Current Smoker: A Clinical COPD Phenotype Affecting Disease Progression and Response to Therapy.

Abstract

Chronic obstructive pulmonary disease (COPD) is a heterogeneous condition of the lungs, characterized by chronic respiratory symptoms, primarily dyspnea, cough, and sputum production, due to airway and/or alveoli abnormalities that cause persistent, and often progressive, airflow obstruction. Although the underlying mechanisms responsible for COPD remain poorly understood, over the last several decades, clinical phenotypes and endotypes have been suggested. These include frequent exacerbator and eosinophilic groups that guide tailored therapies for patients with that clinical expression. In the developed world, smoking is the main known cause of COPD, responsible for ~80% of cases. Active smokers have more severe disease, with more rapid lung function decline and impaired quality of life, than former smokers. Unfortunately, smoking is still highly prevalent. Rates range between 3% and 37% globally, with factors including sex, age, race, education level, and geography influencing the rate of addiction. Importantly, several studies have shown that smoking detrimentally affects treatment efficacy of COPD medications; this is particularly true of inhaled corticosteroids and macrolides. In this review, we discuss the effects of smoking on the pathophysiology of COPD and the clinical impact of smoke exposure in patients with COPD. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives License 4.0 (http://creativecommons.org/licenses/by-nc-nd/4.0/).