Division of Neurology, Department of Medicine, University Health Network, Toronto Western Hospital, Toronto, ON, Canada.
Department of Pediatrics, McMaster University, Hamilton, ON, Canada.
Ann Neurol. 2022 Apr;91(4):568-574. doi: 10.1002/ana.26318. Epub 2022 Feb 28.
Coronavirus disease 2019 (COVID-19) severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2 infection) can lead to intensive care unit (ICU) admission and critical illness myopathy (CIM). We examined 3 ICU patients with COVID-19 who required mechanical ventilation for pneumonia and developed CIM. Pathological examination of the skeletal muscle biopsies revealed myopathic changes consistent with CIM, variable inflammation with autophagic vacuoles, SARS-CoV immunostaining + fibers/granules, and electron microscopy findings of mitochondrial abnormalities and coronavirus-like particles. Although mitochondrial dysfunction with compromised energy production is a critical pathogenic mechanism of non-COVID-19-associated CIM, in our series of COVID-19-associated CIM, myopathic changes including prominent mitochondrial damage suggest a similar mechanism and association with direct SARS-CoV-2 muscle infection. ANN NEUROL 2022;91:568-574.
新型冠状病毒病 2019（COVID-19）严重急性呼吸综合征冠状病毒 2（SARS-CoV-2 感染）可导致入住重症监护病房（ICU）和发生危重病肌病（CIM）。我们检查了 3 例因肺炎需要机械通气而 COVID-19 发展为 CIM 的 ICU 患者。骨骼肌活检的病理检查显示符合 CIM 的肌病变化，伴有自噬空泡的可变炎症、SARS-CoV 免疫染色阳性的纤维/颗粒，以及线粒体异常和冠状病毒样颗粒的电子显微镜发现。虽然线粒体功能障碍导致能量产生受损是非 COVID-19 相关 CIM 的关键发病机制，但在我们的 COVID-19 相关 CIM 系列中，包括突出的线粒体损伤在内的肌病变化表明存在类似的机制，并与直接 SARS-CoV-2 肌肉感染相关。神经病学年鉴 2022；91：568-574.
