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Article Publish Status: FREE
Abstract Title:

Therapeutic blockade of inflammation in severe COVID-19 infection with intravenous N-acetylcysteine.

Abstract Source:

Clin Immunol. 2020 Jul 22 ;219:108544. Epub 2020 Jul 22. PMID: 32707089

Abstract Author(s):

Homam Ibrahim, Andras Perl, Deane Smith, Tyler Lewis, Zachary Kon, Ronald Goldenberg, Kinan Yarta, Cezar Staniloae, Mathew Williams

Article Affiliation:

Homam Ibrahim

Abstract:

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.

Study Type : Human: Case Report

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