Characteristics of Laboratory Confirmed Ethylene Glycol and Methanol Exposures Reported to a Regional Poison Control Center

Tung, Robert C; Thornton, Stephen L.

doi:10.17161/kjm.v11i3.8693

Cited by 4 publications

(2 citation statements)

References 9 publications

(16 reference statements)

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“…«Истинного» варианта сочетанного нарушения КОС установить не представилось возможным -это достаточно характерно для экзогенных интоксикаций. Мы предполагаем, что все же доминирующим вариантом дисбаланса КОС является метаболический ацидоз с высокой анионной разницей в сочетании с другими обменными нарушениями, что согласуется с данными научной литературы [1,[6][7][8].…”

Section: результаты и обсуждениеunclassified

“…Клетки почечных канальцев гибнут по меха-низму одно го из вариантов некроза -онкозиса (осмотического разрыва) [4,5]. Высокие значения анионной разницы при отравлении ЭГ являются значимым фактором риска смерти пациентов [6,7]. При отравлении ЭГ, несмотря на опасность перегрузки объема цир-кулирующей крови, применяют активную инфузионную терапию с помощью антидота фомепизола, этанола и корректора метаболического ацидоза -натрия гидрокарбоната [8,9].…”

Section: Introductionunclassified

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Correction of acid base disorders in rats with acute ethylene glycol poisoning

Сивак

Владимирович²,

Михайлович³

et al. 2020

Medical academic journal

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T The aim of the article. The aim of this study was to evaluation of the effectiveness of standard antidote therapy and dimephosphon administration in rats with acute ethylene glycol poisoning. The tasks of the study included modeling acute ethylene glycol poisoning in rats, conducting experimental therapy with ethanol antidote in combination with sodium bicarbonate and dimephosphon therapy, comparing the effectiveness of drugs in relation to indicators of acid-base state impairment and renal function. Materials and methods. Ethylene glycol (EG) was administered per os to Wistar male rats (190-210 g b.w.) at a single dose of 6 mL / kg b.w. through an atraumatic gastric tube. The animals were divided into 4 groups of 6 individuals each: intact (negative control), EG poisoning (positive control), EG + standard antidote therapy, EG + dimephosphon therapy. Experimental therapy was carried out for first 24 hours using standard antidote therapy: ethanol (30% solution 2 mL / kg b.w. i.p. after 1, 4, 6, 12, 18 hours) and sodium bicarbonate (4% solution 6 mL / kg b.w. i.p. 3 times on the first day), as well as administration of dimephosphon (150 mg / kg i.p. 3 times on the first day, 450 mg / kg b.w. per day). Daily urine on day 3 after poisoning was collected in metabolic cages. Creatinine concentration in urine and blood serum samples were measured, and creatinine clearance was calculated. After 24 hours of therapy, the pH, level of sodium, potassium, calcium, magnesium, chlorides, bicarbonates, lactate, d-3-hydroxybutyrate, albumin, urea and creatinine (measured parameters) were determined in venous blood samples. Anion gap, ∆рН, ∆AG, ∆HCO3, ∆AG/∆HCO3 and ∆Gap were calculated. The mechanism of death was determined for the dead animals. Data processing was performed using GraphPad Prism 6.0. Results. Acute poisoning of rats with ethylene glycol leads to the development of toxic encephalopathy and nephropathy, acid-base abnormalities, high anion gap metabolic acidosis due to the presence of metabolites, as well as lactate-ketoacidosis due to depression of the central nervous system and hunger. 100% of the EG-treated (12 mL / kg b.w.) animals died within 3 days. Metabolic acidosis in combination with hypermagnesemia had provided a cardiodepressive effect, which with direct nephrotoxic and neurotoxic effects contributed to the development of a mixed variant of thanatogenesis and death. Death comes from toxic encephalopathy and nephropathy, high anion gap metabolic acidosis caused by direct nephrotoxic and neurotoxic effects of EG and its metabolites. The standard antidote therapy with ethanol in combination with sodium bicarbonate prevented a pH shift, lactic acidosis and ketoacidosis, an increase in urea, but did not affect the level of bicarbonate (p=0.048), creatinine and its clearance (p=0.037) and the anion gap (p=0.033). The dimephosphon therapy prevented a decrease in creatinine clearance and blood bicarbonate level, limited the increase in lactate dehydrogenase activity, had a more pronounced effect on the AG and ∆AG (p=0.042), but did not affect the hypocalcemia (p=0.0076) and hypoalbuminemia (p=0.021). Conclusion. Acute ethylene glycol poisoning leads to the development of a mixed variant of thanatogenesis with damage to the central nervous and urinary systems, as well as the heart. Autopsy and histopathology confirmed the cause of animal death. In the model at a dose of 6 mL / kg of EG the dimephosphon therapy was more conducive to the correction of the main markers of high anion gap metabolic acidosis (HAGMA) than standard antidote therapy (both measured and calculated, p0.05). The dimephosphon therapy prevented a decrease in creatinine clearance. A comparative analysis of two methods for the correction of high anion gap metabolic acidosis in rats in acute poisoning with ethylene glycol showed that dimephosphon therapy vs. standard antidote therapy had a stronger effect on markers of metabolic acidosis and renal impairment.

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Section: результаты и обсуждениеunclassified

Section: Introductionunclassified

Correction of acid base disorders in rats with acute ethylene glycol poisoning

Сивак

Владимирович²,

Михайлович³

et al. 2020

Medical academic journal

View full text Add to dashboard Cite

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Treating ethylene glycol poisoning with alcohol dehydrogenase inhibition, but without extracorporeal treatments: a systematic review

Beaulieu

Roberts

Gosselin

et al. 2022

Clinical Toxicology

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Estimates of Non-Alcoholic Food-Derived Ethanol and Methanol Exposure in Humans

Gürler

Martz

Taştekin

et al. 2020

Journal of Analytical Toxicology

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Food-derived alcohol is almost not in question due to its low concentration. Nevertheless, could it pose a problem for some risk groups and forensic cases? To answer this, we aimed to simultaneously evaluate ethanol and methanol ingredients of a variety of non-alcoholic foods in two different countries and estimate their possible health and forensic consequences. Alcohols in foods were analyzed by headspace gas chromatography. Human average acute daily food consumptions and food-derived blood alcohol concentrations (BACs) were determined by using the data of The European Food Safety Authority Nutrition Survey. Methanol and ethanol ingredients of similar foods varied between the two cities. Most foods produce higher methanol concentrations than the maximum allowable dose level (23 mg). Especially fruit juices lead to the critical level of ethanol for children (6 mg/kg body weight). Based on the results, adult daily intake of selected food groups does not bear ethanol that exceeds the legal limit of BAC or the limit not allowed from a religious perspective and does not lead to acute alcohol toxicity. But these low levels of ethanol and methanol consumed via non-alcoholic foods for life can raise the vulnerability to chronic health problems (cancer, liver cirrhosis, Alzheimer’s disease, autism, ocular toxicity and alterations in fetal development) and may lead to positive ethanol metabolite results (e.g., ethyl glucuronide) when a low cutoff level is used. Therefore, studies on the alcohol contents of various natural and processed non-alcoholic foods along with their effects on humans and new regulations on labeling the food products and conscious food consumption are of particular importance. It would also be important to consider unintentional alcohol consumption via non-alcoholic foods in the evaluation of clinical and forensic cases.

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Characteristics of Laboratory Confirmed Ethylene Glycol and Methanol Exposures Reported to a Regional Poison Control Center

Cited by 4 publications

References 9 publications

Correction of acid base disorders in rats with acute ethylene glycol poisoning

Correction of acid base disorders in rats with acute ethylene glycol poisoning

Treating ethylene glycol poisoning with alcohol dehydrogenase inhibition, but without extracorporeal treatments: a systematic review

Estimates of Non-Alcoholic Food-Derived Ethanol and Methanol Exposure in Humans

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