Abstract

Critically ill patients often have a dysregulated immune response to the underlying insult leading to varied clinical features and end-organ dysfunction. One of the dysregulated immune responses termed ‘cytokine storm (CS)’ secondary to SARS-COV-2 during the recent COVID-19 pandemic was responsible for unacceptably high morbidity and mortality across the world. Cytokine storm is not unique to just COVID-19 but can also occur due to certain other viruses like H1N1 influenza. This phenomenon accelerated not only our understanding of the underlying pathophysiology and the role of the immune system in critically ill patients but also strengthened the concept of the possible need for an immunomodulator incorporated with standard therapy for treating Acute Respiratory Distress Syndrome(ARDS). Itolizumab, a reformulated anti-CD-6 humanized monoclonal antibody, downregulates the synthesis of proinflammatory cytokines leading to reduced interferon-γ (IFNγ), interleukin (IL-6), and tumour necrosis factor-α (TNFα) levels, along with reduced T-cell infiltration at the inflammatory site. Its usage in the management of CS in non-COVID 19 ARDS seems to be an appealing therapeutic approach given its mechanism of action. The current cases highlight an underlying possible hyperimmune response secondary to H1N1 in two patients who were successfully managed using Itolizumab along with standard treatment of ARDS.

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