ABSTRACT
Background: The effects of asthma, chronic obstructive pulmonary disease (COPD), or asthma-COPD overlap (ACO) on coronavirus disease 2019 (COVID-19) remain unclear. Objective: We aimed to investigate the effects of chronic obstructive airway diseases such as asthma, COPD, and ACO on COVID-19. Methods: In total, 5625 hospitalized patients with COVID-19 were divided into asthma, COPD, ACO, and control groups. A multivariate logistic regression analysis was performed to identify factors affecting the COVID-19 mortality rate. To find out whether chronic obstructive airway diseases such as asthma, COPD, and ACO affect COVID-19 mortality, 1:4 matching was performed, except for the ACO group alone due to a small number of patients. Results: The mortality rates of asthma, COPD, and ACO groups were about 2.3, 4.8, and 5.5 times higher than that of the control group, respectively. Although not statistically significant, the survival probability tended to decrease (asthma, COPD, and combined groups of asthma and ACO, hazard ratio [HR]: 1.84, 1.31, and 1.89, respectively). The survival probability of the combined groups of COPD, ACO, and asthma and the combined groups of COPD and ACO was significantly lower than that of the matched control group (HR: 3.00 and 1.99, respectively). Conclusion: Compared to patients with COVID-19 without chronic obstructive airway disease, patients with these comorbidities are more likely to require oxygen and mechanical ventilators and have a higher mortality rate, which can be considered when classifying and monitoring patients in the era of COVID-19. Therefore, further studies are needed to evaluate the effect of chronic obstructive airway disease, especially ACO, on COVID-19 mortality.
ABSTRACT
BACKGROUND: Angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine subtype 2 (TMPRSS2) are key proteins mediating viral entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although gene expressions of ACE2 and TMPRSS2 have been analyzed in various organs and diseases, their soluble forms have been less studied, particularly in asthma. Therefore, we aimed to measure circulating ACE2 and TMPRSS2 in the serum of asthmatics and examine their relationship with clinical characteristics. METHODS: Clinical data and serum samples of 400 participants were obtained from an asthma cohort. The soluble ACE2 (sACE2) and soluble TMPRSS2 (sTMPRSS2) level was measured by enzyme-linked immunosorbent assay, and the values underwent a natural log transformation. Associations between sACE2 and TMPRSS2 levels and various clinical variables were analyzed. RESULTS: The patients younger than 70 years old, those with eosinophilic asthma (eosinophils ≥ 200 cells/µL), and inhaled corticosteroids (ICS) non-users were associated with higher levels of sACE2. Blood eosinophils and fractionated exhaled nitric oxide levels were positively correlated with serum ACE2. In contrast, lower levels of sTMPRSS2 were noted in patients below 70 years and those with eosinophilic asthma, while no association was noted between ICS use and sTMPRSS2. The level of sTMPRSS2 also differed according to sex, smoking history, coexisting hypertension, and forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) ratio. The proportion of sputum neutrophils was positively correlated with sTMPRSS2, while the FEV1/FVC ratio reported a negative correlation with sTMPRSS2. CONCLUSION: The levels of ACE2 and TMPRSS2 were differently expressed according to age, ICS use, and several inflammatory markers. These findings suggest variable susceptibility and prognosis of SARS-CoV-2 infection among asthmatic patients.