Acute methanol intoxication: physiopathology, prognosis and treatment
Hantson, P.E.
Bulletin et Memoires de l'Academie Royale de Medecine de Belgique 161(6): 425
2006
ISSN/ISBN: 0377-8231 PMID: 17288275 Document Number: 596539
Acute methanol poisoning is mainly the consequence of voluntary or accidental ingestion. The mortality and morbidity rates remain very high despite intensive care therapy. Methanol by itself is poorly toxic. Methanol is transformed in the liver into formaldehyde and thereafter formic acid. Metabolic acidosis is the main biological feature of poisoning. Acidosis is related to formic acid accumulation, and also to a less extent to lactate production. In contrast to rodents, primates are relatively deficient in tetrahydrofolate reductase and therefore formic acid is usually the final metabolite. Formic acid is able to inhibit cytochrome oxidase activity in the mitochondria, leading to histotoxic hypoxia. The most sensitive organs to the effects of formic acid are the brain and the visual pathway, while other organs may also be seriously damaged according to the severity of metabolic acidosis. Hemodialysis remains indicated for the removal of both methanol and formic acid. Fomepizole is a recently approved antidote. It appears safe and effective. Analysis of its cost-effectiveness ratio is still ongoing in methanol poisoning.