Severe 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. Higlights • Severe COVID-19 forms may be related to a hyperinflammatory syndrome. • Severe COVID-19 is associated with clot pathway hyperactivity and sometimes, with thromboses. • Immunosuppression may be a complementary therapy in COVID-19 patients. • Antimalarials, heparin, cytokine blockers, JAK-inhibitors, IVIG could be useful for treating severe COVID-19 patients. • In SARS-CoV-2 infections the effectiveness of the hyperimmune plasma remains uncertain.
【저자키워드】 COVID-19, Treatment, SARS-CoV-2, Cytokine storm, acute respiratory distress syndrome, COVID-19, Coronavirus disease 2019, MERS-CoV, Middle East respiratory syndrome coronavirus, IL, interleukin, immunosuppressive, WHO, World Health Organization, TLR, Toll-like receptor, ACE-2, Angiotensin-Converting Enzyme-2, SARS-COV-2, severe acute respiratory syndrome coronavirus-2, CQ, Chloroquine, HCQ, hydroxychloroquine, RA, Rheumatoid arthritis, TRALI, Transfusion-related acute lung injury, MAS, macrophage activation syndrome, SLE, systemic lupus erythematosus, CDC, Centres for Disease Control, IFNγ, interferon gamma, mTOR, Mammalian target of rapamycin, APC, antigen-presenting cells, ADE, antibody dependent enhancement, TCZ, tocilizumab, AD, Autoimmune diseases, ADRS, Acute distress respiratory syndrome, aPL, Antiphospholipid antibodies, CD, Cluster of differentiation or cluster of designation or classification determinant, CyA, Cyclosporine A, FDA, Food and Drugs Administration, GCS, Glucocorticoids, HPS, Haemophagocytic syndrome, JAK, Janus-Kinase family of enzymes (JAK1, JAK2, JAK3, TYK2), IVIG, Intravenous immunoglobulins, MDA5, Melanoma differentiation-associated gene 5, MHC-II, Major histocompatibility type-II, LMWH, Low-molecular weight heparin, NHC, National Health Council, NK, natural killer cells, NF-kβ, Nuclear Factor-Kβ, PIC, Pulmonary intravascular coagulation, PTE, Pulmonary thromboembolism, TNF-α, Tumour necrosis factor-alpha, TRAASVIR, Thrombotic Risk Associated with Antiphospholipid Syndrome after Viral infection, TGF-β, Transforming growth factor-beta, Tregs, Regulatory T-cells,