Studies on Ethylene Glycol Poisoning

Jacobsen, Dag; Ostby, N; Bredesen, J. E.

doi:10.1111/j.0954-6820.1982.tb03161.x

Cited by 45 publications

(6 citation statements)

References 17 publications

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“…This concern generally arises from clinical observations in humans of EG overdoses (11,15,24,25). After ingestion, EG can be absorbed and metabolized into glycolate and Ox rapidly in the liver.…”

Section: Discussionmentioning

confidence: 99%

Strain differences in urinary factors that promote calcium oxalate crystal formation in the kidneys of ethylene glycol-treated rats

McMartin²

2009

American Journal of Physiology-Renal Physiology

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Ethylene glycol (EG)-induced hyperoxaluria is the most commonly employed experimental regimen as an animal model of calcium oxalate (CaOx) stone formation. The variant sensitivity to CaOx among different rat strains has not been fully explored, although the Wistar rat is known to accumulate more CaOx in kidney tissue after low-dose EG exposure than in the Fischer 344 (F344) rats. Supersaturation of CaOx in tubular fluid contributes to the amount of CaOx crystal formation in the kidney. We hypothesized that the urinary supersaturation of CaOx in Wistar rats is higher than that of F344 rats, thereby allowing for greater CaOx crystal deposition in the Wistar rat. Age-matched male Wistar and F344 rats were treated with 0.75% EG or drinking water for 8 wk. Twenty-four-hour urine was collected at 0, 2, 4, 6, and 8 wk for analysis of key electrolytes to calculate the CaOx supersaturation. Plasma oxalate level was also measured. Our data confirmed the different sensitivity to renal toxicity from EG between the two rat strains (Wistar > F344). After EG treatment, the plasma oxalate level and urine oxalate excretion were markedly greater in the Wistar rats than in the F344 rats, while urine calcium was slightly decreased in Wistars. Thus, the CaOx supersaturation in urine of Wistar rats was higher, which led to a greater crystal deposition in kidney in Wistar rats. These studies suggest that during EG treatment, changes in urine electrolytes and in CaOx supersaturation occur to a greater extent in the Wistar rat, in agreement with its greater sensitivity to EG toxicity.

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Section: Discussionmentioning

confidence: 99%

Strain differences in urinary factors that promote calcium oxalate crystal formation in the kidneys of ethylene glycol-treated rats

McMartin²

2009

American Journal of Physiology-Renal Physiology

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“…Other articles were obtained, although they were not part of the initial systematic literature search, namely relating to dialyzability of EG metabolites [ 292 – 306 ], dialyzability of ethanol [ 307 – 317 ], dialyzability of fomepizole [ 318 – 323 ], and dialyzability of pyridoxine and thiamine [ 324 – 341 ]. Data from publications reporting the same subjects were merged but the citations were only counted once in the systematic review, e.g., [ 15 , 28 , 211 ] and [ 19 , 147 , 151 , 342 ].…”

Section: Resultsmentioning

confidence: 99%

Extracorporeal treatment for ethylene glycol poisoning: systematic review and recommendations from the EXTRIP workgroup

et al. 2023

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Ethylene glycol (EG) is metabolized into glycolate and oxalate and may cause metabolic acidemia, neurotoxicity, acute kidney injury (AKI), and death. Historically, treatment of EG toxicity included supportive care, correction of acid–base disturbances and antidotes (ethanol or fomepizole), and extracorporeal treatments (ECTRs), such as hemodialysis. With the wider availability of fomepizole, the indications for ECTRs in EG poisoning are debated. We conducted systematic reviews of the literature following published EXTRIP methods to determine the utility of ECTRs in the management of EG toxicity. The quality of the evidence and the strength of recommendations, either strong (“we recommend”) or weak/conditional (“we suggest”), were graded according to the GRADE approach. A total of 226 articles met inclusion criteria. EG was assessed as dialyzable by intermittent hemodialysis (level of evidence = B) as was glycolate (Level of evidence = C). Clinical data were available for analysis on 446 patients, in whom overall mortality was 18.7%. In the subgroup of patients with a glycolate concentration ≤ 12 mmol/L (or anion gap ≤ 28 mmol/L), mortality was 3.6%; in this subgroup, outcomes in patients receiving ECTR were not better than in those who did not receive ECTR. The EXTRIP workgroup made the following recommendations for the use of ECTR in addition to supportive care over supportive care alone in the management of EG poisoning (very low quality of evidence for all recommendations): i) Suggest ECTR if fomepizole is used and EG concentration > 50 mmol/L OR osmol gap > 50; or ii) Recommend ECTR if ethanol is used and EG concentration > 50 mmol/L OR osmol gap > 50; or iii) Recommend ECTR if glycolate concentration is > 12 mmol/L or anion gap > 27 mmol/L; or iv) Suggest ECTR if glycolate concentration 8–12 mmol/L or anion gap 23–27 mmol/L; or v) Recommend ECTR if there are severe clinical features (coma, seizures, or AKI). In most settings, the workgroup recommends using intermittent hemodialysis over other ECTRs. If intermittent hemodialysis is not available, CKRT is recommended over other types of ECTR. Cessation of ECTR is recommended once the anion gap is < 18 mmol/L or suggested if EG concentration is < 4 mmol/L. The dosage of antidotes (fomepizole or ethanol) needs to be adjusted during ECTR.

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“…Subsequently, ethylene glycol patients will develop acute kidney injury, coma, seizures and cardiovascular failure . Oxalate crystals in the urine can be observed with increased frequency after 6 h . Methanol‐poisoned victims usually report visual disturbances, gastrointestinal symptoms, chest pain and dyspnoea.…”

Section: Clinical Course Of These Toxicitiesmentioning

confidence: 99%

“…The rationale for this treatment is that ethanol has at least 10 times the affinity for ADH compared to methanol and 20‐fold more than ethylene glycol . Ethanol occupies the active site of the enzyme, thereby reducing production of toxic metabolites as demonstrated in many case reports/series on methanol or ethylene glycol poisoning . Because most patients were also treated with bicarbonate and dialysis, conclusions regarding the efficacy of ethanol therapy alone are limited.…”

Section: Treatment With Ethanolmentioning

confidence: 99%

Antidotes for poisoning by alcohols that form toxic metabolites

McMartin

Jacobsen

Hovda

2016

Brit J Clinical Pharma

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111

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The alcohols, methanol, ethylene glycol and diethylene glycol, have many features in common, the most important of which is the fact that the compounds themselves are relatively non-toxic but are metabolized, initially by alcohol dehydrogenase, to various toxic intermediates. These compounds are readily available worldwide in commercial products as well as in homemade alcoholic beverages, both of which lead to most of the poisoning cases, from either unintentional or intentional ingestion. Although relatively infrequent in overall occurrence, poisonings by metabolically-toxic alcohols do unfortunately occur in outbreaks and can result in severe morbidity and mortality. These poisonings have traditionally been treated with ethanol since it competes for the active site of alcohol dehydrogenase and decreases the formation of toxic metabolites. Although ethanol can be effective in these poisonings, there are substantial practical problems with its use and so fomepizole, a potent competitive inhibitor of alcohol dehydrogenase, was developed for a hopefully better treatment for metabolically-toxic alcohol poisonings. Fomepizole has few side effects and is easy to use in practice and it may obviate the need for haemodialysis in some, but not all, patients. Hence, fomepizole has largely replaced ethanol as the toxic alcohol antidote in many countries. Nevertheless, ethanol remains an important alternative because access to fomepizole can be limited, the cost may appear excessive, or the physician may prefer ethanol due to experience.

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Studies on Ethylene Glycol Poisoning

Cited by 45 publications

References 17 publications

Strain differences in urinary factors that promote calcium oxalate crystal formation in the kidneys of ethylene glycol-treated rats

Strain differences in urinary factors that promote calcium oxalate crystal formation in the kidneys of ethylene glycol-treated rats

Extracorporeal treatment for ethylene glycol poisoning: systematic review and recommendations from the EXTRIP workgroup

Antidotes for poisoning by alcohols that form toxic metabolites

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