Severe acute myopathy following SARS-CoV-2 infection: a case report and review of recent literature.

IF 5.3 2区医学 Q2 CELL BIOLOGY Skeletal Muscle Pub Date : 2021-04-21 DOI:10.1186/s13395-021-00266-5

Badrul Islam, Mohiuddin Ahmed, Zhahirul Islam, S M Begum

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引用次数: 16

Abstract

Background: SARS-CoV2 virus could be potentially myopathic. Serum creatinine phosphokinase (CPK) is frequently found elevated in severe SARS-CoV2 infection, which indicates skeletal muscle damage precipitating limb weakness or even ventilatory failure.

Case presentation: We addressed such a patient in his forties presented with features of severe SARS-CoV2 pneumonia and high serum CPK. He developed severe sepsis and acute respiratory distress syndrome (ARDS) and received intravenous high dose corticosteroid and tocilizumab to counter SARS-CoV2 associated cytokine surge. After 10 days of mechanical ventilation (MV), weaning was unsuccessful albeit apparently clear lung fields, having additionally severe and symmetric limb muscle weakness. Ancillary investigations in addition with serum CPK, including electromyogram, muscle biopsy, and muscle magnetic resonance imaging (MRI) suggested acute myopathy possibly due to skeletal myositis.

Conclusion: We wish to stress that myopathogenic medication in SARS-CoV2 pneumonia should be used with caution. Additionally, serum CPK could be a potential marker to predict respiratory failure in SARS-CoV2 pneumonia as skeletal myopathy affecting chest muscles may contribute ventilatory failure on top of oxygenation failure due to SARS-CoV2 pneumonia.

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SARS-CoV-2感染后严重急性肌病:1例报告及近期文献综述

背景:SARS-CoV2病毒可能具有潜在的肌病性。血清肌酐磷酸激酶(CPK)在严重的SARS-CoV2感染中经常升高，这表明骨骼肌损伤导致肢体无力甚至呼吸衰竭。病例介绍:我们处理了这样一个40多岁的患者，表现为严重的SARS-CoV2肺炎和高血清CPK。他出现严重败血症和急性呼吸窘迫综合征(ARDS)，并接受静脉注射大剂量皮质类固醇和托珠单抗，以对抗SARS-CoV2相关的细胞因子激增。机械通气(MV) 10天后，尽管肺野明显清晰，但脱机失败，并伴有严重和对称的肢体肌肉无力。除血清CPK外的辅助检查，包括肌电图、肌肉活检和肌肉磁共振成像(MRI)提示急性肌病可能由骨骼肌炎引起。结论:提示SARS-CoV2肺炎患者应慎用肌致病性药物。此外，血清CPK可能是预测SARS-CoV2肺炎呼吸衰竭的潜在标志物，因为影响胸肌的骨骼肌病可能是SARS-CoV2肺炎引起的氧合衰竭之外的呼吸衰竭。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Skeletal Muscle CELL BIOLOGY-

CiteScore

9.10

自引率

0.00%

发文量

审稿时长

12 weeks

期刊介绍： The only open access journal in its field, Skeletal Muscle publishes novel, cutting-edge research and technological advancements that investigate the molecular mechanisms underlying the biology of skeletal muscle. Reflecting the breadth of research in this area, the journal welcomes manuscripts about the development, metabolism, the regulation of mass and function, aging, degeneration, dystrophy and regeneration of skeletal muscle, with an emphasis on understanding adult skeletal muscle, its maintenance, and its interactions with non-muscle cell types and regulatory modulators. Main areas of interest include: -differentiation of skeletal muscle- atrophy and hypertrophy of skeletal muscle- aging of skeletal muscle- regeneration and degeneration of skeletal muscle- biology of satellite and satellite-like cells- dystrophic degeneration of skeletal muscle- energy and glucose homeostasis in skeletal muscle- non-dystrophic genetic diseases of skeletal muscle, such as Spinal Muscular Atrophy and myopathies- maintenance of neuromuscular junctions- roles of ryanodine receptors and calcium signaling in skeletal muscle- roles of nuclear receptors in skeletal muscle- roles of GPCRs and GPCR signaling in skeletal muscle- other relevant aspects of skeletal muscle biology. In addition, articles on translational clinical studies that address molecular and cellular mechanisms of skeletal muscle will be published. Case reports are also encouraged for submission. Skeletal Muscle reflects the breadth of research on skeletal muscle and bridges gaps between diverse areas of science for example cardiac cell biology and neurobiology, which share common features with respect to cell differentiation, excitatory membranes, cell-cell communication, and maintenance. Suitable articles are model and mechanism-driven, and apply statistical principles where appropriate; purely descriptive studies are of lesser interest.