tetano
Editor, Senior Moderator
Clin Immunol
. 2020 Jul 21;108544.
doi: 10.1016/j.clim.2020.108544. Online ahead of print.
Therapeutic blockade of inflammation in severe COVID-19 infection with intravenous n-acetylcysteine
Homam Ibrahim[SUP] 1 [/SUP], Andras Perl[SUP] 2 [/SUP], Deane Smith[SUP] 3 [/SUP], Tyler Lewis[SUP] 3 [/SUP], Zachary Kon[SUP] 3 [/SUP], Ronald Goldenberg[SUP] 3 [/SUP], Kinan Yarta[SUP] 3 [/SUP], Cezar Staniloae[SUP] 3 [/SUP], Mathew Williams[SUP] 3 [/SUP]
Affiliations
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 controlled clinical trials.
Keywords: C-reactive protein; COVID-19; Coronavirus 19; Extracorporeal membrane oxygenation; Ferritin; Glucose 6-phosphate dehydrogenase; Glutathione; Mechanistic target of rapamycin; N-acetylcysteine; Respirator.
. 2020 Jul 21;108544.
doi: 10.1016/j.clim.2020.108544. Online ahead of print.
Therapeutic blockade of inflammation in severe COVID-19 infection with intravenous n-acetylcysteine
Homam Ibrahim[SUP] 1 [/SUP], Andras Perl[SUP] 2 [/SUP], Deane Smith[SUP] 3 [/SUP], Tyler Lewis[SUP] 3 [/SUP], Zachary Kon[SUP] 3 [/SUP], Ronald Goldenberg[SUP] 3 [/SUP], Kinan Yarta[SUP] 3 [/SUP], Cezar Staniloae[SUP] 3 [/SUP], Mathew Williams[SUP] 3 [/SUP]
Affiliations
- PMID: 32707089
- DOI: 10.1016/j.clim.2020.108544
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 controlled clinical trials.
Keywords: C-reactive protein; COVID-19; Coronavirus 19; Extracorporeal membrane oxygenation; Ferritin; Glucose 6-phosphate dehydrogenase; Glutathione; Mechanistic target of rapamycin; N-acetylcysteine; Respirator.