Introduction:
The role of comorbid conditions in susceptibility to SARS-CoV-2
infection and the severity of its associated disease, COVID-19, has been
an area of ongoing investigation since the start of the pandemic. It is
well known that viral infections are a common cause for asthma
exacerbations requiring hospitalization, and previous studies have shown
associations between infections with common respiratory viruses as well
as coronaviruses (OC43 and 229E) and asthma exacerbations in both
pediatric and adult patients.1,2 Given that SARS-CoV-2
is a respiratory illness which causes viral pneumonia as a primary
manifestation, experts initially suspected the virus might exert a
similar effect and that those with underlying respiratory illnesses,
such as asthma, might be at higher risk for poor outcomes from infection
with the virus. As such, at the onset of the pandemic, both the Centers
for Disease Control and Prevention (CDC) and World Health Organization
(WHO) advised that patients with asthma may be at greater risk for
severe illness.
Despite this initial hypothesis, the published data regarding the effect
of comorbid asthma on clinical outcomes have been discrepant. Although
findings vary regionally, asthma prevalence in patients hospitalized
with COVID-19 appears to be lower than in the general populations of
Brazil, China, Italy, Russia, Saudi Arabia and
Sweden.3 In addition, several systematic reviews have
reported no increased risk for COVID-19 infection and hospitalization in
asthmatics.4-6 Conversely, in cohorts of COVID-19
patients within the United States, recent studies have revealed the
asthma prevalence to be up to 11% greater than the national
average,7 while also suggesting that asthma may be a
risk factor for poor clinical outcomes. A retrospective, single-center
review of patients who tested positive for SARS-CoV-2 in Washington,
D.C., documented an increased risk for intubation in patients with
asthma as compared to those without asthma.8 However,
in a separate study from Denver, Colorado, there was no association
between asthma and risk for intubation.9 More
recently, a large cohort study from the United Kingdom showed asthmatics
aged 16-49 were more likely to receive critical
care.10 However, the authors note that asthmatics did
not necessarily have more clinically severe disease, so the increased
rates of critical care for these patients may have been due to other
factors, such as provider preference for closer monitoring given
underlying respiratory disease. This same study also showed increased
mortality for severe asthmatics, although the definition of severe
asthma was based on patient self-reports of maintenance medications
taken in the two weeks prior to hospital admission.
Previous studies have also suggested that patients with a non-allergic
asthma phenotype may be at increased risk for severe COVID-19 disease
when compared to patients with allergic asthma.11,12The angiotensin converting enzyme 2 (ACE-2) receptor has previously been
identified as the cellular receptor for SARS-CoV-2 and reduced ACE-2
expression has been reported in patients with allergic asthma, which
would support a possible protective effect of an allergic asthma
phenotype on COVID-19 disease severity.13 A
single-center retrospective analysis of patients presenting to the ED at
a tertiary academic center in the Bronx, New York, supported the role of
pre-existing eosinophilia (AEC ≥150 cells/μL, a biomarker of allergic
inflammation) as a protective characteristic against hospitalization
with COVID-19. 14 Taken together, these findings
suggest the nuanced role of asthma phenotypes in predicting clinical
outcomes of COVID-19. Therefore, the aim of this study was to evaluate
all patients who tested positive for SARS-CoV-2 to determine the impact
of asthma and asthma phenotypes on disease severity and outcomes in
COVID-19 patients.