Introduction
In December 2019, coronavirus disease 2019 (COVID-19) caused by severe
acute respiratory syndrome coronavirus-2 (SARS-CoV-2) occurred in Wuhan,
Hubei Province, China. As of July 20, 2020, 14 348 858 of COVID-19
confirmed cases and 603 691 deaths were reported in over 215 countries
worldwide [1], demanding an urgent need for early identification for
severe cases. The SARS-CoV-2 virus, which belongs to the
betacoronavirus, is highly homologic (with 88% identity) to two
bat-derived SARS-like coronaviruses, while more distant from SARS-CoV
(around 79%) and Middle East respiratory syndrome coronavirus
(MERS-CoV, around 50%) [2]. Clinical evidence has suggested that
SARS-CoV can be transmitted from person to person via direct contact or
through droplets from infected individuals [3, 4]. SARS-CoV-2 is
able to attack the respiratory system through binding the cell entry
receptors angiotensin-converting enzyme 2 (ACE2) on airway epithelial
cells and results in pneumonia and respiratory failure in critically ill
patients.
Chronic bronchitis, chronic obstructive pulmonary disease (COPD), and
asthma are common respiratory diseases with chronic airway inflammation
[5-9]. Eosinophils, neutrophils, and macrophages in innate immune
response significantly increase in the airway and lung during the
initial phase of inflammation. Subsequently, activated adaptive immunity
leads to the recruitment of T and B lymphocytes. Th1, Th2, and Th17
cells play a crucial role in COPD, asthma, and chronic bronchitis,
resulting in mucus overproduction and airflow obstruction [5, 8].
Lymphocytopenia, however, has been reported in several studies in severe
patients infected with SARS-CoV-2 [10-12]. Recently, circulating
eosinophil counts were also reported to be decreased in COVID-19
patients, and associated with the severity of the disease [13, 14].
Therefore, patients with underlying COPD, asthma, and chronic bronchitis
may have different inflammatory states after SARS-CoV-2 infection
compared to patients without chronic airway inflammation. [10-12,
15-17]. In this study, we aimed to identify the potential predictors
for the disease severity of COVID-19 patients with underlying chronic
airway diseases including chronic bronchitis, COPD, and asthma.
In this retrospective cohort study, we reviewed medical records of 59
laboratory-confirmed COVID-19 patients with underlying chronic airway
inflammation and compared the demographic, clinical, and radiological
characteristics as well as laboratory results between severe and
non-severe patients in this cohort. Potential predictors of disease
severity were identified in the abnormal laboratory findings using
univariate and multivariate regression models.