LEADER 01000caa a22002652 4500
001 NLM313464596
003 DE-627
005 20240329234118.0
007 cr uuu---uuuuu
008 231225s2020 xx |||||o 00| ||eng c
024 7 |a 10.1016/j.clim.2020.108555  |2 doi 
028 5 2 |a pubmed24n1354.xml 
035 |a (DE-627)NLM313464596 
035 |a (NLM)32771488 
035 |a (PII)S1521-6616(20)30665-3 
040 |a DE-627  |b ger  |c DE-627  |e rakwb 
041 |a eng 
100 1 |a Laurence, Jeffrey  |e verfasserin  |4 aut 
245 1 0 |a Anti-complement C5 therapy with eculizumab in three cases of critical COVID-19 
264 1 |c 2020 
336 |a Text  |b txt  |2 rdacontent 
337 |a ƒaComputermedien  |b c  |2 rdamedia 
338 |a ƒa Online-Ressource  |b cr  |2 rdacarrier 
500 |a Date Completed 14.09.2020 
500 |a Date Revised 29.03.2024 
500 |a published: Print-Electronic 
500 |a Citation Status MEDLINE 
520 |a Copyright © 2020 Elsevier Inc. All rights reserved. 
520 |a Respiratory failure and acute kidney injury (AKI) are associated with high mortality in SARS-CoV-2-associated Coronavirus disease 2019 (COVID-19). These manifestations are linked to a hypercoaguable, pro-inflammatory state with persistent, systemic complement activation. Three critical COVID-19 patients recalcitrant to multiple interventions had skin biopsies documenting deposition of the terminal complement component C5b-9, the lectin complement pathway enzyme MASP2, and C4d in microvascular endothelium. Administration of anti-C5 monoclonal antibody eculizumab led to a marked decline in D-dimers and neutrophil counts in all three cases, and normalization of liver functions and creatinine in two. One patient with severe heart failure and AKI had a complete remission. The other two individuals had partial remissions, one with resolution of his AKI but ultimately succumbing to respiratory failure, and another with a significant decline in FiO2 requirements, but persistent renal failure. In conclusion, anti-complement therapy may be beneficial in at least some patients with critical COVID-19 
650 4 |a Case Reports 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 4 |a COVID-19 
650 4 |a Complement 
650 4 |a Coronavirus 
650 4 |a Eculizumab 
650 4 |a Lectin pathway 
650 4 |a MASP2 
650 7 |a Antibodies, Monoclonal, Humanized  |2 NLM 
650 7 |a Biomarkers  |2 NLM 
650 7 |a Complement C5  |2 NLM 
650 7 |a Complement Inactivating Agents  |2 NLM 
650 7 |a Complement Membrane Attack Complex  |2 NLM 
650 7 |a Fibrin Fibrinogen Degradation Products  |2 NLM 
650 7 |a Peptide Fragments  |2 NLM 
650 7 |a fibrin fragment D  |2 NLM 
650 7 |a Complement C4b  |2 NLM 
650 7 |a 80295-50-7  |2 NLM 
650 7 |a complement C4d  |2 NLM 
650 7 |a 80295-52-9  |2 NLM 
650 7 |a eculizumab  |2 NLM 
650 7 |a A3ULP0F556  |2 NLM 
650 7 |a MASP2 protein, human  |2 NLM 
650 7 |a EC 3.4.21.-  |2 NLM 
650 7 |a Mannose-Binding Protein-Associated Serine Proteases  |2 NLM 
650 7 |a EC 3.4.21.-  |2 NLM 
700 1 |a Mulvey, J Justin  |e verfasserin  |4 aut 
700 1 |a Seshadri, Madhav  |e verfasserin  |4 aut 
700 1 |a Racanelli, Alexandra  |e verfasserin  |4 aut 
700 1 |a Harp, Joanna  |e verfasserin  |4 aut 
700 1 |a Schenck, Edward J  |e verfasserin  |4 aut 
700 1 |a Zappetti, Dana  |e verfasserin  |4 aut 
700 1 |a Horn, Evelyn M  |e verfasserin  |4 aut 
700 1 |a Magro, Cynthia M  |e verfasserin  |4 aut 
773 0 8 |i Enthalten in  |t Clinical immunology (Orlando, Fla.)  |d 1999  |g 219(2020) vom: 10. Okt., Seite 108555  |w (DE-627)NLM098196855  |x 1521-7035  |7 nnns 
773 1 8 |g volume:219  |g year:2020  |g day:10  |g month:10  |g pages:108555 
856 4 0 |u http://dx.doi.org/10.1016/j.clim.2020.108555  |3 Volltext 
912 |a GBV_USEFLAG_A 
912 |a SYSFLAG_A 
912 |a GBV_NLM 
912 |a GBV_ILN_11 
912 |a GBV_ILN_24 
912 |a GBV_ILN_350 
951 |a AR 
952 |d 219  |j 2020  |b 10  |c 10  |h 108555