西北地区一线患者肌肉流失、化疗诱导神经 毒性及其对生存的影响

Muscle Loss, Chemotherapy-Induced Neurotoxicity and Their Effects on Survival in Frontline Patients in Northwest China

摘要: 目的：本研究通过对人体成分的动态变化研究，探索人体成分及其与化疗诱导的周围神经毒性(CIPN)的相关性，并探索二者对总生存期(OS)的联合影响。方法：本研究为前瞻性观察性研究，纳入2021年9月至2025年2月期间于我院接受含白蛋白紫杉醇方案化疗的癌症患者。最终共56例完成两次随访体成分测量的患者纳入分析，其中一线治疗39例，二线9例，三线8例。采用简明营养状况评估量表(MNSS)评估能量摄入，并依据《中国肿瘤营养治疗指南2020》进行营养管理。在基线及化疗3周期后，分别采用NRS 2002营养风险筛查量表、患者主观整体评估(PG-SGA)、生物电阻抗分析(BIA)及基于第三腰椎(L3) CT图像的骨骼肌指数(L3 SMI)评估营养状况与体成分变化。采用患者神经毒性问卷(PNQ)评估CIPN。使用Cox比例风险模型分析生存影响因素。结果：在纳入的39例一线治疗患者中，化疗期间肌肉质量指标呈下降趋势。中重度CIPN的发生率从第1周期后的8.9%显著上升至第3周期后的28.9%，且在基线低肌肉质量患者中上升更为明显(P = 0.01)。非肌肉减少症患者亦出现显著的肌肉丢失。在生存分析(n = 38)中，CIPN严重程度与总生存期无显著关联(校正后HR = 1.15，95% CI：0.43~3.08，P = 0.78)，但本研究统计效力不足以检测中等的效应量。结论：本研究通过前瞻性动态监测证实，在接受白蛋白紫杉醇化疗的癌症患者中，骨骼肌流失与化疗诱导的周围神经毒性(CIPN)是密切关联、相互影响的合并症。尽管在本研究队列中，基线肌肉减少症状态与总生存期未显示出显著关联，但分析提示骨骼肌质量可能具有保护作用。此外，基线即存在肌肉减少症的患者发生CIPN等级升高的风险显著更高；值得注意的是，非肌肉减少症患者在化疗期间同样面临显著的肌肉质量流失。因此，临床实践中应对所有接受此类化疗的患者进行常规的体成分与神经毒性动态监测。未来，联合营养支持、结构化运动及药物干预的多模式综合策略，可能是预防或缓解肌肉减少症与CIPN、进而改善患者预后的重要方向。

Abstract: Objective: This study aimed to investigate the dynamic changes in body composition during chemotherapy and to explore its correlation with chemotherapy-induced peripheral neuropathy (CIPN), as well as their combined impact on overall survival (OS). Methods: This prospective observational study enrolled cancer patients who received albumin-bound paclitaxel-based chemotherapy at our hospital between September 2021 and February 2025. A total of 56 patients who completed two follow-up body composition assessments were included in the analysis, comprising 39 first-line, 9 second-line, and 8 third-line treatments. Energy intake was assessed using the Mini Nutritional Status Scale (MNSS), and nutritional management followed the Chinese Guidelines for Cancer Nutrition Therapy 2020. Nutritional status and body composition were evaluated at baseline and after three chemotherapy cycles using the NRS 2002 Nutritional Risk Screening Scale, Patient-Generated Subjective Global Assessment (PG-SGA), bioelectrical impedance analysis (BIA), and skeletal muscle index (L3 SMI) derived from third lumbar vertebra (L3) CT images. CIPN was assessed using the Patient Neurotoxicity Questionnaire (PNQ). Cox proportional hazards models were used to analyze survival-related factors. Results: Among the 39 first-line treatment patients, muscle mass indicators showed a declining trend during chemotherapy. The incidence of moderate-to-severe CIPN increased significantly from 8.9% after the first cycle to 28.9% after the third cycle, with a more pronounced increase observed in patients with low baseline muscle mass (P = 0.01). Significant muscle loss was also noted in non-sarcopenic patients. In survival analysis (n = 38), CIPN severity was not significantly associated with OS (adjusted HR = 1.15, 95% CI: 0.43~3.08, P = 0.78), although the study was underpowered to detect moderate effect sizes. Conclusion: This prospective study demonstrated that skeletal muscle loss and CIPN are closely interrelated and mutually exacerbating comorbidities in cancer patients receiving albumin-bound paclitaxel chemotherapy. Although baseline sarcopenia did not show a significant association with OS in this cohort, skeletal muscle mass may exert a protective effect. Notably, patients with baseline sarcopenia had a significantly higher risk of CIPN progression, and non-sarcopenic patients also experienced considerable muscle mass loss during chemotherapy. Therefore, routine dynamic monitoring of body composition and neurotoxicity is recommended for all patients undergoing such chemotherapy. In the future, multimodal strategies combining nutritional support, structured exercise, and pharmacological interventions may represent a promising approach to prevent or mitigate sarcopenia and CIPN, thereby improving patient outcomes.