We report the case of a patient with muscle‐specific kinase (MuSK) antibody–positive myasthenia gravis (MG) who developed coronavirus disease‐2019 (COVID‐19). We report the clinical course of COVID‐19 focusing on the MG postintervention status in this patient. The patient, a 66‐year‐old woman, was diagnosed with MG at 44 years of age. At the time of initial MG diagnosis, she presented with dysphagia, dysarthria, ptosis, and diplopia. Symptoms worsened, with difficulty walking and culminated in respiratory muscle weakness necessitating mechanical ventilation. The diagnosis of MG was confirmed with a positive edrophonium test. Antibody testing 7 years earlier revealed a negative acetylcholine receptor–binding antibody and a positive MuSK antibody. She was initially treated with plasmapheresis, prednisone, and pyridostigmine. Subsequently, azathioprine was started while prednisone was tapered. Prednisone was stopped 5 years after diagnosis, and she had been in pharmacological remission since that time. Comorbidities were diabetes, warfarin anticoagulation for the history of deep venous thrombosis, and chronic kidney disease. She presented to the emergency department with fever and shortness of breath. Polymerase chain reaction testing for severe acute respiratory syndrome coronavirus‐2 was positive. Examination in the emergency department showed no ptosis, diplopia, facial, bulbar, or limb weakness. Chest X ray revealed perihilar and ill‐defined peripheral and lower zone predominant opacities. Arterial blood gas (ABG) before intubation showed hypoxemia without hypercapnia (partial pressure of oxygen 77 mmHg, partial pressure of carbon dioxide 34 mmHg, pH 7.43, bicarbonate 22 mEq/L). She was intubated for hypoxemic respiratory failure. Her hospital course was also complicated by hypotension and acute renal failure for which she was placed on continuous renal replacement therapy followed by intermittent hemodialysis. COVID‐19 was treated with hydroxychloroquine for 5 days, tocilizumab, and intravenous immunoglobulin (IVIg) 1 g/kg daily for 2 consecutive days. We avoided azithromycin as a COVID‐19 treatment due to its potential for exacerbating MG. We adjusted the dose of azathioprine according to the patient's renal status. She slowly improved and was extubated after 17 days then discharged to inpatient rehabilitation. After extubation, negative inspiratory pressure measurements were normal (−60 cmH₂O) with frequent monitoring. As of this writing, at 2.5 months after extubation, she has continued to receive intermittent hemodialysis for renal failure and has not developed any symptoms suggestive of worsening of MG.

A recent report on patients with myasthenia gravis and COVID‐19 included one patient with MuSK MG who had worsening of MG as a result of the COVID‐19, and was treated with an increased dose of prednisone and with IVIg. Mechanical ventilation was not needed.1 Our patient did not have ptosis, diplopia, bulbar, or limb weakness before intubation or after extubation. Also, we did not measure forced vital capacity or maximal inspiratory and expiratory pressures in the emergency department due to absence of symptoms and signs of MG exacerbation. The lack of hypercapnia on ABG before intubation suggests that the patient did not develop respiratory muscle weakness; however, we cannot entirely rule out subtle MG worsening in the intensive care unit due to inherent difficulties in assessing sedated and ventilated patients. Moreover, the treatment of our patient with IVIg for COVID‐19 may have masked symptoms of MG exacerbation. The normal measurements of negative inspiratory pressure after extubation suggested no respiratory muscle weakness.

Our case report lends support to individualized therapy of MG in the context of COVID‐19 and is consistent with published guidance for the management of MG during the COVID‐19 pandemic.2

我们报告了一例患有肌肉特异性激酶 (MusK) 抗体阳性重症肌无力 (MG) 的患者，该患者出现了 2019 年冠状病毒病 (COVID-19)。我们报告了 COVID-19 的临床过程，重点关注该患者的 MG 干预后状态。患者为 66 岁女性，在 44 岁时被诊断为 MG。在最初诊断为 MG 时，她出现吞咽困难、构音障碍、上睑下垂和复视。症状恶化，行走困难，最终导致呼吸肌无力，需要机械通气。MG的诊断通过阳性的edrophonium试验得到证实。7 年前的抗体检测显示乙酰胆碱受体结合抗体呈阴性，MuSK 抗体呈阳性。她最初接受了血浆置换术、泼尼松和吡啶斯的明治疗。随后，在泼尼松逐渐减量时开始使用硫唑嘌呤。泼尼松在诊断后 5 年停用，从那时起她一直处于药物缓解状态。合并症是糖尿病、有深静脉血栓形成史的华法林抗凝剂和慢性肾病。她因发烧和呼吸急促而到急诊室就诊。严重急性呼吸综合征冠状病毒-2的聚合酶链反应检测呈阳性。急诊科检查未发现上睑下垂、复视、面部、延髓或四肢无力。胸部 X 线显示肺门周围和边界不清的周边和下部区域主要混浊。插管前动脉血气（ABG）显示低氧血症，无高碳酸血症（氧分压 77 mmHg，二氧化碳分压 34 mmHg，pH 7.43，碳酸氢盐 22 mEq/L）。她因低氧性呼吸衰竭而被插管。她的住院病程还因低血压和急性肾功能衰竭而复杂化，为此她接受了持续的肾脏替代治疗，然后进行了间歇性血液透析。COVID-19 用羟氯喹治疗 5 天，托珠单抗和静脉注射免疫球蛋白 (IVIg) 每天 1 g/kg，连续 2 天。我们避免将阿奇霉素作为 COVID-19 治疗，因为它有可能加重 MG。我们根据患者的肾脏状况调整了硫唑嘌呤的剂量。她慢慢好转，17天后拔管，然后出院接受住院康复治疗。拔管后，吸气负压测量值正常（-60 cmH 她的住院病程还因低血压和急性肾功能衰竭而复杂化，为此她接受了持续的肾脏替代治疗，然后进行了间歇性血液透析。COVID-19 用羟氯喹治疗 5 天，托珠单抗和静脉注射免疫球蛋白 (IVIg) 每天 1 g/kg，连续 2 天。我们避免将阿奇霉素作为 COVID-19 治疗，因为它有可能加重 MG。我们根据患者的肾脏状况调整了硫唑嘌呤的剂量。她慢慢好转，17天后拔管，然后出院接受住院康复治疗。拔管后，吸气负压测量值正常（-60 cmH 她的住院病程还因低血压和急性肾功能衰竭而复杂化，为此她接受了持续的肾脏替代治疗，然后进行了间歇性血液透析。COVID-19 用羟氯喹治疗 5 天，托珠单抗和静脉注射免疫球蛋白 (IVIg) 每天 1 g/kg，连续 2 天。我们避免将阿奇霉素作为 COVID-19 治疗，因为它有可能加重 MG。我们根据患者的肾脏状况调整了硫唑嘌呤的剂量。她慢慢好转，17天后拔管，然后出院接受住院康复治疗。拔管后，吸气负压测量值正常（-60 cmH 和静脉注射免疫球蛋白 (IVIg) 每天 1 g/kg，连续 2 天。我们避免将阿奇霉素作为 COVID-19 治疗，因为它有可能加重 MG。我们根据患者的肾脏状况调整了硫唑嘌呤的剂量。她慢慢好转，17天后拔管，然后出院接受住院康复治疗。拔管后，吸气负压测量值正常（-60 cmH 和静脉注射免疫球蛋白 (IVIg) 每天 1 g/kg，连续 2 天。我们避免将阿奇霉素作为 COVID-19 治疗，因为它有可能加重 MG。我们根据患者的肾脏状况调整了硫唑嘌呤的剂量。她慢慢好转，17天后拔管，然后出院接受住院康复治疗。拔管后，吸气负压测量值正常（-60 cmH₂ O) 经常监测。在撰写本文时，拔管后 2.5 个月，她继续接受间歇性血液透析治疗肾功能衰竭，并且没有出现任何提示 MG 恶化的症状。

最近一份关于重症肌无力和 COVID-19 患者的报告包括一名 MuSK MG 患者，该患者因 COVID-19 导致 MG 恶化，并接受了增加剂量的强的松和 IVIg 治疗。不需要机械通气。1我们的患者在插管前或拔管后没有上睑下垂、复视、延髓或肢体无力。此外，由于没有 MG 恶化的症状和体征，我们没有测量急诊科的用力肺活量或最大吸气和呼气压力。插管前 ABG 无高碳酸血症提示患者未出现呼吸肌无力；然而，由于评估镇静和通气患者的固有困难，我们不能完全排除重症监护病房中轻微的 MG 恶化。此外，我们的患者用 IVIg 治疗 COVID-19 可能掩盖了 MG 恶化的症状。拔管后吸气负压的正常测量表明没有呼吸肌无力。

我们的病例报告支持在 COVID-19 的背景下对 MG 进行个体化治疗，并与已发表的 COVID-19 大流行期间 MG 管理指南一致。2