In 2001, a consensus of professionals in the treatment of chronic pulmonary disease (COPD) released the first version of the Global Initiative for Obstructive Pulmonary Disease (GOLD), with the purpose of establishing a consistent approach to a disease that still has significant world mortality. COPD is also a significant cause of worldwide disability.
The GOLD guidelines were revised in 2006 and again in 2011. Further refinements were made to the guidelines in 2015. Now there is another revision in 2017 as experts continue to learn about this condition.
Most doctors who diagnose and treat chronic lung disease will tell you that, unlike the new treatments that continue to evolve in cardiac medicine (because of new discoveries in the many diseases classified as heart disease), there’s really nothing new in COPD. So why the need to update the guidelines?
The many new issues
In the past, almost all of the definitions used to diagnose COPD focused on its most common cause: cigarette smoking. The guidelines have now been revised to recognize the importance of “host factors.” This includes the unique genetic make-up of each individual, which can explain why some patients have accelerated aging and, consequently, abnormal lung development.
Experts have known for years that some individuals have a deficiency of the enzyme alpha-one antitrypsin (AAT). This enzyme counteracts another enzyme called neutrophil elastase, which inhibits the normal elasticity of the lungs. As a result of AAT deficiency, the lungs lose their elasticity and emphysema develops. What has been surprising is the discovery that large numbers of people have the gene for this deficiency, even if it is not expressed until adulthood.
Some other familial observations suggest that there is a genetic basis for the production of matrix metalloproteinases, which are substances involved in the potential destruction of the lung matrix.
Another interesting finding is that smoking during pregnancy, in addition to posing a number of known risks to mother and child, was also found to specifically raise the risk of abnormal lung development in the developing baby, by negatively priming the immune system.
The effect of exposure in the workplace on the development of COPD was apparent from data collected in the National Health and Nutrition Examination Survey (NHANES III). Researchers determined from this survey that an estimated 19 percent of individuals had COPD that was attributable to the workplace (workplace exposures), and 31 percent of individuals diagnosed with COPD had never smoked. Note that until this data was interpreted, it was assumed that asthma was the only workplace-related pulmonary disease.
Another 2017 GOLD report update and change pertains to the effect of air pollution. The effect of air pollution is still considered relatively small compared to cigarette smoking in causing chronic lung disease, except in children, where it is now noted to have a significant impact on lung development.
Perhaps the most notable change in the present GOLD report is the realization that the most prominent factor in accelerating damage to the lung is the effect of accumulated exacerbations. Previously it was thought that constant exposure to irritants such as cigarette smoke was the continuing source of inflammation that causes the damage. Experts now realize it is the accumulation of exacerbations, comonnly referred to as flare ups, that is mostly driving inflammation and damage to the lungs in chronic lung disease.
It is apparent that one exacerbation will trigger an inflammatory process that doesn’t simply end, even after effective treatment. This phenomenon may help to explain why, among all heavy daily smokers, only a minority will go on to develop COPD.
This “amplified inflammation” may be at least partially genetically determined and then extended by oxidative stress. We now also know that this lung inflammation may persist, even in some people who stop smoking.All of these recently noted findings have further solidified the importance of prevention of disease progression, by anticipating and preventing exacerbations.
A new subset of COPD patients
One new subset of individuals with COPD was identified based on the elevation of a subtype of white blood cells called eosinophils. These are cells that play a role in allergies and were thought to be prominent (elevated blood levels) only in asthma. It is now apparent that some individuals with COPD who have high levels of eosinophils should be treated differently from standard COPD care, with much more emphasis on the use of inhaled corticosteroids. Usually inhaled steroids are the mainstay treatment of asthma, not COPD.
Another new approach is that the classification of COPD (mild, moderate, and severe disease) does not just take into account spirometry findings, like in the past. An earlier revision of the GOLD included a grid that specifically factored spirometry findings of vital capacity and subjective symptoms of shortness of breath. This was done by a questionnaire called the Modified British Medical Research Council Assessment of Shortness of Breath (mMRC)
Now, the latest 2017 revision includes an additional factor that has been added to those two metrics: whether someone has experienced a minimum of two exacerbations in the previous year. This is considered to be a better formula for assessment and treatment decisions.
One final change worth noting is that oxygen is no longer recommended as a routine treatment for stable COPD patients. The new indication for supplemental oxygen is the diagnosis of severe resting hypoxia in a COPD patient.
COPD continues to be one of the most dominant causes of high mortality and high cost to healthcare. The GOLD current ABCD treatment parameters will likely continue to be refined based on future research.
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