Pharmacologic Treatment of Chronic Obstructive Pulmonary Disease
Pharmacologic Treatment of Chronic Obstructive Pulmonary Disease
Pharmacologic treatment of chronic obstructive pulmonary disease (COPD) has evolved considerably during the past several decades. Initial treatment of the disease was accomplished primarily through antibiotics, mucolytic agents, and nonselective sympathomimetic agents. Up-to-date treatment guidelines stratified according to strength of evidence are published in the National Heart, Lung, and Blood Institute-World Health Organization workshop report on the Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease. Current drug therapy for stable COPD focuses primarily on bronchodilation through inhaled β2-agonists and anticholinergic agents, immunization, and elimination of smoking as a risk factor. Although many pharmacologic agents are available to treat COPD, no drug has demonstrated effectiveness in halting progression of the disease. Rather, the goal of drug therapy at this time is to maintain control of symptoms and prevent COPD exacerbations. Compared with asthma, research into treatment for COPD has been minimal. However, a long-acting anticholinergic agent, tiotropium, has received approval status by the United States Food and Drug Administration. The drug has been shown to improve spirometric parameters, quality of life, and utilization of health care resources. In addition, several new targets for the treatment of COPD are being studied, and a few agents, including some that theoretically may slow functional decline in patients with COPD, are in development.
Chronic obstructive pulmonary disease (COPD), unlike most other diseases, is increasing in prevalence worldwide. This increase, at least in part, is likely due to the population surviving longer overall and escalating cigarette consumption in developing countries. In addition, although exposure to cigarette smoke is by far the leading identifiable cause of COPD, exposure to certain occupational dusts and chemicals (grain, isocyanates, cadmium, coal, welding fumes), exposures in the home (cooking smoke, fuel used for heating), and genetic predisposition (primarily α1-antitrypsin deficiency) have been linked to the disease. Chronic obstructive pulmonary disease is the fourth leading cause of death in the United States. By the third decade of the 21st century, COPD is likely to become the number three cause of death if this increase in prevalence continues. The number of patients with COPD in fact may be greater than statistics indicate, since typically, the disease is not diagnosed until the patient presents with a first exacerbation.
Compared with asthma, results of research aimed at improving treatment for COPD have been slow in coming. The mechanisms involved in COPD are much less well understood than are those of asthma. In addition, a general misperception exists that COPD is untreatable because of difficulty in reversing airway obstruction. Owing to its link to smoking, COPD sometimes is thought of as the fault of the patient. Smoking cessation is, in fact, the only intervention identified to date that slows the progression of the disease. In essence, COPD is an increase in the rate of normal functional decline of the lungs caused by the inhalation of proinflammatory particles. By definition, patients with COPD have restriction of airflow that is usually progressive and significantly, but not entirely, limited in its reversibility.
Bronchiolitis, an inflammation of the small airways that causes narrowing of the lumen and active constriction, and emphysema, the destruction of the parenchyma of the lung, are the pathologic hallmarks of COPD. The ultimate effect is limitation of airflow, with a forced expiratory volume in 1 second (FEV1):forced vital capacity (FVC) ratio less than 70% of the predicted value being the criteria for diagnosis.
The Global Initiative for Chronic Obstructive Lung Disease (GOLD) executive summary published through the National Heart, Lung, and Blood Institute-World Health Organization summarizes current COPD treatment guidelines and recommendations for disease staging. According to the GOLD report, patients experiencing symptoms (chronic cough and sputum production) despite having normal spirometric parameters are classified as stage 0, at risk. Patients with an FEV1:FVC ratio less than 70% and an FEV1 greater than 80% of predicted are classified as stage I, mild COPD. These individuals may not yet have chronic cough and sputum production and may be unaware that their lung function has deteriorated. Stage II, moderate COPD, is characterized by the same FEV1:FVC ratio as that of mild disease, but with an FEV1 less than 80% of predicted. Patients in this group may or may not experience chronic cough, sputum production, or dyspnea. These individuals are further separated into stage IIA (50% ≤ FEV1 < 80% of predicted) or IIB (30% ≤ FEV1 < 50% of predicted). The final staging category is stage III, severe COPD, representing those patients with an FEV1:FVC ratio less than 70% and an FEV1 of 30-49% of predicted in addition to respiratory failure or symptoms consistent with right-sided heart failure.
Pharmacologic treatment of chronic obstructive pulmonary disease (COPD) has evolved considerably during the past several decades. Initial treatment of the disease was accomplished primarily through antibiotics, mucolytic agents, and nonselective sympathomimetic agents. Up-to-date treatment guidelines stratified according to strength of evidence are published in the National Heart, Lung, and Blood Institute-World Health Organization workshop report on the Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease. Current drug therapy for stable COPD focuses primarily on bronchodilation through inhaled β2-agonists and anticholinergic agents, immunization, and elimination of smoking as a risk factor. Although many pharmacologic agents are available to treat COPD, no drug has demonstrated effectiveness in halting progression of the disease. Rather, the goal of drug therapy at this time is to maintain control of symptoms and prevent COPD exacerbations. Compared with asthma, research into treatment for COPD has been minimal. However, a long-acting anticholinergic agent, tiotropium, has received approval status by the United States Food and Drug Administration. The drug has been shown to improve spirometric parameters, quality of life, and utilization of health care resources. In addition, several new targets for the treatment of COPD are being studied, and a few agents, including some that theoretically may slow functional decline in patients with COPD, are in development.
Chronic obstructive pulmonary disease (COPD), unlike most other diseases, is increasing in prevalence worldwide. This increase, at least in part, is likely due to the population surviving longer overall and escalating cigarette consumption in developing countries. In addition, although exposure to cigarette smoke is by far the leading identifiable cause of COPD, exposure to certain occupational dusts and chemicals (grain, isocyanates, cadmium, coal, welding fumes), exposures in the home (cooking smoke, fuel used for heating), and genetic predisposition (primarily α1-antitrypsin deficiency) have been linked to the disease. Chronic obstructive pulmonary disease is the fourth leading cause of death in the United States. By the third decade of the 21st century, COPD is likely to become the number three cause of death if this increase in prevalence continues. The number of patients with COPD in fact may be greater than statistics indicate, since typically, the disease is not diagnosed until the patient presents with a first exacerbation.
Compared with asthma, results of research aimed at improving treatment for COPD have been slow in coming. The mechanisms involved in COPD are much less well understood than are those of asthma. In addition, a general misperception exists that COPD is untreatable because of difficulty in reversing airway obstruction. Owing to its link to smoking, COPD sometimes is thought of as the fault of the patient. Smoking cessation is, in fact, the only intervention identified to date that slows the progression of the disease. In essence, COPD is an increase in the rate of normal functional decline of the lungs caused by the inhalation of proinflammatory particles. By definition, patients with COPD have restriction of airflow that is usually progressive and significantly, but not entirely, limited in its reversibility.
Bronchiolitis, an inflammation of the small airways that causes narrowing of the lumen and active constriction, and emphysema, the destruction of the parenchyma of the lung, are the pathologic hallmarks of COPD. The ultimate effect is limitation of airflow, with a forced expiratory volume in 1 second (FEV1):forced vital capacity (FVC) ratio less than 70% of the predicted value being the criteria for diagnosis.
The Global Initiative for Chronic Obstructive Lung Disease (GOLD) executive summary published through the National Heart, Lung, and Blood Institute-World Health Organization summarizes current COPD treatment guidelines and recommendations for disease staging. According to the GOLD report, patients experiencing symptoms (chronic cough and sputum production) despite having normal spirometric parameters are classified as stage 0, at risk. Patients with an FEV1:FVC ratio less than 70% and an FEV1 greater than 80% of predicted are classified as stage I, mild COPD. These individuals may not yet have chronic cough and sputum production and may be unaware that their lung function has deteriorated. Stage II, moderate COPD, is characterized by the same FEV1:FVC ratio as that of mild disease, but with an FEV1 less than 80% of predicted. Patients in this group may or may not experience chronic cough, sputum production, or dyspnea. These individuals are further separated into stage IIA (50% ≤ FEV1 < 80% of predicted) or IIB (30% ≤ FEV1 < 50% of predicted). The final staging category is stage III, severe COPD, representing those patients with an FEV1:FVC ratio less than 70% and an FEV1 of 30-49% of predicted in addition to respiratory failure or symptoms consistent with right-sided heart failure.
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