Abstract
Objective. This study aimed to investigate improvements in inflammatory mediator levels in induced sputum and airway hyperresponsiveness (AHR) in cough variant asthma (CVA) during long-term inhaled corticosteroid (ICS) treatment. Patients and Methods. Patients with CVA (N = 35) and classic asthma (N = 26) and healthy subjects (N = 24) were recruited into this study. All patients were treated with budesonide (400 μg/day). Measurement of inflammatory mediators in induced sputum and PD20-FEV1 (the accumulated provocative dose resulting in a 20% decrease in FEV1) in histamine-challenged subjects was performed every three months after the start of medication. Interleukin- (IL-) 5 and IL-10 were assayed by ELISA, and the percentage of eosinophils was detected with Giemsa stain. Trends during the follow-up period were analyzed using a general linear model. Results. Inflammatory mediator levels in induced sputum and PD20-FEV1 in patients with CVA and classic asthma differed from those in the control group, although no differences were found in the two asthmatic groups. PD20-FEV1 significantly increased in CVA patients after ICS treatment for 3 months, while classic asthma patients exhibited a delayed change in AHR. After ICS treatment, levels of IL-5 and IL-10 as well as the percentage of eosinophils in the CVA group were altered at 3 months and 6 months, respectively. Accordingly, the level of inflammatory mediators in classic asthma changed more slowly. Conclusion. CVA has a greater improvement in airway inflammation and airway hyperresponsiveness (AHR) than classic asthma with respect to inhaled corticosteroid (ICS). Short-term ICS considerably reduces AHR although longer treatment is required for complete control of airway inflammation.
Highlights
Cough variant asthma (CVA), a variant form of classic asthma that presents solely with a cough and responds to bronchodilator treatment, is considered to be the most common cause of chronic coughs [1]
There were no significant differences between the CVA and asthma groups with respect to age, sex, total immunoglobulin E (IgE), forced expiratory volume in 1 second (FEV1)% predicted, FEV1/forced vital capacity (FVC), hemocytes, and atopy (Table 1)
Evidence suggests that an imbalance in Th1 and Th2 lymphocyte responses plays a critical role in the pathogenesis of chronic asthma [12]
Summary
Cough variant asthma (CVA), a variant form of classic asthma that presents solely with a cough and responds to bronchodilator treatment, is considered to be the most common cause of chronic coughs [1]. As a precursor of classic asthma, it has been demonstrated that nearly 30% of untreated CVA patients eventually develop classic asthma. Budesonide can reduce the percentage of eosinophils in induced sputum in CVA patients. Long-term ICS may prevent the development of classic asthma from CVA by reducing bronchial responsiveness [4]. More recent studies have demonstrated that atopic/asthmatic individuals have an inherent defect in regulatory T cells, which suppress potentially harmful immune responses by releasing anti-inflammatory cytokines such as IL-10 and TGF-β [7]
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