• Jaume Alijotas-Reig, Enrique Esteve-Valverde, Cristina Belizna, Albert Selva-O'Callaghan, Josep Pardos-Gea, Angela Quintana, Arsene Mekinian, Ariadna Anunciacion-Llunell, and Francesc Miró-Mur.
• Systemic Autoimmune Diseases Unit, Department of Internal Medicine-1, Vall d'Hebron University Hospital, Barcelona, Spain; Systemic Autoimmune Research Unit, Vall d'Hebron Reseacrh Institute, Spain; Department of Medicine, Universitat Autònoma de Barcelona, Barcelona, Spain. Electronic address: jalijotas@vhebron.net.
• Autoimmun Rev. 2020 Jul 1; 19 (7): 102569.

AbstractSevere Acute Respiratory Syndrome related to Coronavirus-2 (SARS-CoV-2), coronavirus disease-2019 (COVID-19) may cause severe illness in 20% of patients. This may be in part due to an uncontrolled immune-response to SARS-CoV-2 infection triggering a systemic hyperinflammatory response, the so-called "cytokine storm". The reduction of this inflammatory immune-response could be considered as a potential therapeutic target against severe COVID-19. The relationship between inflammation and clot activation must also be considered. Furthermore, we must keep in mind that currently, no specific antiviral treatment is available for SARS-CoV-2. While moderate-severe forms need in-hospital surveillance plus antivirals and/or hydroxychloroquine; in severe and life-threating subsets a high intensity anti-inflammatory and immunomodulatory therapy could be a therapeutic option. However, right data on the effectiveness of different immunomodulating drugs are scarce. Herein, we discuss the pathogenesis and the possible role played by drugs such as: antimalarials, anti-IL6, anti-IL-1, calcineurin and JAK inhibitors, corticosteroids, immunoglobulins, heparins, angiotensin-converting enzyme agonists and statins in severe COVID-19.Copyright © 2020. Published by Elsevier B.V.

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