Min Feng1,2,3, Xin Zhang1,2,3, Wen Wen Wu1, Zhi Hong Chen4, Brian G Oliver5,6, Vanessa M McDonald7, Hong Ping Zhang1, Min Xie8, Ling Qin9, Jie Zhang10, Lei Wang1,3, Wei Min Li2, Gang Wang11,12, Peter G Gibson7. 1. Pneumology Group, Department of Integrated Traditional Chinese and Western Medicine, Clinical Research Center for Respiratory Disease, West China Hospital, Sichuan University, Chengdu, China. 2. Department of Respiratory and Critical Care Medicine, Clinical Research Center for Respiratory Disease, West China Hospital, Sichuan University, Chengdu, China. 3. Laboratory of Pulmonary Immunology and Inflammation, Frontiers Science Center for Disease-related Molecular Network, Sichuan University, Chengdu, China. 4. Shanghai Institute of Respiratory Disease, Respiratory Division of Zhongshan Hospital, Fudan University, Shanghai, China. 5. School of Life Sciences, University of Technology Sydney, Ultimo, New South Wales, Australia. 6. Respiratory Cellular and Molecule Biology, Woolcock Institute of Medical Research, The University of Sydney, Sydney, New South Wales, Australia. 7. Priority Research Centre for Healthy Lungs, Hunter Medical Research Institute, The University of Newcastle, Newcastle, New South Wales, Australia. 8. Department of Respiratory and Critical Care Medicine, Tongji Hospital, Huazhong University of Science & Technology, Wuhan, China. 9. Department of Respiratory and Critical Care Medicine, Xiangya Hospital, Central South University, Changsha, China. 10. Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Jilin University, Changchun, China. 11. Department of Respiratory and Critical Care Medicine, Clinical Research Center for Respiratory Disease, West China Hospital, Sichuan University, Chengdu, China, wcums-respiration@hotmail.com. 12. Laboratory of Pulmonary Immunology and Inflammation, Frontiers Science Center for Disease-related Molecular Network, Sichuan University, Chengdu, China, wcums-respiration@hotmail.com.
Abstract
BACKGROUND: Reducing asthma exacerbations is a major target of current clinical guidelines, but identifying features of exacerbation-prone asthma (EPA) using multidimensional assessment (MDA) is lacking. OBJECTIVE: To systemically explore the clinical and inflammatory features of adults with EPA in a Chinese population. METHODS: We designed a cross-sectional study using the Severe Asthma Web-based Database from the Australasian Severe Asthma Network (ASAN). Eligible Chinese adults with asthma (n = 546) were assessed using MDA. We stratified patients based on exacerbation frequency: none, few (1 or 2), and exacerbation prone (≥3). Univariate and multivariable negative binomial regression analyses were performed to investigate features associated with the frequency of exacerbations. RESULTS: Of 546 participants, 61.9% had no exacerbations (n = 338), 29.6% had few exacerbations (n = 162), and 8.4% were exacerbation prone (n = 46) within the preceding year. EPA patients were characterized by elevated blood and sputum eosinophils but less atopy, with more controller therapies but worse asthma control and quality of life (all p < 0.05). In multivariable models, blood and sputum eosinophils (adjusted rate ratio = 2.23, 95% confidence interval = [1.26, 3.84] and 1.67 [1.27, 2.21], respectively), FEV1 (0.90 [0.84, 0.96]), bronchodilator responsiveness (1.16 [1.05, 1.27]), COPD (2.22 [1.41, 3.51]), bronchiectasis (2.87 [1.69, 4.89]), anxiety (2.56 [1.10, 5.95]), and depression (1.94 [1.20, 3.13]) were found. Further, upper respiratory tract infection (1.83 [1.32, 2.54]) and food allergy (1.67 [1.23, 2.25]) were at high risk of asthma symptom triggers. CONCLUSION: EPA is a clinically recognizable phenotype associated with several recognizable traits that could be addressed by targeted treatment.
BACKGROUND: Reducing asthma exacerbations is a major target of current clinical guidelines, but identifying features of exacerbation-prone asthma (EPA) using multidimensional assessment (MDA) is lacking. OBJECTIVE: To systemically explore the clinical and inflammatory features of adults with EPA in a Chinese population. METHODS: We designed a cross-sectional study using the Severe Asthma Web-based Database from the Australasian Severe Asthma Network (ASAN). Eligible Chinese adults with asthma (n = 546) were assessed using MDA. We stratified patients based on exacerbation frequency: none, few (1 or 2), and exacerbation prone (≥3). Univariate and multivariable negative binomial regression analyses were performed to investigate features associated with the frequency of exacerbations. RESULTS: Of 546 participants, 61.9% had no exacerbations (n = 338), 29.6% had few exacerbations (n = 162), and 8.4% were exacerbation prone (n = 46) within the preceding year. EPApatients were characterized by elevated blood and sputum eosinophils but less atopy, with more controller therapies but worse asthma control and quality of life (all p < 0.05). In multivariable models, blood and sputum eosinophils (adjusted rate ratio = 2.23, 95% confidence interval = [1.26, 3.84] and 1.67 [1.27, 2.21], respectively), FEV1 (0.90 [0.84, 0.96]), bronchodilator responsiveness (1.16 [1.05, 1.27]), COPD (2.22 [1.41, 3.51]), bronchiectasis (2.87 [1.69, 4.89]), anxiety (2.56 [1.10, 5.95]), and depression (1.94 [1.20, 3.13]) were found. Further, upper respiratory tract infection (1.83 [1.32, 2.54]) and food allergy (1.67 [1.23, 2.25]) were at high risk of asthma symptom triggers. CONCLUSION:EPA is a clinically recognizable phenotype associated with several recognizable traits that could be addressed by targeted treatment.