Clinical implications of airway hyper-responsiveness in COPD

Abstract

COPD represents one of the leading causes of mortality in the general population. This study aimed at evaluating the relationship between airway hyperresponsiveness (AHR) and COPD and its relevance for clinical practice. We performed a MEDLINE search that yielded a total of 1919 articles. Eligible studies were defined as articles that addressed specific aspects of AHR in COPD, such as prevalence, pathogenesis, or prognosis. AHR appears to be present in at least one out of two individuals with COPD. The occurrence of AHR in COPD is influenced by multiple mechanisms, among which impairment of factors that oppose airway narrowing plays an important role. The main determinants of AHR are reduction in lung function and smoking status. We envision a dual role of AHR: in suspected COPD, specific determinants of AHR, such as reactivity and the plateau response, may help the physician to discriminate COPD from asthma; in definite COPD, AHR may be relevant for the prognosis. Indeed, AHR is an independent predictor of mortality in COPD patients. Smoking cessation has been shown to reduce AHR. Further studies are needed to elucidate whether this functional change is associated with improvement in lung function and respiratory symptoms.

Brain-Derived Neurotrophic Factor in Cigarette Smoke–Induced Airway Hyperreactivity

“…Airway diseases such as asthma and chronic obstructive pulmonary disease (COPD) can be triggered or exacerbated by cigarette smoke and secondhand smoke exposure (1)(2)(3)(4). Furthermore, in people with preexisting airway diseases such as asthma, acute exposure to cigarette smoke can produce a bronchospastic response.…”

Genome-Wide Association Study Identification of Novel Loci Associated with Airway Responsiveness in Chronic Obstructive Pulmonary Disease

“…The development of airway responsiveness in COPD probably involves multiple mechanisms, including increased airway smooth muscle contractility, increased smooth muscle mass in the small airways, decreased elastic recoil, epithelial cell dysfunction, and increased airway wall thickness (23). The mechanism by which the novel targets identified in this GWAS may affect airway responsiveness remains unknown; however, the locus on chromosome 5, SGCD (sarcoglycan, d), is a component of the dystrophin-glycoprotein complex (DGC).…”

Asthma, Chronic Obstructive Pulmonary Disease (COPD), and the Overlap Syndrome

“…13 Asthma and COPD resemble each other in that they both may show variable severity of AHR and hence bronchodilator reversibility. 14,15 AHR is present in almost all patients with asthma, at least when they are experiencing symptoms, and in up to two thirds of patients with COPD, especially when reassessed overtime.…”

“…Long-acting bronchodilators are effective when used as monotherapy in patients with COPD, but they should always be combined with an anti-inflammatory medication (eg, an ICS or a leukotriene-modifying agent) when treating persistent asthma of any severity. 1,15 While inhaled ␤2-agonists are considered to be first-line bronchodilators in the treatment of asthma, inhaled anticholinergics, when given at effective doses, can cause significant bronchodilation that is comparable to that found after treatment with ␤2-agonists. [41][42][43][44] There is increasing evidence that long-acting anticholinergics could be as effective as long-acting ␤2-agonists in controlling asthma symptoms.…”