SARS-CoV2 in Asthmatic Children: Same Consequences in Different Endotypes?

During the early stages of the SARS-CoV2 pandemic, there was considerable concern about the risk of infection in asthmatic children, one of the most common chronic conditions in childhood and a major cause of hospitalization in pediatric settings. Contrary to initial expectations, studies conducted on children with asthma have shown fewer upper respiratory tract infections, emergency room admissions, asthma flare-ups and hospitalizations for bronchospasm in the pandemic period than in the healthy population. The literature has also shown that the majority of COVID-19 cases in asthmatic children have been mild, but cases of critical and fatal infection, often related to specific clinical features of the patient, are not negligible. It is therefore these characteristics that make risk stratification possible for young people at severe COVID-19 risk. In this regard, obesity is considered not only an important comorbidity in patients with difficult-to-treat asthma but also a risk factor for more severe forms of COVID-19. These observations are of even greater concern in the context of an increase in childhood obesity that began even before the SARS-CoV2 pandemic and has continued also as a consequence of it. It is therefore imperative to consider the effects of COVID-19 infection on asthmatic children by addressing asthma in all its complexity, dwelling on the presence of different endotypes, which can describe the distinct pathophysiological mechanisms at the cellular and molecular level of each asthmatic phenotype. This is possible through a detailed analysis of the complex metabolic pathways that correlate asthma, COVID-19 infection and obesity thanks to new high-through-put technologies, especially metabolomics, which with minimally invasive sampling, including on exhaled breath condensate (EBC), can provide precise and unbiased evidence in support of existing endotypes, making it possible to identify not only the most vulnerable individuals and thus risk stratification through specific biomarkers, but also new molecular and therapeutic targets.