Morawska Marta, Grzasko Norbert, Kostyra Magdalena, Wojciechowicz Jolanta, Hus Marek
Hemato-oncology and Bone Marrow Transplantation Clinic, SPSK1, Lublin, Poland.
Face and Jaw Surgery Clinic, SPSK1, Lublin, Poland.
Hematol Oncol. 2015 Dec;33(4):113-9. doi: 10.1002/hon.2149. Epub 2014 Nov 14.
This review discusses the most common issues concerning multiple myeloma (MM)-related peripheral neuropathy (PN). This is an important MM complication, observed in up to 54% of newly diagnosed patients, caused by the disease itself or its treatment. Although its aetiology is largely unknown, a number of mechanisms are suspected. It is important to know the neurological status of a patient, as many new antimyeloma medicines can trigger or exacerbate any pre-existing neuropathy. Examples include thalidomide-induced and bortezomib-induced PN (TiPN and BiTN, respectively), which are key MM treatment options. TiPN is usually sensory and sensorimotor, whereas BiPN is typically sensory. The mechanisms of chemotherapy-induced neurotoxicity in MM are well known; thalidomide seems to induce PN through its antiangiogenic properties, whereas bortezomib neurotoxicity is connected with disrupted calcium homeostasis. TiPN incidence ranges from 25% to 75%, and its prevalence and severity appears to be dose-dependent. BiPN incidence is almost 40% and is dose-related as well. Poor (25%) reversibility of TiPN prompted the recommendations for dose and exposure reduction, whereas BiPN cases are mostly reversible (64%). Peripheral sensory neuropathy is very rare in patients receiving bendamustine monotherapy. Because of this favourable toxicity profile, bendamustine may be considered a promising option for combination therapies in pre-existing PN in myeloma patients. Considering the lack of curative therapy for treatment-emergent PN, prevention is a key management strategy in MM patients. All patients should be evaluated for PN before the administration of a neurotoxic drug, and those under treatment should be closely monitored by a neurologist.
本综述讨论了与多发性骨髓瘤（MM）相关的周围神经病变（PN）的最常见问题。这是一种重要的MM并发症，在高达54%的新诊断患者中可见，由疾病本身或其治疗引起。尽管其病因大多未知，但怀疑有多种机制。了解患者的神经状态很重要，因为许多新型抗骨髓瘤药物会引发或加重任何已有的神经病变。例如沙利度胺诱导的PN和硼替佐米诱导的PN（分别为TiPN和BiPN），它们是MM的关键治疗选择。TiPN通常为感觉性和感觉运动性，而BiPN通常为感觉性。MM中化疗诱导的神经毒性机制已为人熟知；沙利度胺似乎通过其抗血管生成特性诱导PN，而硼替佐米的神经毒性与钙稳态破坏有关。TiPN的发生率在25%至75%之间，其患病率和严重程度似乎与剂量有关。BiPN的发生率近40%，也与剂量有关。TiPN的可逆性较差（25%），因此建议减少剂量和暴露，而BiPN病例大多是可逆的（64%）。接受苯达莫司汀单药治疗的患者很少发生周围感觉神经病变。由于这种有利的毒性特征，苯达莫司汀可被视为骨髓瘤患者已有PN的联合治疗的一个有前景的选择。考虑到对于治疗引起的PN缺乏治愈性疗法，预防是MM患者的关键管理策略。所有患者在使用神经毒性药物前都应评估是否存在PN，正在接受治疗的患者应由神经科医生密切监测。
