COPD: it is time to change!

Abstract

COPD is a common cause of disability, morbidity and mortality worldwide and a major global health problem with enormous direct and indirect health care costs. Different reasons can be advanced to explain it, but among them the possibility that the recommended diagnostic and therapeutic approaches to COPD were less effective than they could be, should be also considered. The pharmacological baseline treatment of stable COPD has been widely based on the severity of airflow obstruction and recently, of chronic symptoms and on the annual number of previous exacerbations. These recommendations do not take into account the underlying prevalent disease that should be treated and the future risk. Our suggestion is that the therapy must be firstly tailored on the prevalent disease leading to COPD, independently from the degree of FEV1 reduction and chronic dyspnea and only after that, according to the severity of the disorder (and age of patient), to establish the level of the treatment in order to freeze, when possible, and not to follow the underlying pathological process, running after it. Moreover, given the relevance of exacerbations in the natural history of COPD, greater effort should be placed on recognition of their prevalent type in frequent exacerbators and to prevent them using more tailored and specific treatment.

Keywords: COPD; prevention of COPD exacerbations; therapeutic approach of COPD.

Figure 1

The baseline pharmacological approach to COPD according to the prevalent underlying disease. Notes: ^aJudged according to persistence of daytime and/or nighttime symptoms, resting dynamic hyperinflation, lung function deterioration (in terms of FEV₁ annual decline and plethysmographic lung volume changes) and limited exercise tolerance (based on patient’s lifestyle). ^bIf eosinophilic inflammation (or surrogates: significant acute reversibility of airway obstruction, presence of airway hyperresponsiveness, high FENO); fluticasone dipropionate: high dose =1,000γ equivalent/daily; low dose =500γ equivalent/daily. Abbreviations: bid, twice daily; FEV₁, forced expiratory volume in 1 second; ICS, inhaled corticosteroids; FENO, fractional exhaled nitric oxide; LABA, long-acting beta-adrenoceptor agonist; LAMA, long-acting muscarinic antagonist; U-LABA, ultralong-acting beta-adrenoceptor agonist; U-LAMA, ultralong-acting muscarinic antagonist.

Figure 2

The different preventive approach to acute exacerbation in COPD. Notes: ^aIf eosinophilic exacerbations only. ^bIf chronic bronchitis, if environmental pollution, if still current smoker (carbocistein – N-acetyl carbocysteine high doses). ^cIf bacterial AECOPD, expected in the presence of bronchiectasis, chronic bronchitis, and bacterial colonization (macrolides). ^dOther causes of exacerbations (not infectious, not eosinophilic, and not induced by oxidative stress) according to etiology. Abbreviations: AECOPD, acute exacerbations of chronic obstructive pulmonary disease; vit, vitamin; ICS, inhaled corticosteroids; C-PAP, continuous positive airway pressure.