Peripheral Neurotoxicity in Gynecologic Oncology Patients who Received Paclitaxel

Paclitaxel is commonly used with carboplatin as standard chemotherapy in the treatment of gynecologic cancer patients especially in cases of ovarian and endometrial cancer [1]. The principle mechanism of paclitaxel is to stabilize microtubules, block the late G2 mitotic phase of the cell cycle by polymerization and induce cell death while the action of carboplatin is predominantly at the interstrand DNA cross -link [2,3]. The major side effect of paclitaxel is peripheral neuropathy and has been previously reported to be as high as 60% [4]. The pathogenesis of this event is believed to be the interference of many systems such as microtubule-based axonal transportation, macrophage activation at both the dorsal root ganglion and peripheral nerve and spinal cord microglial activation [2]. Whereas the neurotoxicity caused by carboplatin was reported as being very low, only 6%, in the former study [5]. However, when a paclitaxel plus carboplatin regimen was used there were additive effects regarding peripheral neuropathy [2]. Typically, patients affected by paclitaxel induced peripheral neuropathy presented with paresthesia, numbness, and/or neuropathic pain in a stockingand-glove distribution and myalgia. This toxicity can show minimal improvement a long time after stopping treatment [4]. Although paclitaxel and carboplatin are widely used in Thai gynecologic oncology patients, the incidence and severity of peripheral neuropathy in these patients were unclear. Hence, we conducted this prospective study to evaluate the incidence of paclitaxel plus carboplatin induced peripheral neuropathy.