LAUSR

Bronchiectasis is defined as abnormal and irreversible dilation of the bronchi, and is the final outcome of several diseases that have a common pathophysiology.1 Changes in local defense mechanisms or the immune response make it harder for the body to eliminate potentially pathogenic microorganisms, and trigger an inflammatory and cytotoxic cascade that damages the epithelium of the airway, completing the vicious circle of obstruction-inflammationinfection that forms the pathogenic axis of bronchiectasis.2,3 Bronchiectasis is generally classified as cystic fibrosis-related (CF) or non-CF-related (non-CF). Non-CF has different causes and affects a more heterogeneous population. Interest in bronchiectasis has been growing in recent years, due to an increased prevalence, a greater diagnostic capacity offered by high-resolution computed tomography, the increasing identification of diseases associated with bronchiectasis (asthma, COPD, autoimmune diseases, etc.), and the development of new treatments.4 Bronchiectasis is a chronic, progressive disease, and its prognosis is associated with the underlying disease, the extent of the lesions, the impact on lung function, and the frequency and severity of exacerbations. In patients with chronic obstructive pulmonary disease (COPD), bronchiectasis is related with a greater number and greater severity of exacerbations and increased mortality.5 For this reason, the severity of the bronchiectasis must be evaluated, and prevention, diagnosis, and early treatment of exacerbations are essential.6 Potentially pathogenic microorganisms usually isolated in the sputum of bronchiectasis patients include Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, Staphylococcus aureus, and Pseudomonas aeruginosa (PsA).7,8 However, not all potentially pathogenic microorganisms affect bronchiectasis patients in the same way. Chronic PsA colonization, generally observed in patients with more severe obstruction, is associated to an increase in healthcare costs generated by hospital admissions and inhaled antibiotic treatment,4 and has been defined as a predictor of mortality.9 Macrolide antibiotics, such as azithromycin, exhibit bacteriostatic activity by altering the 50S ribosomal subunit, with the subsequent interruption and inhibition of protein synthesis. Important characteristics of azithromycin are that it achieves