Disulfiram Neuropathy: Two Case Reports

Anh Thu Tran; Richard A. Rison; Said R. Beydoun

Disclosures

J Med Case Reports. 2016;10(72) 

In This Article

Background

Disulfiram is typically used as a second-line agent for treating chronic alcoholism. Alcohol is metabolized by alcohol dehydrogenase to acetaldehyde, which is then broken down by aldehyde dehydrogenase to acetic acid and excreted. Disulfiram's main mechanism of action is to inhibit aldehyde dehydrogenase, thereby increasing serum acetaldehyde levels. When alcohol is taken in conjunction with disulfiram, the drug interaction results in high levels of acetaldehyde. This produces an unpleasant physiologic reaction, causing patients to have "hangover" symptoms such as nausea, palpitations, flushing, vertigo, and chest pain. Adverse reactions have been documented in both the central and peripheral nervous systems. In the central nervous system, adverse reactions include drowsiness, headache, fatigue, polyneuritis, and psychosis. Adverse reactions in the peripheral nervous system include peripheral neuritis and peripheral neuropathy. Several authors have suggested that this physiologic reaction is dose-dependent and related to an accumulation of carbon disulfide, which is a by-product of the metabolism of disulfiram in the liver.[1] Disulfiram neuropathy has been described as a distal axonopathy related to the "dying-back" effect of axonal degeneration.[2–4] The frequency of these adverse reactions has not been defined. A brief literature review showed that the adverse reaction of peripheral neuropathy is uncommon.

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