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COVID-19 相关危重症肌病与直接病毒作用。

COVID-19-Associated Critical Illness Myopathy with Direct Viral Effects.

机构信息

Division of Neurology, Department of Medicine, University Health Network, Toronto Western Hospital, Toronto, ON, Canada.

Department of Pediatrics, McMaster University, Hamilton, ON, Canada.

出版信息

Ann Neurol. 2022 Apr;91(4):568-574. doi: 10.1002/ana.26318. Epub 2022 Feb 28.

Abstract

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.

摘要

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.

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