## Ethanol as Antidote in Methanol Poisoning ### Mechanism of Action **Key Point:** Ethanol acts as a **competitive inhibitor of alcohol dehydrogenase (ADH)**, reducing the conversion of methanol to its toxic metabolites. ### How It Works ```mermaid flowchart LR A[Methanol + Ethanol]:::outcome --> B{ADH present}:::decision B -->|High ethanol concentration| C[Ethanol preferentially metabolized]:::action B -->|Methanol metabolism inhibited| D[Methanol excreted unchanged in urine]:::action E[Formic acid NOT formed]:::action C --> E D --> F[Toxicity prevented]:::outcome ``` ### Pharmacokinetic Basis 1. **ADH has higher affinity for ethanol** than methanol 2. **Ethanol saturates ADH** at therapeutic concentrations (100–150 mg/dL) 3. **Methanol metabolism is blocked**, preventing formation of formaldehyde and formic acid 4. **Unchanged methanol is excreted** renally (non-toxic elimination) **High-Yield:** This is a classic example of **competitive enzyme inhibition** in toxicology. ### Clinical Application - **Ethanol loading dose**: 10 mL/kg of 10% ethanol IV - **Maintenance**: 1–2 mL/kg/hr to maintain blood ethanol at 100–150 mg/dL - **Duration**: Until methanol is undetectable or formic acid is cleared - **Modern alternative**: Fomepizole (4-methylpyrazole) — a more selective ADH inhibitor with fewer side effects **Clinical Pearl:** Fomepizole is now preferred in many centres because it does not cause CNS depression or hypoglycemia like ethanol does.
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