Anklesaria Zafia, Frankman Jonathan, Gordin Jonathan, Zhan Jennifer, Liu Antonio K
Pulmonary and Critical Care, California Hospital Medical Center, Los Angeles, USA.
Family Medicine, California Hospital Medical Center, Los Angeles, USA.
Cureus. 2020 Oct 26;12(10):e11186. doi: 10.7759/cureus.11186.
It is well-established by now that COVID-19 can have a wide variety of neuromuscular manifestations, including rhabdomyolysis. Weakness and elevated creatinine kinase (CK) have been documented as the initial presentation of COVID-19. Myopathy from statin use has also been well-established since the introduction of this class of medication, and the common pathologic mechanism of both entities may have been mitochondrial dysfunction. We present here the case of a COVID-19 patient on rosuvastatin who developed rhabdomyolysis with CK above 1,000,000 units/L. The patient did not present with any respiratory difficulty and responded poorly to treatment, resulting in his untimely demise. COVID-19 may have accentuated an otherwise survivable condition by means of extra stress on mitochondrial homeostasis. Understanding the actual mechanism will be important in the development and utilization of medications in the fight against COVID-19.
目前已经明确，新冠病毒病（COVID-19）可出现多种神经肌肉表现，包括横纹肌溶解。虚弱和肌酐激酶（CK）升高已被记录为COVID-19的初始表现。自这类药物引入以来，他汀类药物所致肌病也已得到充分证实，这两种情况的常见病理机制可能都是线粒体功能障碍。我们在此报告一例服用瑞舒伐他汀的COVID-19患者发生横纹肌溶解，CK超过1,000,000单位/升。该患者未出现任何呼吸困难，对治疗反应不佳，最终不幸死亡。COVID-19可能通过对线粒体稳态施加额外压力，使原本可存活的病情恶化。了解实际机制对于开发和使用抗击COVID-19的药物至关重要。
