摘要目的:报道3例分别与服用氯喹、羟氯喹及秋水仙碱相关的药物中毒性溶酶体肌病的病例，并结合相关文献复习，总结该类疾病的临床表现、肌肉核磁共振成像（MRI）特点及肌肉活组织检查（活检）病理特征。方法:回顾性收集2023—2024年于山东大学齐鲁医院就诊且经肌肉活检确诊为药物中毒性溶酶体肌病患者的完整临床资料，包括详细病史、体格检查、实验室检查、肌肉MRI、肌肉活检病理及肌电图检查结果等。同时，系统检索国内外数据库的相关文献，分析该类疾病的临床表现和肌肉活检病理特征。基于临床和病理数据，采用多因素Logistic回归分析探讨与该疾病预后相关的影响因素。结果:3例患者均为中老年人（50、61、76岁）。例1和例2分别在服用氯喹及羟氯喹后出现原有肌无力症状加重，例3在服用秋水仙碱后出现新发肌无力。体格检查显示，3例患者均表现为四肢近端肌无力。肌电图均提示肌源性损害，可伴或不伴神经源性损害。肌肉MRI显示受累肌群呈水肿样改变，其中例1和例3血清肌酸激酶水平升高（分别为700、2 124 U/L）。肌肉活检均可见肌纤维内自噬性空泡形成，符合溶酶体肌病的病理特征。文献复习结果显示，药物中毒性溶酶体肌病多见于中老年人，临床以近端肌无力为主要表现，肌肉活检常见自噬性空泡，停用致病药物后多数患者相关症状均有不同程度的恢复。多因素Logistic回归分析结果显示，服用秋水仙碱的患者恢复时间短于服用氯喹/羟氯喹的患者（ OR=5.380，95% CI 1.492~19.405， P=0.010）。 结论:对于服用氯喹、羟氯喹或秋水仙碱的患者，若出现新发肌无力或原有肌无力加重和（或）血清肌酸激酶升高，肌肉MRI提示受累肌群的水肿样改变，且肌肉活检可见肌纤维内自噬性空泡形成，应考虑药物中毒性溶酶体肌病的可能，停药后多数患者预后良好。

abstractsObjective:To report 3 cases of drug-induced toxic lysosomal myopathy induced by chloroquine, hydroxychloroquine, and colchicine, respectively, and to summarize their clinical manifestations, muscle magnetic resonance imaging (MRI) features, and histopathological characteristics through a literature review.Methods:Clinical data of patients diagnosed with drug-induced toxic lysosomal myopathy by muscle biopsy at Qilu Hospital of Shandong University between 2023 and 2024 were retrospectively collected, including medical history, physical examination findings, laboratory results, muscle MRI, muscle biopsy, and electromyography. Relevant literature was systematically reviewed to analyze clinicopathological characteristics. Multivariate Logistic regression analysis was performed to identify prognostic factors.Results:All 3 patients were middle-aged or elderly and presented with proximal limb weakness. Patients 1 and 2 experienced exacerbation of pre-existing muscle weakness following chloroquine or hydroxychloroquine treatment, whereas patient 3 developed new-onset muscle weakness after colchicine administration. Physical examination revealed proximal myopathy in all cases. Muscle MRI demonstrated edema-like changes in the affected muscles. Elevated serum creatine kinase levels were observed in patients 1 and 3 (700 and 2 124 U/L, respectively). Muscle biopsy in all cases showed the presence of autophagic vacuoles, consistent with lysosomal myopathy. Literature review indicated that drug-induced toxic lysosomal myopathy predominantly affected middle-aged and elderly individuals and was characterized by proximal muscle weakness and autophagic vacuoles on muscle biopsy. Most patients achieved varying degrees of recovery, after discontinuation of the offending drug. Multivariate Logistic regression analysis indicated that patients with colchicine-induced myopathy had a significantly shorter recovery time compared with those induced by chloroquine/hydroxychloroquine ( OR=5.380, 95% CI 1.492-19.405, P=0.010). Conclusions:For patients treated with chloroquine, hydroxychloroquine, or colchicine, if new-onset muscle weakness, exacerbation of pre-existing weakness, and (or) elevated serum creatine kinase levels occur, with muscle MRI showing edema-like changes in the affected muscle groups and muscle biopsy revealing autophagic vacuole formation within muscle fibers, the possibility of drug-induced toxic lysosomal myopathy should be considered. Most patients have a good prognosis after discontinuation of the drug.