Methanol Toxicity Medication
- Author: Kalyani Korabathina, MD; Chief Editor: Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS more...
Ethanol and fomepizole can be administered to delay methanol metabolism until the methanol is eliminated from the patient’s system (either naturally or with dialysis). These antidotes work via competitive inhibition; ethanol and fomepizole are metabolized by ADH, just as methanol is, but the enzyme has a higher affinity for both antidotes than it does for methanol. For example, the affinity of ADH for ethanol is 10-20 times greater than it is for methanol. The use of fomepizole is limited because of its high cost and lack of availability.
These agents inhibit the toxic effects of methanol via competitive inhibition.
Ethanol is believed to compete with methanol for ADH, thus preventing metabolism of methanol to its toxic by-products. ADH has a 10- to 20-fold greater affinity for ethanol than for methanol. By slowing the degradation of methanol, ethanol is assumed to prevent the accumulation of high levels of formic acid.
The goal of ethanol therapy is to achieve an ethanol blood concentration of 100 mg/dL. At this level, ethanol is thought to become a competitive substrate for ADH and to be sufficient to block methanol metabolism.
Fomepizole acts similarly to ethanol. It is a stronger competitive inhibitor of ADH and, in addition, does not cause hypoglycemia or sedation. Fomepizole is relatively easier to administer than ethanol. It does not require monitoring of serum concentrations.
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