) is an odorless, colorless, sweet-tasting liquid, which is used in many manufacturing processes. Domestically, it is probably most commonly encountered in antifreeze. It is absorbed somewhat rapidly from the gastrointestinal tract, and peak concentrations are observed 1-4 hours after ingestion. [8]

Ethylene glycol itself is nontoxic, but it is metabolized into toxic compounds. Ethylene glycol is oxidized via alcohol dehydrogenase into glycoaldehyde, which then undergoes metabolism via aldehyde dehydrogenase into glycolic acid. [11] The conversion to glycolic acid is somewhat rapid. In contrast, the conversion of glycolic acid to glyoxylic acid is slower and is the rate-limiting step in the metabolism of ethylene glycol.

Glyoxylic acid is subsequently metabolized into several different products, including oxalic acid (oxalate), glycine, and alpha-hydroxy-beta-ketoadipate. The conversion to glycine requires pyridoxine as a cofactor, while the conversion to alpha-hydroxy-beta-ketoadipate requires thiamine as a cofactor. The oxalic acid combines with calcium to form calcium oxalate crystals.

In the presence of normal renal function and no competitive inhibition for alcohol dehydrogenase, the excretion half-life of ethylene glycol is approximately 3 hours. However, in the presence of fomepizole or ethanol, alcohol dehydrogenase undergoes competitive inhibition, and the resulting excretion half-life increases to approximately 17-20 hours.

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