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.