Intermittent hemodialysis is superior to continuous veno-venous hemodialysis/hemodiafiltration to eliminate methanol and formate during treatment for methanol poisoning

Zakharov, Sergey; Pelclová, Daniela; Navrátil, Tomáš; Běláček, Jaromír; Kurcová, Ivana; Komzak, Ondrej; Skalický, T; Latta, Jiří; Turek, Radovan; Bocek, Robert; Kucera, Cyril; Hubacek, Jaroslav A.; Fenclová, Zdeňka; Petrik, Vit; Čermák, Martin; Hovda, Knut Erik

doi:10.1038/ki.2014.60

Cited by 72 publications

(58 citation statements)

References 36 publications

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“…Formic acid, the main toxic metabolite of methanol, induces cellular toxicity through inhibition of cytochrome c oxidase, which impairs oxygen utilization, causing a shift from aerobic to anaerobic metabolism [14,15]. If ADH is blocked by antidote (ethanol or fomepizole), formic acid is effectively eliminated by hemodialysis with a half-life of 1.6-3.6 h and acidemia is corrected during the first hours after hospital treatment initiation [33,34]. In addition to its primary cytotoxic effect, formic acid induces secondary effects including ischemia, edema, BBB disruption, hemorrhages, reactive oxidative damage, axonal demyelination, neuronal degeneration, and cell death.…”

Section: Discussionmentioning

confidence: 99%

“…Finally, the patients treated with IHD had higher concentration of cys-LTs than those treated with CRRT. This fact can be explained by more rapid elimination of formic acid and correction of acidemia in patients treated with IHD [33,34].…”

Section: Discussionmentioning

confidence: 99%

“…Intermittent hemodialysis (IHD) or continuous veno-venous hemodialysis/hemodiafiltration (CRRT) was performed to eliminate formic acid and methanol and to correct academia [33,34]. Folates were administered to substitute the internal pool (folinic or folic acid) [35].…”

Section: Selection Of Participants and Treatmentmentioning

confidence: 99%

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Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning

Zakharov

Kotikova

Nurieva

et al. 2017

Clinical Toxicology

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Context: The role of neuroinflammation in methanol-induced toxic brain damage has not been studied. Objective: We studied acute concentrations and the dynamics of leukotrienes (LT) in serum in hospitalized patients with acute methanol poisoning and in survivors. Methods: Series of acute cysteinyl-LT and LTB4 concentration measurements were performed in 28/101 hospitalized patients (mean observation time: 88 ± 20 h). In 36 survivors, control LT measurements were performed 2 years after discharge. Results: The acute maximum (C max ) LT concentrations were higher than concentrations in survivors: C max for LTC4 was 80.7 ± 5.6 versus 47.9 ± 4.5 pg/mL; for LTD4, 51.0 ± 6.6 versus 23.1 ± 2.1 pg/mL; for LTE4, 64.2 ± 6.0 versus 26.2 ± 3.9 pg/mL; for LTB4, 59.8 ± 6.2 versus 27.2 ± 1.4 pg/mL (all p < 0.001). The patients who survived had higher LT concentrations than those who died (all p < 0.01). Among survivors, patients with CNS sequelae had lower LTE4 and LTB4 than did those without sequelae (both p < 0.05). The LT concentrations increased at a rate of 0.4-0.5 pg/mL/h and peaked 4-5 days after admission. The patients with better outcomes had higher cys-LTs (all p < 0.01) and LTB4 (p < 0.05). More severely poisoned patients had lower acute LT concentrations than those with minor acidemia. The follow-up LT concentrations in survivors with and without CNS sequelae did not differ (all p > 0.05). The mean decrease in LT concentration was 30.9 ± 9.0 pg/mL for LTC4, 26.3 ± 8.6 pg/mL for LTD4, 37.3 ± 6.4 pg/mL for LTE4, and 32.0 ± 8.8 pg/mL for LTB4. Conclusions: Our findings suggest that leukotriene-mediated neuroinflammation may play an important role in the mechanisms of toxic brain damage in acute methanol poisoning in humans. Acute elevation of LT concentrations was moderate, transitory, and was not followed by chronic neuroinflammation in survivors.ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning

Zakharov

Kotikova

Nurieva

et al. 2017

Clinical Toxicology

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“…The accumulation of formic acid results in metabolic acidosis, lactacidemia, visual impairment and damage to the basal ganglia, especially when the concentration rises to 9-11 mmol/L (approximately 300-400 mg/L) (ref. [8][9][10][11] ). The role of ethanol in the treatment of acute methanol poisonings is well-established 12,13 .…”

Section: Introductionmentioning

confidence: 99%

Fomepizole in the treatment of acute methanol poisonings: Experience from the Czech mass methanol outbreak 2012-2013

Zakharov¹,

Navrátil²,

Pelclová³

2014

BIOMED PAP

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Objective. During an outbreak of mass methanol poisonings in the Czech Republic in 2012-2013, fomepizole was applied as an alternative antidote to ethanol. We present the laboratory data, clinical features, adverse reactions, and treatment outcomes in all patients treated with fomepizole. Methods. Combined retrospective and prospective case series study in 25 patients, median age 50 (16-73) years, 18 males and 7 females. Results. There were 24% fatalities, 36% survivors without health impairment, and 40% survivors with sequelae. All the patients who died were comatose on admission; the mortality was 50% among patients in a coma. The median intensive care unit length of stay was six (2-22) days. The median total dose of fomepizole was 2 (1-9) g. Complications were observed in 7/25 cases: aspiration pneumonia (4), sepsis (2), bleeding (2), malignant arrhythmia (1), delirium tremens (1), and rebound of acidosis (1). The patients who survived without impairment were less acidotic than those who died or survived with sequelae (P<0.01). No difference in serum methanol and formate was found between the three groups. Conclusion. There is no evidence whether fomepizole is a more efficient antidote than ethanol with regards to the hospital mortality. The possibility of delirium tremens in the patients with a history of chronic alcohol abuse has to be taken in consideration. The benefits of fomepizole were indirect: no need to monitor serum ethanol's level during the hemodialysis in severely poisoned patients and less working overload on ICU doctors treating several poisoned patients simultaneously.

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“…In cases of methanol poisoning, hemodialysis significantly reduces the half-life formate: 1.8 h comparing to 6.0 h in untreated case 101 . Intermittent hemodialysis, continuous veno-venous hemodialysis and hemodiafiltration can be exampled as other effective techniques 102 . Hyperventilation is presented as another available supporting therapy during severe poisoning 103 .…”

Section: Treatment Of Poisoning With the Alcoholsmentioning

confidence: 99%

Toxicology and the biological role of methanol and ethanol: Current view

Pohanka¹

2016

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Background. Alcohol variants such as ethanol and methanol are simple organic compounds widely used in foods, pharmaceuticals, chemical synthesis, etc. Both are becoming an emerging health problem; abuse of ethanol containing beverages can lead to disparate health problems and methanol is highly toxic and unfit for consumption. Methods and Results. This review summarizes the basic knowledge about ethanol and methanol toxicity, the effect mechanism on the body, the current care of poisoned individuals and the implication of alcohols in the development of diseases. Alcohol related dementia, stroke, metabolic syndrome and hepatitis are discussed as well. Besides ethanol, methanol toxicity and its biodegradation pathways are addressed. Conclusions. The impact of ethanol and methanol on the body is shown as case reports, along with a discussion on the possible implication of alcohol in Alzheimer's disease and antidotal therapy for methanol poisoning. The role of ethanol in cancer and degenerative disorders seems to be underestimated given the current knowledge. Treatment in case of poisoning is another issue that remains unresolved even though effective protocols and drugs exist.

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Intermittent hemodialysis is superior to continuous veno-venous hemodialysis/hemodiafiltration to eliminate methanol and formate during treatment for methanol poisoning

Cited by 72 publications

References 36 publications

Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning

Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning

Fomepizole in the treatment of acute methanol poisonings: Experience from the Czech mass methanol outbreak 2012-2013

Toxicology and the biological role of methanol and ethanol: Current view

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