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Diethylene glycol (DEG) is a solvent with physical and chemical properties similar to propylene glycol, a xenobiotic that is used throughout the chemical industry. Pharmaceutical-grade propylene glycol is a safe and commonly used solvent for water-insoluble pharmaceuticals (Chap. 46). However, unlike propylene glycol, DEG is a potent nephrotoxic and neurotoxic chemical. Substitution of DEG for propylene glycol and other diluents such as glycerin in oral pharmaceutical elixirs has repeatedly caused epidemics of mass poisoning (Chap. 2). This substitution usually occurred early in the pharmaceutical manufacturing process because of a variety of reasons, including the intentional mislabeling of DEG as an inexpensive replacement diluent for pharmaceutical-grade glycerin, for financial gain and various other reasons.37,45 As medication-associated DEG mass poisonings recurred over time, numerous quality assurance and control guidelines were developed to identify DEG-contaminated materials. Failure to adhere to these guidelines throughout the pharmaceutical manufacturing and distribution process contributes to this persistent public health problem.45 In DEG poisoning, patients develop acute kidney injury (AKI) that often rapidly progresses to kidney failure. Patients who developed AKI and do not die quickly after exposure, often become dialysis dependent. A subset who survive the initial poisoning also develop neurological signs and symptoms. These patients either deteriorate further after the onset of neurologic signs and symptoms and die, or they recover from their initial poisoning event, but suffer neurologic sequelae that tends to improve with time.42,47

The metabolism of DEG and the pathophysiology of DEG-associated disease are incompletely understood and most of what is known comes from animal studies. Indeed, very little data regarding DEG and its metabolites are available from biological samples of humans poisoned by DEG. It was once thought that DEG was metabolized to 2 ethylene glycol molecules, which, when metabolized to glycolic acid and oxalic acid, caused AKI; this theory has been disproven.20 Current evidence supports that the terminal DEG metabolite diglycolic acid (DGA) is the nephrotoxin.10,28,38 Diglycolic acid is neurotoxic as well based on a single published case report of DGA ingestion.40 This Special Consideration will provide a brief history and epidemiology of DEG poisoning, describe existing pharmacokinetic and toxicokinetic data collected primarily from animal studies, and then discuss available information on the toxic dose, pathophysiology, clinical manifestations, testing and treatment for DEG poisoning. When specific doses of DEG in the literature were reported in milliliters per kilogram, they were converted to grams per kilogram by taking into account the density of DEG (1.118 g/mL) and the concentration. If information on concentration was not provided, then a 100% concentration was assumed. For the reader’s convenience, the original dose (if it was in milliliters per kilogram) and commensurate DEG concentration are provided following the converted dose in grams per kilogram or milligrams per kilogram.

Diethylene glycol is produced ...

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