TY - JOUR
T1 - Coronavirus disease 2019
T2 - investigational therapies in the prevention and treatment of hyperinflammation
AU - on behalf of the COVID-19 Global Rheumatology Alliance
AU - Amigues, Isabelle
AU - Pearlman, Alexander H.
AU - Patel, Aarat
AU - Reid, Pankti
AU - Robinson, Philip C.
AU - Sinha, Rashmi
AU - Kim, Alfred Hj
AU - Youngstein, Taryn
AU - Jayatilleke, Arundathi
AU - Konig, Maximilian
N1 - Funding Information:
This paper was not funded. The views expressed here are those of the authors and participating members of the COVID-19 Global Rheumatology Alliance, and do not necessarily represent the views of the American College of Rheumatology, the European League Against Rheumatism, or any other organization.
Funding Information:
I. Amigues reports personal fees from Abbvie unrelated to this manuscript. A. Kim was supported by grants from NIH/NIAMS and Rheumatology Research Foundation, and personal fees from Exagen Diagnostics, Inc. and GlaxoSmithKline, unrelated to this manuscript. A. Patel reports personal fees from Abbvie, Celgene and Eli Lilly unrelated to this manuscript. M. Konig was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health under Award no. T32AR048522, and received personal fees from Bristol-Myers Squibb and Celltrion, unrelated to this manuscript. P. Robinson reports personal fees from Abbvie, Eli Lilly, Gilead, Janssen, Novartis, Pfizer, Roche and UCB, research grants from Janssen, Novartis, Pfizer and UCB, and non-financial support from BMS, all unrelated to this manuscript. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
Publisher Copyright:
© 2020 Informa UK Limited, trading as Taylor & Francis Group.
PY - 2020
Y1 - 2020
N2 - Introduction: The mortality of coronavirus disease 2019 (COVID-19) is frequently driven by an injurious immune response characterized by the development of acute respiratory distress syndrome (ARDS), endotheliitis, coagulopathy, and multi-organ failure. This spectrum of hyperinflammation in COVID-19 is commonly referred to as cytokine storm syndrome (CSS). Areas covered: Medline and Google Scholar were searched up until 15th of August 2020 for relevant literature. Evidence supports a role of dysregulated immune responses in the immunopathogenesis of severe COVID-19. CSS associated with SARS-CoV-2 shows similarities to the exuberant cytokine production in some patients with viral infection (e.g.SARS-CoV-1) and may be confused with other syndromes of hyperinflammation like the cytokine release syndrome (CRS) in CAR-T cell therapy. Interleukin (IL)-6, IL-8, and tumor necrosis factor-alpha have emerged as predictors of COVID-19 severity and in-hospital mortality. Expert opinion: Despite similarities, COVID-19-CSS appears to be distinct from HLH, MAS, and CRS, and the application of HLH diagnostic scores and criteria to COVID-19 is not supported by emerging data. While immunosuppressive therapy with glucocorticoids has shown a mortality benefit, cytokine inhibitors may hold promise as ‘rescue therapies’ in severe COVID-19. Given the arguably limited benefit in advanced disease, strategies to prevent the development of COVID-19-CSS are needed.
AB - Introduction: The mortality of coronavirus disease 2019 (COVID-19) is frequently driven by an injurious immune response characterized by the development of acute respiratory distress syndrome (ARDS), endotheliitis, coagulopathy, and multi-organ failure. This spectrum of hyperinflammation in COVID-19 is commonly referred to as cytokine storm syndrome (CSS). Areas covered: Medline and Google Scholar were searched up until 15th of August 2020 for relevant literature. Evidence supports a role of dysregulated immune responses in the immunopathogenesis of severe COVID-19. CSS associated with SARS-CoV-2 shows similarities to the exuberant cytokine production in some patients with viral infection (e.g.SARS-CoV-1) and may be confused with other syndromes of hyperinflammation like the cytokine release syndrome (CRS) in CAR-T cell therapy. Interleukin (IL)-6, IL-8, and tumor necrosis factor-alpha have emerged as predictors of COVID-19 severity and in-hospital mortality. Expert opinion: Despite similarities, COVID-19-CSS appears to be distinct from HLH, MAS, and CRS, and the application of HLH diagnostic scores and criteria to COVID-19 is not supported by emerging data. While immunosuppressive therapy with glucocorticoids has shown a mortality benefit, cytokine inhibitors may hold promise as ‘rescue therapies’ in severe COVID-19. Given the arguably limited benefit in advanced disease, strategies to prevent the development of COVID-19-CSS are needed.
KW - Coronavirus disease 2019 (COVID-19)
KW - cytokine release syndrome
KW - cytokine storm syndrome
KW - hemophagocytic lymphohistiocytosis
KW - hyperinflammation
UR - http://www.scopus.com/inward/record.url?scp=85096587695&partnerID=8YFLogxK
U2 - 10.1080/1744666X.2021.1847084
DO - 10.1080/1744666X.2021.1847084
M3 - Review article
C2 - 33146561
AN - SCOPUS:85096587695
SN - 1744-666X
VL - 16
SP - 1185
EP - 1204
JO - Expert Review of Clinical Immunology
JF - Expert Review of Clinical Immunology
IS - 12
ER -