Comorbid Asthma May Not Increase Risk for Severe COVID-19
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The COVID-19 pandemic has created a global crisis that has led to substantial morbidity and mortality and has devastated health systems and economies. In response, the global scientific community has mobilized to seek insights to better understand, limit, and treat this disease. In severe SARS-CoV-2 infection, a complex immunopathology exists that comprises active viral replication and an armed, overactive immune, and inflammatory response.

Cytokines (such as IL-6 and IL-1) can evoke a cytokine storm syndrome (CSS) that features elevated markers of inflammation (such as high sensitivity C-reactive protein, lactic dehydrogenase, and ferritin) and an acquired immunodeficiency (eg, lymphopenia with reductions in T cells).

Disruption of the coagulation cascade (fibrinogen, factor VIII, and platelets) in CSS can lead to a coagulopathy with elevated D-dimers and fibrin split products, reflecting a generalized severe endovascular process. Tissue injury may then ensue from macro- and microthrombi in the veins and arteries of major organs including the lungs, heart, kidneys, and brain. Evidence of CSS is present in a high proportion of severely ill patients.

However, critical questions remain about the biologic and clinical features that predispose to CSS and critical illness, including underlying comorbidities such as asthma and the medications used to treat them.

The investigators concluded that the findings suggest a hypothesis that patients with asthma appear to be protected from COVID-19 because they have a low expression of ACE2 in their epithelial cells. A major limitation of the current analysis is the fact that all of the epidemiologic data were obtained retrospectively or on a cross-sectional basis, with no tests conducted for IFN production or ACE2 expression in patients with COVID-19, particularly in those who had comorbid asthma.

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