Glucose 6-phosphate dehydrogenase (G6PD) deficiency facilitates human coronavirus infection due to glutathione depletion. G6PD deficiency may especially predispose to hemolysis upon coronavirus disease-2019 (COVID-19) infection when employing pro-oxidant therapy. However, glutathione depletion is reversible by N-acetylcysteine (NAC) administration. We describe a severe case of COVID-19 infection in a G6PD-deficient patient treated with hydroxychloroquine who benefited from intravenous (IV) NAC beyond reversal of hemolysis. NAC blocked hemolysis and elevation of liver enzymes, C-reactive protein (CRP), and ferritin and allowed removal from respirator and veno-venous extracorporeal membrane oxygenator and full recovery of the G6PD-deficient patient. NAC was also administered to 9 additional respirator-dependent COVID-19-infected patients without G6PD deficiency. NAC elicited clinical improvement and markedly reduced CRP in all patients and ferritin in 9/10 patients. NAC mechanism of action may involve the blockade of viral infection and the ensuing cytokine storm that warrant follow-up confirmatory studies in the setting of controlled clinical trials.

6-磷酸葡萄糖脱氢酶（G6PD）缺乏会导致由于谷胱甘肽耗竭而导致人类冠状病毒感染。当采用促氧化剂疗法时，G6PD缺乏症尤其容易导致冠状病毒病-2019（COVID-19）感染后发生溶血。然而，谷胱甘肽耗竭是可逆通过Ñ-乙酰半胱氨酸（NAC）给药。我们描述了在接受羟氯喹治疗的G6PD缺陷患者中发生的严重COVID-19感染的严重病例，他从溶血逆转中受益于静脉（IV）NAC。NAC阻止了肝酶，C反应蛋白（CRP）和铁蛋白的溶血和升高，并允许从呼吸器和静脉-静脉体外膜充氧器中移除，并完全康复了G6PD缺陷患者。NAC还用于另外9名没有G6PD缺乏症的呼吸依赖COVID-19感染患者。NAC引起临床改善，所有患者的CRP明显降低，9/10患者的铁蛋白降低。NAC的作用机制可能涉及病毒感染的阻断和随后发生的细胞因子风暴，因此有必要在对照临床试验中进行后续的确认研究。