Paclitaxel-induced peripheral neuropathy occurs in 59 to 78% of patients receiving paclitaxel therapy, and its severity is proportional to the cumulative dose and is often the dose-limiting toxicity. In the present study, Ito et al. investigated the effect of etodolac on mechanical allodynia and compared it with that of other COX inhibitors and analgesic agents used to treat peripheral neuropathic pain. The decrease in the paw-withdrawal threshold induced by paclitaxel was reversed by oral administration of etodolac but was not affected by indomethacin, diclofenac, or celecoxib. The antiallodynic effect of etodolac gradually increased during repeated administration. There was almost no difference in the distribution of etodolac and diclofenac in nervous tissue, indicating that COX inhibition is unlikely to be involved in the antiallodynic effect of etodolac. The action of etodolac in paclitaxel-induced neuropathy is likely to be mediated by a mechanism other than COX inhibition, and the mechanism remains under investigation, with a focus on transient receptor potential channels. Etodolac has a good reputation for safety in long-term use because of the low levels of gastrointestinal ulceration associated with its use, and it may contribute to the welfare of cancer patients suffering from the adverse neurological effects of paclitaxel chemotherapy.
See article at J Pharmacol Exp Ther 2012, 342:53–60.
- Copyright © 2012 by The American Society for Pharmacology and Experimental Therapeutics