Pancreatic Injury Following Acute Methanol Poisoning

Hantson, Philippe; Mahieu, Paul

doi:10.1081/clt-100100935

Cited by 57 publications

(26 citation statements)

References 19 publications

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“…The toxic dose of methanol is estimated to be between 0.3 and 1.0 g/kg. Extensive evidence indicates that excessive production of formic acid leads to metabolic acidosis and elevated blood formate ion concentrations which can reach 10 to 20 mM or more in severe human cases (Tong, 1982;Sejersted et al, 1983;Hantson and Mahieu, 2000;Timbrell, 2000;Fox and Boyes, 2001;Barceloux et al, 2002).…”

Section: Resultsmentioning

confidence: 99%

“…Dietary sources of methanol include fruit juices (average 140 mg of methanol/liter; range 12-640 mg/liter) and fermented beverages which can contain up to 1.5 g of methanol/liter (Stegink et al, 1983;Kavat and Nauss, 1990). Consumption of large quantities of methanol by humans or nonhuman primates leads to toxic consequences including metabolic acidosis, visual disturbances progressing to permanent blindness, and death (Tong, 1982;Sejersted et al, 1983;Hantson and Mahieu, 2000;Timbrell, 2000;Fox and Boyes, 2001;Barceloux et al, 2002). The toxic dose of methanol is estimated to be between 0.3 and 1.0 g/kg.…”

Section: Resultsmentioning

confidence: 99%

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Absorption and Elimination of Formate Following Oral Administration of Calcium Formate in Female Human Subjects

Hanzlik

Fowler²,

Eells³

2004

Drug Metab Dispos

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ABSTRACT:Calcium formate is a water-soluble salt of an essential mineral nutrient with potential for use as a dietary calcium supplement. Formate ion is a product of endogenous and xenobiotic metabolism, but sustained high plasma formate concentrations (such as occur in cases of methanol poisoning) are toxic to the retina and optic nerve. Humans and primates have reduced capacity for formate oxidation compared with rodents and dogs and are thus more sensitive to methanol (and formate) intoxication. To assess the potential for accumulation of formate ion upon repeated administration of calcium formate as a potential dietary calcium supplement, we measured plasma concentrations of formate in 14 adult human subjects before and after oral administration of a single large dose of calcium formate (3900 mg; ca. 3-6 times the anticipated dose for calcium supplementation). Plasma formate concentrations increased briskly from 0.024 ؎ 0.008 mM (endogenous formate) to reach C max (0.50 ؎ 0.04 mM) at 60 min postdose and then declined with a half-life of 59 ؎ 7 min. By 225 min postdose, plasma formate concentration had returned to baseline. With such a short half-life, repeated use of calcium formate as a dietary supplement, even three times daily, should not lead to progressive accumulation of formate. These findings are discussed in light of the production of formate by endogenous and xenobiotic metabolism and the kinetics of formate during methanol poisoning.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Absorption and Elimination of Formate Following Oral Administration of Calcium Formate in Female Human Subjects

Hanzlik

Fowler²,

Eells³

2004

Drug Metab Dispos

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“…Epidemiologic data indicate a higher frequency of alcohol-induced acute pancreatitis in the areas where surrogates or homemade alcohol are easily available 42 . In particular, methanol poisoning can produce pancreatic injury 43 . Nonpurified synthetic alcohol and self-made beverages can have a relatively high methanol concentration 21 .…”

Section: Health Care Life Expectancy and Alcoholmentioning

confidence: 99%

Rusya'da Alkol ve Alkolizm: Politikalar ve Etkileri

Jargin¹

2017

Arşiv Kaynak Tarama Dergisi

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The purpose of this review was to draw attention to certain aspects of alcohol consumption in Russia related to the public health: consequences of governmental anti-alcohol policies, use of alcoholrelated topics to distract public attention from shortages of public health and assistance, toxicity of some legally sold alcoholic beverages, offences against alcoholics and people with alcohol-related dementia.

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“…Formic acid is responsible for the characteristic signs and symptoms of methanol toxicity such as coma, seizure, visual disturbances, and metabolic acidosis with a high plasma anion gap [1][2][3][4]. Also, due to inhibition of mitochondrial cytochrome oxidase by formate, lactic acid accumulation can occur [5][6][7][8][9][10][11]. Two antidotes for methanol intoxication include ethanol and fomepizole since they both are competitive inhibitors of ADH [1,12,13].…”

mentioning

confidence: 99%