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10.1016/j.clim.2020.108544 http://scihub22266oqcxt.onion/10.1016/j.clim.2020.108544 32707089!7374140!32707089     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Clin+Immunol 2020 ; 219 (ä): 108544 Nephropedia Template TP {{tp|p=32707089|t=2020. Therapeutic blockade of inflammation in severe COVID-19 infection with intravenous N-acetylcysteine |pdf=|usr=}}{{32707089}} gab.com Text Therapeutic blockade of inflammation in severe COVID-19 infection with intravenous N-acetylcysteine JO: Clin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=32707089 #FOAvip 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. Twit Text FOAVip Therapeutic blockade of inflammation in severe COVID-19 infection with intravenous N-acetylcysteine ????Clin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=32707089 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32707089 #FOAvip English Wikipedia <ref>{{Cite pmid|32707089}}</ref> Therapeutic blockade of inflammation in severe COVID-19 infection with intravenous N-acetylcysteine #MMPMID32707089 Ibrahim H; Perl A; Smith D; Lewis T; Kon Z; Goldenberg R; Yarta K; Staniloae C; Williams M Clin Immunol 2020[Oct]; 219 (ä): 108544 PMID32707089show ga 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. |Acetylcysteine/*therapeutic use[MESH] |Adult[MESH] |Antioxidants/*therapeutic use[MESH] |Antirheumatic Agents/therapeutic use[MESH] |Betacoronavirus/*pathogenicity[MESH] |Biomarkers/blood[MESH] |C-Reactive Protein/metabolism[MESH] |COVID-19[MESH] |Coronavirus Infections/blood/complications/*drug therapy/virology[MESH] |Cytokine Release Syndrome/blood/complications/*drug therapy/virology[MESH] |Drug Administration Schedule[MESH] |Ferritins/blood[MESH] |Fibrin Fibrinogen Degradation Products/metabolism[MESH] |Glucosephosphate Dehydrogenase Deficiency/blood/complications/*drug therapy/virology[MESH] |Humans[MESH] |Hydroxychloroquine/therapeutic use[MESH] |Inflammation/prevention & control[MESH] |Male[MESH] |Pandemics[MESH] |Pneumonia, Viral/blood/complications/*drug therapy/virology[MESH] |SARS-CoV-2[MESH]Therapeutic blockade of inflammation in severe COVID-19 infection with(epmc).pdf DeepDyve Pubget Overpricing