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紫杉烷神经毒性的机制。

Mechanism of taxane neurotoxicity.

作者信息

Hagiwara Hiroki, Sunada Yoshihide

机构信息

Division of Neurology, Department of Internal Medicine, Kawasaki Medical School, 577 Matsushima, Kurashiki-City, Okayama 701-0192, Japan.

出版信息

Breast Cancer. 2004;11(1):82-5. doi: 10.1007/BF02968008.

Abstract

The two taxanes (paclitaxel and docetaxel) are widely employed in standard antineoplastic practice. Although these agents are now well established, some toxic side effects have been reported. Toxicity of these agents includes bone marrow suppression (principally neutropenia), hypersensitivity reactions, cutaneous reactions, edema and neurotoxicity. The most prominent neurotoxicity is a sensory neuropathy. Controlling neuropathy is crucial for maintaining the quality of life of patients because it is usually persistent and hard to manage. The precise mechanism for taxane-induced neuropathy is still unknown. The taxanes are known to promote aggregation of intracellular microtubules. Abnormal aggregation of microtubules in the neuronal cells may cause this neuropathy. In addition, the taxanes have been suggested to have intrinsic toxicity and directly injure the cells. A better understanding of the mechanism for this neuropathy may improve the quality of life of patients who undergo taxane antineoplastic therapy.

摘要

两种紫杉烷类药物(紫杉醇和多西他赛)在标准抗肿瘤治疗中被广泛应用。尽管这些药物如今已被广泛认可,但仍有一些毒性副作用的报道。这些药物的毒性包括骨髓抑制(主要是中性粒细胞减少)、过敏反应、皮肤反应、水肿和神经毒性。最突出的神经毒性是感觉神经病变。控制神经病变对于维持患者的生活质量至关重要,因为它通常持续存在且难以处理。紫杉烷类药物诱发神经病变的确切机制仍然未知。已知紫杉烷类药物会促进细胞内微管的聚集。神经元细胞中微管的异常聚集可能导致这种神经病变。此外,有人提出紫杉烷类药物具有内在毒性并直接损伤细胞。更好地理解这种神经病变的机制可能会改善接受紫杉烷类抗肿瘤治疗患者的生活质量。

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