Oxaliplatin-induced neurotoxicity: changes in axonal excitability precede development of neuropathy
نویسندگان
چکیده
منابع مشابه
Oxaliplatin-induced neurotoxicity: changes in axonal excitability precede development of neuropathy.
Administration of oxaliplatin, a platinum-based chemotherapy used extensively in the treatment of colorectal cancer, is complicated by prominent dose-limiting neurotoxicity. Acute neurotoxicity develops following oxaliplatin infusion and resolves within days, while chronic neuropathy develops progressively with higher cumulative doses. To investigate the pathophysiology of oxaliplatin-induced n...
متن کاملOxaliplatin and axonal Na+ channel function in vivo.
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 Exc...
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Chemotherapy-induced neurotoxicity is a serious consequence of cancer treatment, which occurs with some of the most commonly used chemotherapies(1,2). Chemotherapy-induced peripheral neuropathy produces symptoms of numbness and paraesthesia in the limbs and may progress to difficulties with fine motor skills and walking, leading to functional impairment. In addition to producing troubling sympt...
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Oxaliplatin-induced peripheral neuropathy (OXAIPN) is of great clinical interest as it ranks among the most common dose limiting toxicities of oxaliplatin (OXA) administration with an obvious impact on the outcome of cancer patients. In addition, OXAIPN has a detrimental effect on the quality of life of cancer patients because it can be long lasting or even permanent. It has a unique spectrum o...
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Oxaliplatin use in palliative and adjuvant treatment of colon cancer is frequently limited by cumulative neurotoxicity, leading to reduced quality of life and decreased dose. The mechanism of this neurotoxicity is unclear, but may relate to neuronal voltage-gated sodium channels involving calcium chelation by a metabolite of the drug. Various preventative measures have been tested to reduce the...
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ژورنال
عنوان ژورنال: Brain
سال: 2009
ISSN: 1460-2156,0006-8950
DOI: 10.1093/brain/awp219