Chronic Obstructive Pulmonary Disease (COPD)

Chronic obstructive pulmonary disease, or COPD, is the name given to a group of disorders characterized by narrowing of the breathing tubes that limits (obstructs) the movement of air in and out of the lungs.

Jakarta, Indonesia (prHWY.com) April 10, 2012 - INTRODUCTION

Chronic obstructive pulmonary disease, or COPD, is the name given to a group of disorders characterized by narrowing of the breathing tubes that limits (obstructs) the movement of air in and out of the lungs. Specific diseases in this group include chronic bronchitis and emphysema. In most cases, COPD is associated with cigarette smoking. In the older literature and in certain parts of the world, COPD has been called chronic obstructive lung disease (COLD) or chronic obstructive airway disease (COAD), but the term COPD is now preferred.

COPD is often confused with asthma, because some of the symptoms and physical signs are similar. The major difference is that in asthma, most (or in many cases all) of the obstruction to airflow in the bronchial tubes is reversible. In other words, when asthmatic patients are examined or tested in between attacks of their asthma, their lung function is often normal. In contrast, once COPD is established, the lung function is never normal. When patients have flares or "exacerbations" of COPD, they typically get better with administration of medication, but their lung function never normalizes, although it may return to their pre-exacerbation baseline.

Chronic Bronchitis is a clinical diagnosis, based on a history of cough and sputum production on most days, for 3 months of the year, for 2 consecutive years. In contrast, a diagnosis of Emphysema cannot be made on clinical grounds alone. Because emphysema involves destruction of lung tissue, evidence of that destruction is required to confirm the diagnosis. In the past a definitive diagnosis could not be made without pathologic examination of lung tissue (e.g., at autopsy or in surgically resected lung), although a reduction in diffusing capacity (a lung function measurement that reflects the number and integrity of small blood vessels involved in oxygen exchange in the lung) has been used to infer the presence of emphysema. Today, computed tomography (CT) scans of the chest can visualize emphysema.

The number of cases of COPD is increasing worldwide, and data suggest that the true number of cases is far greater than appreciated, because COPD often goes undiagnosed. Even more concerning is the fact that deaths from COPD are increasing at a time when deaths from most other major diseases are unchanged or decreasing. COPD is not "curable," but there are several interventions that can positively impact the natural history of the disease. In addition, there are a number of approaches, including medications and non-pharmacologic interventions, which can significantly improve function and quality of life in patients with COPD.


HOW DOES COPD DEVELOP?

In 2001, a panel convened jointly by the US National Heart, Lung & Blood Institute and the World Health Organization released a report of their Global Initiative for Chronic Obstructive Lung Disease, commonly referred to as the "GOLD Guidelines" (1). In this report, COPD is defined as "a disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases."

Most COPD is associated with smoking, and 80-90% of patients with COPD have a smoking history of at least 10-20 "pack years." ("Pack years" is a convenient term that permits quantification of an individual's smoking history. To calculate pack years, the average number of packs smoked per day is multiplied by the number of years: e.g., 1 pack per day x 20 years = 20 pack years.) Although cigarette smoking is the most important risk factor for COPD in the United States and most of the developed world, exposure to fumes from biomass fuels is a major factor in the developing world. The World Health Organization (WHO) estimates that there are 400,000 COPD deaths per year related to exposure to biomass fuels.

In the right setting, these noxious or environmental exposures initiate an inflammatory response in the lungs and airways that results in damage to the lung tissue. The inflammatory response is characterized by increased numbers of specific inflammatory cells that migrate from the bloodstream into the lung and airways. Most investigators believe that the cell that contributes most to the lung damage in COPD is the neutrophil. Neutrophils are one type of white blood cell that plays an important role in the body's response to infection. However, when present in large numbers, especially in the absence of infection, the potent chemicals they release can damage the tissues. Neutrophil products, especially proteases, have many effects in the lungs and airways. They may result in:
* Increased mucus (phlegm) production
* Damage to the thin walls of lung air spaces (alveoli)
* Loss of elasticity of the lung tissue
* Scarring and narrowing of the small bronchial tubes

All of these contribute to the breathing difficulties experienced by patients with COPD. Inflammation around the airways leads to swelling and sometimes scarring that results in a reduction in the size of the bronchial tubes themselves. Obviously, it is harder to move air in and out of the lungs if the tubes are smaller than normal. Loss of elasticity of the lung tissue, caused by specific proteases that degrade elastic fibers (e.g., neutrophil elastase), results in collapse of airways during exhalation, which makes it much harder to breathe. Increased mucus stimulates coughing, but the patient with COPD often has difficulty coughing up this mucus through narrowed bronchial tubes. In addition, mucus can sometimes plug up small airways far out in the lungs, thereby interfering with the ability of fresh air (and oxygen) to reach the site in the lung where it is absorbed into the bloodstream.

Genetics may be important. Although 80-90% of patients with COPD have a history of smoking, only about 20% of smokers develop COPD. This suggests an interaction between exposure to smoke and another risk factor. It seems likely that genetic factors predispose individuals to the damage produced by smoke - what is often referred to as a "gene-by-environment interaction." The best understood genetic factor is alpha1-antitrypsin deficiency. This is a recessive trait, found mainly in individuals of Northern European ancestry. It is estimated that approximately 100,000 Americans have this gene mutation that results in the reduced ability to inhibit the activity of some of the proteases that cause lung damage. A number of other genes have been studied, but to date, no mutations other than alpha 1-antitrypsin have been convincingly linked to the development of COPD.


HOW COMMON IS COPD?

Studies from the US Centers for Disease Control report that approximately 12 million adults had a diagnosis of COPD in 2001. However, COPD is clearly underdiagnosed, and the National Health and Nutrition Examination Survey (NHANES III) http://www.cdc.gov/nchs/products/elec_prods/subject/nhanes3.htm of 20,050 adults in the United States suggests that as many as 24 million Americans are affected. The WHO estimates that as of 2007, there were 210 million people throughout the world with COPD. In addition, the WHO estimates 1.1 billion smokers worldwide, increasing to 1.6 billion by 2025. As public sentiment and policy make smoking less acceptable in Europe and North America, tobacco companies have focused their marketing efforts on low- and middle-income countries where the rates of smoking are increasing at an alarming rate.

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