Prospective study of paclitaxel-induced peripheral neuropathy with quantitative sensory testing
Prospective study of paclitaxel-induced peripheral neuropathy with quantitative sensory testing
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DOI：
10.1023/a:1005805907311
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发表时间：
1997-10-01
影响因子：
3.9
通讯作者：
DeAngelis, LM
中科院分区：
文献类型：
--
作者：
Forsyth, PA;Balmaceda, C;DeAngelis, LM
背景紫杉醇诱导的周围神经病变（PN）在初始剂量大于或等于275 mg/M-2时可能是重度和剂量限制性的，但其在剂量小于或等于250 mg/M-2时的神经毒性尚未完全表征。本研究的目的是表征和量化紫杉醇诱导的PN，并确定定量感觉测试（QST）的实用性。方法.我们前瞻性地研究了临床和QST 37例转移性乳腺癌妇女，用紫杉醇（200-250 mg/m2）治疗（平均周期数= 7.3，平均20.1周）。QST包括热阈（TT）和振动阈（VT）。结果31例（84%）患者在平均1.7个周期和平均累积剂量371.5 mg/M-2后出现感觉异常。26例（84%）患者在第一次或第二次给药后出现症状，10例（32%）患者症状稳定，13例（42%）患者症状改善（尽管继续治疗），6例（19%）患者症状完全缓解，2例（7%）患者症状进展。仅（3%）例患者因神经毒性而停用紫杉醇，无患者因PN而需要降低剂量。36例（97%）出现PN体征。最敏感的QST是大脚趾VT，但QST不能预测或识别任何患者的亚临床PN。12例（32%）患者发生了PN以外的神经系统综合征，7例是由于转移性癌症。结论. 1)紫杉醇诱导的PN主要是感觉性的，并在第一次或第二次给药后开始。在这些剂量下，神经病变是轻度的，很少有剂量限制性。2)QST定量神经病变，但不如临床检查敏感。3)了解紫杉醇PN的特征可以将其与其他可能提示肿瘤进展的神经系统综合征区分开来。
Background. Paclitaxel-induced peripheral neuropathy (PN) may be severe and dose-limiting at initial doses greater than or equal to 275 mg/M-2, but its neurotoxicity at doses less than or equal to 250 mg/M-2 has been incompletely characterized. The purposes of this study were to characterize and quantify paclitaxel-induced PN and to determine the utility of quantitative sensory testing (QST). Methods. We prospectively examined clinically and by QST 37 women with metastatic breast cancer, treated with paclitaxel (200-250 mg/m2) (average number of cycles = 7.3 over an average of 20.1 weeks). QST included thermal threshold (TT) and vibration threshold (VT). Results. Paresthesias appeared in 31 (84%) patients after an average of 1.7 cycles and an average cumulative dose of 371.5 mg/M-2. Symptoms occurred after the first or second dose in 26 (84%) patients and then stabilized in 10 (32%), improved in 13 (42%) despite continued treatment, resolved completely in 6 (19%), and were progressive in 2 (7%). Paclitaxel was discontinued in only (3%) patient because of neurotoxicity and no patient required dose reduction because of PN. Thirty-six (97%) developed signs of PN. The most sensitive QST was great toe VT but QST did not predict or identify subclinical PN in any patient. Neurologic syndromes other than PN developed in 12 (32%) patients, and 7 were due to metastatic cancer. Conclusions. 1) Paclitaxel-induced PN is mostly sensory, and begins after the first or second dose. At these doses the neuropathy is mild, and rarely dose-limiting. 2) QST quantified the neuropathy but was less sensitive than the clinical examination. 3) Knowledge of the features of paclitaxel's PN allows it to be differentiated from other neurologic syndromes which may signal tumor progression.