Methanol intoxication

Methanol intoxication can cause blindness due to damage to ganglion cells in the retina. The blindness results from the accumulation of formaldehyde and formic acid, which are metabolites of methanol. Chemical compounds can also damage the visual cortex, for example, visual damage was observed among the victims of organic mercury intoxication in Japan (the fishermen of Minamata Bay). ... 

Osterloh JD et al Serum formate concentrations in methanol intoxication as a criterion for hemodialysis. Ann Intern Med 104 200-203, 1986... 

Ethylene glycol or methanol intoxication IV infusion 15 mg/kg as loading dose, followed by 10mg/kgql2hfor4 doses, then 15 mg/kg ql2h until ethylene glycol or methanol concentrations are below 20 mg/dl. All doses should be administered as a slow IV infusion over 30 min. 

The administration of ethanol to a patient suffering from methanol intoxication will competitively inhibit the metabolism of methanol to formaldehyde and... 

Methanol intoxication of rats (3 g/kg) was found to decrease TAC of their liver homogenates (S19). 

A 44-year-old man suffering from methanol intoxication was found comatose and had a serum concentration of 5830 pg/ml on admission. The subject died 40 hours later and the following postmortem concentrations were found (pg/ml or pg/g) blood 1420, bile 1750, brain 1590, heart 930, kidney 1300, liver 1070, lung 1270, vitreous humour 1730 (N. B. Wu Chen etal., J. forens. Sci., 1985, 30, 213-216). 

ADH also oxygenates methanol into toxic formaldehyde. Consequently, ethanol should be administered in order to inhibit the breakdown of methanol in cases of methanol intoxication. 

Onder F, llker S, KansuT, et al. Acute blindness and putaminal necrosis in methanol intoxication, /nf Ophthalmol. 1998-1999 22 81 -84... 

Hsu HH, Chen CY, Chen FH, et al. Optic atrophy and cerebral infarcts caused by methanol intoxication MRI. Neuroradlology. 1997 39 192-194... 

Erlanson PH, Fritz KE, Hagstam B, Liljenberg N,Tryding N,VoigtG. Severe methanol intoxication. Acta Med Scand 1965 177 393-407. 

Hoy WE, Scand ling JD, Carbonneau RJ. Hemodialysis treatment of methanol intoxication. Artif Organs 1983 7 479-481. 

Friedlaender MM, Rosenmann E, Rubinger D, Silver J, Moskovici A, Dranitzki-Elhalel M, Popovtzer MM, Berlatzky Y, Eid A. Successful renal transplantation from two donors with methanol intoxication. Transplantation 1996 61 (10) 1549-1552. 

Laakso O, Haapala M, Jaakkola P, Laaksonen R> Luomanmaki K, Nieminen J, et al FT-IR breath test in the diagnosis and control of treatment of methanol intoxications. J Anal Toxicol 2001 25 ... 

Matsumoto K, Moriya F, Nanikawa R. 1990. The movement of blood formaldehyde in methanol intoxication. II Tire movement of blood formaldehyde and its metabolism in the rabbit. Jpn J Legal Med 44(3) 205-211. 

Kidney damage results from precipitation of oxalate crystals in the convoluted tubules. The elevated anion-gap metabolic acidosis is caused by glycolic acid and lactic acid. The latter is formed from pyruvate due to a shift in the redox potential favoring the production of lactate. The treatment is the same as that for methanol intoxication. 

In all poisoning situations, it is important to establish adequate respiration. Bicarbonate may be needed to counteract metabolic acidosis. In patients with suspected methanol intoxication, ethanol (10% solution) is often given intravenously before laboratory diagnosis is confirmed to block the formation of toxic products of ADH-catalyzed metabolism of methanol. Blood levels of methanol in excess of 50 mg/dL are an absolute indication for hemodialysis. Activated charcoal does not bind alcohols. The answer is (B). 

A. In the first few hours after ingestion, methanol-intoxicated patients present with inebriation and gastritis. Acidosis is not usually present because metabolism to toxic products has not yet occurred. There may be a noticeable elevation in the osmolar gap (see p 32) an osmolar gap of as little as 10 mOsm/L is consistent with toxic concentrations of methanol. 

I. Pharmacology. Leucovorin (folinic acid or citrovomm factor) Is a metabolically functional form of folic acid. Unlike folic acid, leucovorin does not require reduction by dihydrofolate reductase, and therefore it can participate directly in the one-carbon transfer reactions necessary for purine biosynthesis and cellular DNA and RNA production. In animal models of methanol intoxication, replace-... 

Clinical samples of urine, blood, expired air, and tissue have been examined using headspace sampling approaches. Thus, chlorinated organic compounds, methanol, acetone, methyl ethyl ketone, and phenols have been determined in urine. Volatile substances in urine have also been used as a guide to acute poisoning, and the determination of stimulants in urine has been proposed as screening test for field use. The determination of the concentration of blood alcohol is the most well-known application of headspace techniques to biological samples. Blood has also been examined for cyanide, methyl sulfide, and formaldehyde levels, the last as a measure of methanol intoxication. The headspace approach for blood samples overcomes the difficulties associated with the alternative direct injection of two-phase samples. 

Methanol and Formate. - Methanol intoxication can result from both accidental and deliberate ingestion. The alcohol undergoes ADH-catalysed oxidation to formaldehyde, which is then rapidly metabolised to formic add, resulting in metabolic acidosis. 

The diagnosis of methanol intoxication includes the observation of the preceding symptoms. The combination of the characteristic visual disturbances and a history of methanol oqrosure is usually considered a confirmative diagnosis. Confirmation can also be reached by a urine test with positive formic acid or methanol presence. 

The human toxicology of methanol has been studied [6,71,72]. The skin absorption rate has been reported to be 0.19 m cm2/min [73]. Methanol vapor uptake by the lungs is effective, usually 7080% (74). In the liver, methanol goes through oxidation metabolism catalyzed by alcohol dehydrogenase (an enzyme), producing toxic formaldehyde and formic acid. The accumulation of formic acid leads to acidosis, dama g the nervous system, particularly the optic nerves, and the retina. In the copresence of ethanol, ethanol is selectively metabolized by alcohol dehydrogenase over methanol this delays methanol intoxication and allows detoxication by the natural elimination of methanol via respiration and urination. The methanol elimination half-life is about 23 h [6]. Because of the slow elimination, methanol can be re rded as a cumulative poison [68]. Chronic oq)osure may result in sufficient methanol accumulation in the body, and illness. 

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