**1. Introduction**

Chronic obstructive lung disease (COPD) is defined as a common, preventable, and treatable disease that is characterized by persistent respiratory symptoms (shortness of breath, chronic cough, sputum production) and by airway obstruction (airflow limitation) that will not return to the normal range [1]. It is considered that COPD is

complex and heterogeneous in symptoms, disease progression, functional outcomes, and response to therapies based on the etiology, pathogenesis, and type of lung pathology [2]. To address this complexity and heterogeneity, it is desirable to meaningfully identify and classify groups of patients with similar clinical characteristics, prognosis, and/or therapeutic needs, referred to as clinical phenotypes. However, it has not established to classify patients with COPD into defined subtypes according to distinct phenotypes. The Genetic Epidemiology of Chronic Obstructive Pulmonary Disease (COPDGene) study, which is a longitudinal cohort study of more than 10,000 smokers, is being carried out to identify the etiology, progression, and heterogeneity of COPD. This cohort study is probably useful for research and development of treatable trait toward precision medicine or personalized medicine for COPD [3–5].

Chronic lung inflammation, which is caused by cigarette smoke and other environmental exposures (biomass fuel, air pollution etc.), contributes to the pathogenesis of this disease. This chronic lung inflammation related to neutrophils and macrophages is normal response in many people, but appears to be modified in patients who develop COPD, leading to emphysema and small airway fibrosis, which are essential characteristics in pathology of this disease. COPD is diagnosed only by persistent airflow limitation in spirometry, but other variables in lung function test may be relevant to diagnosis and prognosis of this disease. Since not only FEV1 but also FEV1/FVC physiologically decreases with age, the fixed cutoff point for FEV1/ FVC ratio may be inaccurate to use for diagnosis of COPD. Airflow limitation is progressive, and a decline of FEV1 varies in each patient.

The pathological alterations cause not only airflow limitation mediated by the loss of alveolar attachment to the small airways but also gas trapping (an increase in residual volume (RV) or a decrease in inspiratory capacity (IC)). Moreover, these structural alterations also cause a decrease in lung elastic recoil (a reduction in dynamic elastance). Since COPD is associated with not only small airway but also alveolar disease [6], some patients with COPD have a low diffusing capacity of the lung for carbon monoxide (DLCO). It has been recognized that chronic airflow obstruction could be seen in a variety of overlapping conditions among airway diseases, most notably in patients with COPD and asthma [7, 8]. The overlap of asthma and COPD has been proposed as a distinct COPD phenotype, refers to a set of observable characteristics of an organism.

When infections or heart failure occurs in patients, the stable periods of COPD may be interrupted by acute worsening of respiratory symptoms (exacerbations). Moreover, significant chronic diseases are concomitant with most patients with COPD (comorbidity) [9]. The prognosis of each patient with COPD is probably dependent on frequency of exacerbations and coexisting diseases. Hence, COPD is a heterogeneous disease in symptoms, exacerbations, disease progression, functional outcomes, and response to therapies (clinical phenotypes) [10]. A unique phenotype, which has similar underlying biologic (physiologic or molecular) mechanisms that define subtypes (referred to as "endotypes") to guide the development of therapy, is sheared between COPD and asthma [11]. In COPD, individual patients with similar degrees of airflow limitation most likely are different in terms of symptoms, exercise capacity, and exacerbation risk. Ever since 2011, Global Initiative for Chronic Obstructive Lung Disease (GOLD) states a multidimensional assessment of patients with COPD that includes two new dimensions: symptoms experienced by the patient and the risk of future exacerbations [1].

Since COPD is heterogeneous, patients with this disease can be stratified according to clinical phenotypes [3, 4, 10]. However, different clinical characteristics are mixed in various proportions in individual patients with COPD. This chapter

*New Perspectives in Pharmacological Therapy for COPD: Phenotype Classification and… DOI: http://dx.doi.org/10.5772/intechopen.106949*

describes multiple dimensions including clinical, physiologic, imaging, and endotyping dimensions in COPD [9]; moreover, describes effectiveness of corticosteroids with bronchodilators to patients with COPD who have airway eosinophilia and airway hyperresponsiveness as phenotypes in order to search treatable trait for COPD [12].
