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Oxaliplatin and Axonal Na⁺ Channel Function In vivo

Authors' Affiliations: ¹ Institutes of Neurological Sciences and ² Medical Oncology, Prince of Wales Hospital; and ³ Prince of Wales Medical Research Institute and Prince of Wales Clinical School, University of New South Wales, Randwick, Sydney, New South Wales, Australia

Requests for reprints: Matthew C. Kiernan, Prince of Wales Medical Research Institute, Barker Street, Randwick, Sydney, New South Wales 2031, Australia. Phone: 61-2-9382-2422; Fax: 61-2-9382-2437; E-mail: M.kiernan{at}unsw.edu.au.

Purpose: The aim of the study was to investigate the pathophysiology of oxaliplatin-induced neurotoxicity using clinical nerve excitability techniques that provide information about axonal ion channel function.

Experimental Design: Excitability studies were combined with standard nerve conduction studies and clinical assessment in 22 patients undergoing treatment with oxaliplatin.

Results: Excitability studies recorded before and immediately after oxaliplatin infusion for 89 treatment cycles revealed significant increases in refractoriness and relative refractory period postinfusion in all patients, consistent with an effect of oxaliplatin on axonal Na⁺ channels. However, those patients that developed chronic neuropathy had significantly greater changes. Following cessation of oxaliplatin treatment, 41% of patients had persistent symptoms and nerve conduction abnormalities consistent with the development of chronic neuropathy.

Conclusion: The present study provides evidence that oxaliplatin-induced neurotoxicity is mediated through an effect on axonal Na⁺ channels. Clinical nerve excitability techniques may prove beneficial in monitoring for early signs of neurotoxicity and in the assessment of future prophylactic therapies.

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				S. B. Park, D. Goldstein, C. S.-Y. Lin, A. V. Krishnan, M. L. Friedlander, and M. C. Kiernan Acute Abnormalities of Sensory Nerve Function Associated With Oxaliplatin-Induced Neurotoxicity J. Clin. Oncol., March 10, 2009; 27(8): 1243 - 1249. [Abstract] [Full Text] [PDF]