目的:探讨新型冠状病毒(COVID-19，也称严重急性呼吸综合征冠状病毒2型，SARS-CoV-2)对骨骼肌损伤的机制。方法:分析两例COVID-19患者骨骼肌相关的临床和实验室特征以及组织病理学发现，其中1例来自多器官功能衰竭死亡后患者腓肠肌穿刺标本，另1例来自血栓形成所致左下肢截肢的标本。结果:患者均出现肌肉疼痛症状、实验室检查显示与骨骼肌损伤有关的生化指标异常，如肌酸激酶同工酶和乳酸脱氢酶升高；病理改变较轻微，在所检查的两个肌肉病例中未发现明显的急性组织学改变或炎症。1#患者的病理显示主要是散在的肌纤维萎缩，而2#患者则出现肌纤维坏死和轻微炎症。CD68和白细胞共同抗原(LCA)免疫组织化学染色证实浸润的炎性细胞主要是组织细胞和淋巴细胞。1#患者鉴别诊断包括慢性神经肌肉疾病，2#患者则存在血栓形成引起的筋膜室综合征的可能性。结论:两例COVID-19患者与骨骼肌损伤有关的临床证据和病理改变表明SARS-CoV-2与肌肉组织之间可能存在一些潜在的作用部位。“,”Objective:To study the mechanism of skeletal muscle injury in patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2, also known as coronavirus disease-19, COVID-19).Methods:We reported relevant clinical and laboratory features and histopathological findings in skeletal muscle of two COVID-19 patients: one from a gastrocnemius puncture specimen from a patient who died of multiorgan failure and the other from a left lower extremity amputation due to thrombosis.Results:The patients presented with the symptom of muscle ache and laboratory examination showed abnormal biochemical parameters related to skeletal muscle injury such as increased creatine kinase-MB and lactate dehydrogenase. The pathological findings were mild, and no significant acute histological changes or inflammation were identified in the two muscle cases examined. The pathological findings in patient 1 were mainly scattered atrophic muscles, while fiber necrosis and minor inflammation were identified in patient 2. The mild infiltration was confirmed by CD68 and leukocyte common antigen (LCA) staining to be predominantly macrophages and lymphocytes. The differential diagnosis included chronic neuromuscular disease in patient 1 and the possibility of fascial compartment syndrome due to thrombosis in patient 2.Conclusion:From the clinical evidence and pathological changes related to skeletal muscle injury found in the two patients with COVID-19, we speculated that there may be some potential sites of action between SARS-CoV-2 and muscle tissue.