Advances in peripheral neuropathy induced by chemotherapy and its prevention and treatment

Abstract

Peripheral neuropathy (CIPN) induced by chemotherapy is the common dose-limiting adverse reactions of platinum, taxol and vinblastine. The mechanisms of CIPN due to platinum, taxol and vinblastine may be related to injury of dorsal root ganglion, inhibition of tubulin depolymerization and changing axonal transport, inhibition of association of tubulin from protein subunit, deletion of tubulin and dysfunction of axonal transport, respectively. Pain, numbness, acanthesthesia, burning sensation, sensory deprivation, myodynamia weakness or paralysation, constipation, sexual dysfunction, change of vision, and anaudia are the main clinical manifestations of CIPN. Usually, the amplitude and the conduction velocity of sensory nerve action potential are decreased, while the amplitude and the conduction velocity of motor nerve are normal or slightly changed before the clinical symptoms of CIPN appearance. The development of CIPN are related with sex (female), age (agedness), habits and customs (smoking history), tumor type (oophoroma), primary disease and combination with neurotoxic drug. The more the chemotherapeutics accumulated dose is, the higher the incidence of CIPN. The shorter the administration interval of chemotherapy is, the higher the incidence of CIPN. There is no effective drug for prevention of CIPN at present. Duloxetine is the the only one drug recommended by American Society of Clinical Oncology for treatment of CIPN. Key words: Drug therapy; Peripheral nerve injuries