Neuropathy in the setting of alcoholism-an entity less thought of

Disulfiram is a commonly used adjunctive treatment in the management of alcohol dependency. It has been noted that disulfiram can induce peripheral neuropathy, the mechanism of which has not been clearly determined. A 35-year-old patient, reformed alcoholic, on disulfiram presented with complaints of painful distal dysesthesias and foot drop. Clinical examination revealed bilateral foot drop without any objective sensory loss. Patient was evaluated for the same and routine blood investigations including vitamin B-12, inflammatory and virological markers were found to be normal. Nerve conductions studies revealed in excitable bilateral common peroneal and tibial nerves. Possibility of disulfiram induced peripheral neuropathy was thought of and drug was withdrawn. Patient was followed up and after two months improvement in motor power and reduction in paraesthesia’s was noted. Disulfiram is a commonly used drug, the uncommon side effect of which is distal predominant axonal neuropathy. This must be kept be kept in mind when evaluating a patient presenting with features of peripheral neuropathy, on a background of alcohol abuse.

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Genome-Wide Screen Identifies Drug-Induced Regulation of the Gene Giant Axonal Neuropathy (Gan) in a Mouse Model of Antiretroviral-Induced Painful Peripheral Neuropathy

Biological Research For Nursing ◽

10.1177/1099800409332726 ◽

2009 ◽

Vol 11 (1) ◽

pp. 7-16 ◽

Cited By ~ 18

Author(s):

Susan G. Dorsey ◽

Carmen C. Leitch ◽

Cynthia L. Renn ◽

Sherrie Lessans ◽

Barbara A. Smith ◽

...

Keyword(s):

Peripheral Neuropathy ◽

Mouse Model ◽

Side Effect ◽

Quantitative Polymerase Chain Reaction ◽

Axonal Neuropathy ◽

Protein Product ◽

Hiv Treatment ◽

Patient Comfort ◽

Giant Axonal Neuropathy ◽

Drug Induced

Painful peripheral neuropathy is a debilitating complication of the treatment of HIV with nucleoside reverse transcriptase inhibitors (NRTIs). Patients are living longer with these drugs; however many develop excruciating, unremitting, and often treatment-limiting neuropathy that is resistant to conventional pain management therapies. Improving patient comfort and quality of life is paramount and depends on a clearer understanding of this devastating side effect. The mechanisms underlying the development of NRTI-induced neuropathy, however, remain unclear. Using a mouse model of NRTI-induced neuropathy, the authors conducted an unbiased whole-genome microarray screen to identify molecular targets in the spinal dorsal horn, which is the location where integration of ascending sensory transmission and descending modulatory effects occur. Analysis of the microarray data identified a change in the gene giant axonal neuropathy 1 (Gan1). Mutation of this gene has been linked to the development of giant axonal neuropathy (GAN), a rare autosomal recessive condition characterized by a progressive sensorimotor neuropathy. Gan1 has not been previously linked to nerve pathologies in other populations. In this study, downregulation of the Gan1 gene and the gene protein product, gigaxonin, was validated via quantitative polymerase chain reaction ([qPCR] gene expression) and Western blot analyses (protein level). Our report is the first to suggest that Gan1 might be a novel molecular target in the development of NRTI-induced peripheral neuropathy with implications for new therapeutic approaches to preventing or reducing a significant side effect of HIV treatment.

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