• Pritikanta Paul, Geoffrey Campbell, Anastasia Zekeridou, Michelle Mauermann, and Elie Naddaf.
• Department of Neurology and Rehabilitation, University of Illinois at Chicago, Chicago, IL.
• Mayo Clin. Proc. 2024 Jul 5.

AbstractWith the lack of distinctive features or diagnostic biomarkers, peripheral neuropathy in patients with excessive alcohol consumption is often misdiagnosed as alcohol-related neuropathy, influenced by underlying implicit and explicit bias against patients with an alcohol use disorder (AUD). Alcohol-related nerve toxicity has been attributed to various underlying mechanisms including altered trophic factor signaling, disrupted protein synthesis, free radical injury from oxidative stress, and nutritional deficiencies. Alcohol-related neuropathy has been most described as mild but painful, predominantly affecting small sensory fibers, without major functional limitations. This phenotype may be indistinguishable from a chronic idiopathic axonal neuropathy; hence, a causal relationship with AUD cannot be established with certainty. Searching for alternative causes is warranted, especially in patients with a more severe or rapidly progressive peripheral neuropathy. At the same time, there is underlying implicit and explicit bias in the medical field against patients with AUDs. Patients often experience devaluation and stigma, which can affect their adherence to medical advice and may lead to social reclusion. Addressing biases in health care workers is crucial to ensure that individuals receive proper care and are not subjected to stigmatization. In this article, we present a comprehensive narrative review of the literature on the clinical presentation and underlying pathomechanisms of alcohol-related peripheral neuropathy, raising awareness of the bias in the medical field against patients with AUD.Copyright © 2024 Mayo Foundation for Medical Education and Research. Published by Elsevier Inc. All rights reserved.

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