TY - JOUR
T1 - Weathering the Cytokine Storm in COVID-19: Therapeutic Implications
AU - Iannaccone, Giulia
AU - Scacciavillani, Roberto
AU - Del Buono, Marco Giuseppe
AU - Camilli, Massimiliano
AU - Ronco, Claudio
AU - Lavie, Carl J.
AU - Abbate, Antonio
AU - Crea, Filippo
AU - Massetti, Massimo
AU - Aspromonte, Nadia
PY - 2020
Y1 - 2020
N2 - Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) recently emerged in Wuhan, Hubei-China, as responsible for the coronavirus disease 2019 (COVID-19) and then spread rapidly worldwide. While most individuals remain asymptomatic or develop only mild symptoms, approximately 5% develop severe forms of COVID-19 characterized by acute respiratory distress syndrome (ARDS) and multiple-organ failure (MOF) that usually require intensive-care support and often yield a poor prognosis. Summary: The pathophysiology of COVID-19 is far from being completely understood, and the lack of effective treatments leads to a sense of urgency to develop new therapeutic strategies based on pathophysiological assumptions. The exaggerated cytokine release in response to viral infection, a condition known as cytokine release syndrome (CRS) or cytokine storm, is emerging as the mechanism leading to ARDS and MOF in COVID-19, thus endorsing the hypothesis that properly timed anti-inflammatory therapeutic strategies could improve patients' clinical outcomes and prognosis. Key Messages: The objective of this article is to explore and comment on the potential role of the promising immunomodulatory therapies using pharmacological and nonpharmacological approaches to overcome the dysregulated proinflammatory response in COVID-19.
AB - Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) recently emerged in Wuhan, Hubei-China, as responsible for the coronavirus disease 2019 (COVID-19) and then spread rapidly worldwide. While most individuals remain asymptomatic or develop only mild symptoms, approximately 5% develop severe forms of COVID-19 characterized by acute respiratory distress syndrome (ARDS) and multiple-organ failure (MOF) that usually require intensive-care support and often yield a poor prognosis. Summary: The pathophysiology of COVID-19 is far from being completely understood, and the lack of effective treatments leads to a sense of urgency to develop new therapeutic strategies based on pathophysiological assumptions. The exaggerated cytokine release in response to viral infection, a condition known as cytokine release syndrome (CRS) or cytokine storm, is emerging as the mechanism leading to ARDS and MOF in COVID-19, thus endorsing the hypothesis that properly timed anti-inflammatory therapeutic strategies could improve patients' clinical outcomes and prognosis. Key Messages: The objective of this article is to explore and comment on the potential role of the promising immunomodulatory therapies using pharmacological and nonpharmacological approaches to overcome the dysregulated proinflammatory response in COVID-19.
KW - Adrenal Cortex Hormones
KW - Antibodies, Monoclonal, Humanized
KW - Betacoronavirus
KW - CCR5 Receptor Antagonists
KW - COVID-19
KW - Chloroquine
KW - Coronavirus Infections
KW - Cytokine Release Syndrome
KW - Cytokine storm
KW - Enzyme Inhibitors
KW - Extracorporeal Membrane Oxygenation
KW - HIV Antibodies
KW - Hemoperfusion
KW - Humans
KW - Hydroxychloroquine
KW - Immunization, Passive
KW - Immunoglobulins, Intravenous
KW - Immunologic Factors
KW - Immunomodulation
KW - Interleukin 1 Receptor Antagonist Protein
KW - Janus Kinase Inhibitors
KW - Lung Injury
KW - Mesenchymal Stem Cell Transplantation
KW - Multiple Organ Failure
KW - Pandemics
KW - Plasma Exchange
KW - Plasmapheresis
KW - Pneumonia, Viral
KW - Receptors, Interleukin-6
KW - Respiratory Distress Syndrome
KW - SARS-CoV-2
KW - Therapy
KW - Tumor Necrosis Factor Inhibitors
KW - Adrenal Cortex Hormones
KW - Antibodies, Monoclonal, Humanized
KW - Betacoronavirus
KW - CCR5 Receptor Antagonists
KW - COVID-19
KW - Chloroquine
KW - Coronavirus Infections
KW - Cytokine Release Syndrome
KW - Cytokine storm
KW - Enzyme Inhibitors
KW - Extracorporeal Membrane Oxygenation
KW - HIV Antibodies
KW - Hemoperfusion
KW - Humans
KW - Hydroxychloroquine
KW - Immunization, Passive
KW - Immunoglobulins, Intravenous
KW - Immunologic Factors
KW - Immunomodulation
KW - Interleukin 1 Receptor Antagonist Protein
KW - Janus Kinase Inhibitors
KW - Lung Injury
KW - Mesenchymal Stem Cell Transplantation
KW - Multiple Organ Failure
KW - Pandemics
KW - Plasma Exchange
KW - Plasmapheresis
KW - Pneumonia, Viral
KW - Receptors, Interleukin-6
KW - Respiratory Distress Syndrome
KW - SARS-CoV-2
KW - Therapy
KW - Tumor Necrosis Factor Inhibitors
UR - http://hdl.handle.net/10807/166527
U2 - 10.1159/000509483
DO - 10.1159/000509483
M3 - Article
SN - 1664-3828
VL - 10
SP - 277
EP - 287
JO - CardioRenal Medicine
JF - CardioRenal Medicine
ER -