Abstract

Interleukin-6 is pro-inflammatory cytokine which plays a role in cytokine storm and brought into notice with corona virus disease of 2019. Lymphopenia and dysregulated immune response were seen in the critically ill patients of corona virus disease of 2019. IL-6 inhibitors were proposed as a treatment option in this pandemic with a concept that it will reduce inflammation, infection and organ failure. Tocilizumab, a monoclonal antibody against soluble and membrane IL‐6 receptors was considered as forefront treatment option as it was used previously in rheumatologic disorder as a licensed agent. Tocilizumab is an immunosuppressive agent and serious or fatal infections could occur. Presence of superimposed bacterial infections in critically ill patients with corona virus disease of 2019 should be aggressively treated. However clinical experiences showed higher rates of superimposed bacterial infections which renders for extreme caution while prescribing such therapies. Perspective is needed when using the rheumatologic literature of IL-6 into corona virus disease of 2019 and their range observed in these conditions.

Highlights

  • Interleukin-6 blockade and cytokine release syndrome in coronavirus disease of 2019: Is that a lot? Thoughts from the emergency department

  • Dear Editor, Cytokine storm remains the main feature in pathophysiology of the coronavirus disease 2019 (COVID-19) causing adverse effects from interleukin (IL) 1β, 6, and tumor necrosis factor-α

  • Experimental studies show that elevated IL-6 is found in severe infection, cytokine storm blockers and immune host modulators are used to deal with overwhelming inflammation (2-5)

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Summary

Introduction

Interleukin-6 blockade and cytokine release syndrome in coronavirus disease of 2019: Is that a lot? Sadaf Sheikh* Emergency Medicine Department, Sultan Qaboos University Hospital, Muscat, Oman Dear Editor, Cytokine storm remains the main feature in pathophysiology of the coronavirus disease 2019 (COVID-19) causing adverse effects from interleukin (IL) 1β, 6, and tumor necrosis factor-α.

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