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Therapeutic blockade of inflammation in severe COVID-19 infection with intravenous N-acetylcysteine.
Clin Immunol. 2020 10; 219:108544.CI

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.

Authors+Show Affiliations

New York University Grossman School of Medicine, NY, New York, United States of America. Electronic address: Homam.ibrahim@NYUlangone.org.Upstate Medical University Hospital, Syracuse, New York, United States of America. Electronic address: perla@upstate.edu.New York University Grossman School of Medicine, NY, New York, United States of America.New York University Grossman School of Medicine, NY, New York, United States of America.New York University Grossman School of Medicine, NY, New York, United States of America.New York University Grossman School of Medicine, NY, New York, United States of America.New York University Grossman School of Medicine, NY, New York, United States of America.New York University Grossman School of Medicine, NY, New York, United States of America.New York University Grossman School of Medicine, NY, New York, United States of America.

Pub Type(s)

Case Reports
Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

32707089

Citation

Ibrahim, Homam, et al. "Therapeutic Blockade of Inflammation in Severe COVID-19 Infection With Intravenous N-acetylcysteine." Clinical Immunology (Orlando, Fla.), vol. 219, 2020, p. 108544.
Ibrahim H, Perl A, Smith D, et al. Therapeutic blockade of inflammation in severe COVID-19 infection with intravenous N-acetylcysteine. Clin Immunol. 2020;219:108544.
Ibrahim, H., Perl, A., Smith, D., Lewis, T., Kon, Z., Goldenberg, R., Yarta, K., Staniloae, C., & Williams, M. (2020). Therapeutic blockade of inflammation in severe COVID-19 infection with intravenous N-acetylcysteine. Clinical Immunology (Orlando, Fla.), 219, 108544. https://doi.org/10.1016/j.clim.2020.108544
Ibrahim H, et al. Therapeutic Blockade of Inflammation in Severe COVID-19 Infection With Intravenous N-acetylcysteine. Clin Immunol. 2020;219:108544. PubMed PMID: 32707089.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Therapeutic blockade of inflammation in severe COVID-19 infection with intravenous N-acetylcysteine. AU - Ibrahim,Homam, AU - Perl,Andras, AU - Smith,Deane, AU - Lewis,Tyler, AU - Kon,Zachary, AU - Goldenberg,Ronald, AU - Yarta,Kinan, AU - Staniloae,Cezar, AU - Williams,Mathew, Y1 - 2020/07/22/ PY - 2020/07/11/received PY - 2020/07/17/revised PY - 2020/07/17/accepted PY - 2020/7/25/pubmed PY - 2020/9/15/medline PY - 2020/7/25/entrez KW - C-reactive protein KW - COVID-19 KW - Coronavirus 19 KW - Extracorporeal membrane oxygenation KW - Ferritin KW - Glucose 6-phosphate dehydrogenase KW - Glutathione KW - Mechanistic target of rapamycin KW - N-acetylcysteine KW - Respirator SP - 108544 EP - 108544 JF - Clinical immunology (Orlando, Fla.) JO - Clin Immunol VL - 219 N2 - 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. SN - 1521-7035 UR - https://www.unboundmedicine.com/medline/citation/32707089/Therapeutic_blockade_of_inflammation_in_severe_COVID_19_infection_with_intravenous_N_acetylcysteine_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1521-6616(20)30651-3 DB - PRIME DP - Unbound Medicine ER -