Asthma is a heterogenous illness, characterized by airway inflammation and expressing mainly with wheezing, dyspnea, chest tightness and cough. These symptoms vary, regarding intensity and time. Chronic Obstructive Pulmonary Disease (COPD) is a preventable and treatable disease, where you can notice persistent airflow obstruction, usually progressive. Enhanced chronic inflammatory response in noxious particles or gases is associated with COPD. There is a strong relation of asthma with allergies and atopy, displayed mainly in childhood, while COPD is related with smoking and concerns people over 40 years old, having worse prognosis compared to asthma. Multiple recent reviews of literature try to define the asthma-COPD coexistence, using mainly the word overlap. American Thoracic Society-ATS guidelines of 1995 already, define asthma, chronic bronchitis, emphysema, COPD, airway obstruction, recognizing 11 different syndromes, with overlap in six of them. There are three common clinical characteristics in airway diseases: airway inflammation, airway obstruction and bronchial hyper responsiveness. The inflammation in asthma is mostly eosinophilic, driven by CD4 cells, in contrast with COPD where inflammation is neutrophilic, driven by CD8 cells. Eosinophilic inflammation is adequately controlled with steroids, while smoking promotes neutrophilic inflammation which is corticosteroids resistant. Remodeling, especially of distal, small airways happening in long standing asthma, as well as in COPD, is responsible for pulmonary function decline (airway obstruction). It is impressive the fact that up to 16% of asthmatics develop insufficient airway reversibility, after a period of 21-33 years. Bronchial hyper responsiveness is present in almost all asthmatics and in up to 2/3 of COPD patients. A cohort study proved that 17% of general population had positive challenge test in metacholine, while 50% of them were asymptomatic. Why overlap happens? “Dutch hypothesis” supports the theory that asthma and bronchial hyper responsiveness evolve in COPD later, and that asthma, COPD, chronic bronchitis and emphysema constitute different expressions of a single disease that are affected of host and environmental factors. In the biomarkers field, recent clinical trials have shown that increased levels of sputum NGAL (Neutrophil Gelatinase-Associated Lipocalin), puts the diagnosis of asthma-COPD overlap syndrome, and that overlap patients have elevated values of IL-6. Summarizing, given the fact that overlap patients are presenting more frequent exacerbations, have poorer quality of life, a more rapid decline in lung function, and higher hospital impact and mortality, in comparison to asthmatics or COPD patients, it is crucial to study further the pathogenesis of overlap syndrome, in order to understand and even to modificate the progressive functionality decline that leads to COPD.
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