Abstract
Neurotoxicity complicates the use of several commonly administered chemotherapeutic agents (platinum based alkylating agents, taxanes and vinca alkaloids), with chemotherapy-induced peripheral neuropathy being the most common manifestation. Structural damage to the peripheral nervous system results in positive symptoms, e.g., allodynia, hyperalgesia and pain with unpleasant features as burning and shooting. Patients are unable to complete full or optimal treatment schedules. The pathophysiologic basis of nerve injury in chemotherapy-induced peripheral neuropathy is incompletely understood and appears to be unique for each class of the chemotherapeutic agents. Erythropoeitin (EPO), a well-established hematopoietic factor, is a very effective and widely used treatment for anemia in cancer patients undergoing chemotherapy. It also possesses generalized neuroprotective and neurotrophic properties. Co-treatment of chemotherapy and erythropoietin has been proposed for preventing or reversing the disabling peripheral neuropathy induced by the different chemotherapeutic agents. This study first describes the pathophysiological background of the clinically relevant chemotherapeutic agents-inducing peripheral neuropathy. Secondly, the possible mechanisms that might underlie the neuroprotective effect of erythropoietin in chemotherapy-induced neuropathy. Further clinical trials of EPO in cancer patients receiving chemotherapy and suffering from neurological symptoms seem to be warranted in the future. This might improve the quality of life in cancer patients.
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