Management of Chronic Obstructive Pulmonary Disease—A Review of the Latest Therapies


effects on several outcomes independent of the degree of airway obstruction.9


The existence of different phenotypes, particularly associated with the systemic consequences of the disease, highlights the need for more tailored treatment strategies. Moreover, multidimensional grading systems that take into account not only lung function but also parameters reflecting the patient’s perception and the systemic impact of the disease show a greater ability to predict important outcomes such as mortality compared with lung function assessment alone.10


Prevention Primary Prevention


Objectives for primary prevention in COPD are summarized in Table 1. Cigarette smoking is the main etiological factor in COPD; second-hand smoke is also known to affect lung function.11


Therefore, COPD is a


potentially preventable disease and efforts should be made to prevent the population, particularly young people, from starting smoking through comprehensive tobacco control policies.


suggesting that genetic factors could influence this susceptibility. The best documented genetic risk factor is the hereditary deficiency of the antiprotease alpha-1 antitrypsin.13


Several regions of


However, the results of these genetic association studies have been largely inconsistent between different populations, and functional genetic variants influencing the development of COPD (other than alpha-1 antitrypsin deficiency) have not been definitively identified.17


the genome that are likely to contain COPD-susceptibility genes have been identified.14–16


Although cigarette smoke is by far the main etiological factor, other factors may contribute to the development of COPD, including exposure to occupational dusts and chemicals, indoor air pollutants—particularly biomass fuels burned in poorly ventilated homes—and outdoor air pollution.18–20


In a population of 120 woman from a Spanish study,20 wood


or charcoal alone both independently increased the risk for COPD (odds ratio [OR] 1.8 and 1.5, respectively), but only the combination of the two was statistically significant (OR 4.5). Policies directed at controling air pollution are required.


COPD preferentially affects elderly individuals. Indeed, if individuals lived for 150 years, most would develop COPD, at least as assessed by airflow limitation and increased lung compliance.21


Physiological aging


of the lungs is associated with enlargement of the distal air spaces, a decrease in the distal air space surface area and loss of supporting tissue for peripheral airways (‘senile emphysema’).21


Medical research


has contributed to a significantly increased life expectancy in the 20th century; however, this can be associated with an increased risk for developing chronic degenerative diseases such as COPD. An accelerated rate of lung function decline with age is a major defining feature of COPD.22


A smoker susceptible to developing COPD may stop smoking at 55 years of age and develop symptoms at 65 years of age, as shown in Fletcher and Peto’s well-defined curve of age-associated lung function decline.22


US RESPIRATORY DISEASE


COPD is a classic example of a condition caused by gene–environment interactions, as not all smokers develop COPD. A significant familial risk for airflow obstruction has been observed in smokers with severe COPD,12


Table 1: Goals for Primary Prevention in Chronic Obstructive Pulmonary Disease


Preventing smoking initiation Smoking cessation programs Reducing indoor pollutants


Policies for reducing outdoor air pollutants Promoting healthy lifestyle (promoting physical activity) Early diagnosis


Interestingly, regular physical activity is associated with reduced age-related lung function decline and reduces the risk for developing COPD in smokers.23


Thus, regular physical activity should be encouraged in the general population and particularly in smokers. Efforts should be directed towards encouraging a healthier lifestyle.


COPD may have a long sub-clinical phase, which is a factor in the underdiagnosis of COPD.6,7


Early diagnosis could help to initiate


treatment of the disease in its early stages; therefore, efforts should be directed to diagnosing COPD in its early stages in the primary care environment. Spirometry should be considered in individuals over 40 years of age with dyspnea, chronic cough, sputum production, or a history of exposure to risk factors for the disease to confirm the diagnosis.24


so chronic airflow limitation should also be considered in symptomatic never-smokers.


Secondary Prevention


Once COPD has been diagnosed, there is still a case for secondary prevention. Smoking cessation, prevention of exacerbations, prevention and treatment of comorbidities, encouraging physical activity, and vaccination are the main strategies of secondary prevention for COPD patients.


Smoking cessation is the most important component of therapy in continuing smokers.5,24,26 in current smokers.22,27


It is well documented that FEV1 declines faster The factors that drive patients to smoke are


multifactorial; therefore, smoking cessation programs should involve interventions at different levels and require a multifaceted approach. Effective interventions include counseling from physicians, nicotine replacement, self-help, and group programs. According to the US Public Health Service guidelines for smoking cessation,28


seven first-line


pharmacotherapies for tobacco dependence are effective and at least one of these should be prescribed: bupropion, nicotine gum, nicotine inhaler, nicotine lozenge, nicotine nasal spray, nicotine spray, and varenicline. Monotherapy with the aforementioned drugs has been shown to be effective compared with placebo, with an estimated OR of 1.5–3.1.29


Exacerbations of COPD (ECOPD) are associated with a faster decline in FEV1,27


in muscle function,31,32


poor health-related quality of life (HRQoL),30 a high mortality rate,33,34


Recurrent exacerbations are a particularly important causal factor in the decline in lung function and exercise tolerance in COPD.36


deterioration and a worse prognosis.35 Therefore, 15


Among the population of never-smokers, the prevalence of significant non-reversible airway obstruction (Global Initiative for Chronic Obstructive Lung Disease [GOLD] stage >II) is about 2.6%,25


Page 1  |  Page 2  |  Page 3  |  Page 4  |  Page 5  |  Page 6  |  Page 7  |  Page 8  |  Page 9  |  Page 10  |  Page 11  |  Page 12  |  Page 13  |  Page 14  |  Page 15  |  Page 16  |  Page 17  |  Page 18  |  Page 19  |  Page 20  |  Page 21  |  Page 22  |  Page 23  |  Page 24  |  Page 25  |  Page 26  |  Page 27  |  Page 28  |  Page 29  |  Page 30  |  Page 31  |  Page 32  |  Page 33  |  Page 34  |  Page 35  |  Page 36  |  Page 37  |  Page 38  |  Page 39  |  Page 40  |  Page 41  |  Page 42  |  Page 43  |  Page 44  |  Page 45  |  Page 46  |  Page 47  |  Page 48  |  Page 49  |  Page 50  |  Page 51  |  Page 52  |  Page 53  |  Page 54  |  Page 55  |  Page 56  |  Page 57  |  Page 58  |  Page 59  |  Page 60  |  Page 61  |  Page 62  |  Page 63  |  Page 64  |  Page 65  |  Page 66  |  Page 67  |  Page 68  |  Page 69  |  Page 70  |  Page 71  |  Page 72  |  Page 73  |  Page 74  |  Page 75  |  Page 76  |  Page 77  |  Page 78  |  Page 79  |  Page 80  |  Page 81  |  Page 82  |  Page 83  |  Page 84