Unlike ethanol and isopropyl alcohol, MeOH/EG/DEG produce less CNS depression and cause more metabolic toxicity - the earliest finding may be the presence of an osmol gap created by the parent compound.
The enzymes responsible for the transformation from a “safe” to “toxic” alcohol or glycol are primarily Alcohol dehydrogenase and Aldehyde Dehydrogenase (ADH). DEG toxicity is also managed with this antidote. Providers have now largely replaced ethanol with fomepizole (4-methylpyrazole, 4-MP) as the ADH-blocker of choice. By the late 1940’s to early 1950’s, medical practice came to recognize that toxicity is prevented or limited by the co-administration of ethanol, an inhibitor of the ADH enzyme.
However, recovery was often partial, with MeOH and EG causing neural damage and renal failure, respectively. Historically, toxic alcohol poisoned patients were managed with sodium bicarbonate (for acidosis) and with supportive care until recovery or death. Today, methanol (MeOH), diethylene glycol (DEG), and ethylene glycol (EG) are still used in “antifreeze” products and continue to be implicated in poisonings and fatalities. Throughout the early 20th century, people drank ethylene glycol products meant for cooling internal combustion engines. In 1938, a sulfanilamide elixir was “sweetened” with diethylene glycol. During Prohibition in the 1920’s– 1930’s, ethanol (drinking alcohol) was contaminated with methanol.
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