Conclusions and Proposals for Future Work

Identification

COPD is a relatively new diagnosis, but is nonetheless a controversial one. There are defining characteristics of COPD (namely, irreversible lung damage, constriction of airways, unresponsiveness to steroids), but not a clear, distinct definition. Some view COPD as an “umbrella term” of respiratory diseases. In fact, in the process of researching this disease, I talked to a resident who mentioned something along the lines of “sometimes, we diagnose a patient with COPD when they have multiple respiratory complaints that are of a certain severity and have been correlated with COPD and we can’t find another, more fitting answer”. While this scenario may not sit well with the average individual, it does reflect a very real shortcoming of medicine when it comes to COPD. Besides performing lung biopsies or checking chest CT’s (and exposing those with risk factors for lung cancer to intense radiation that can cause cancer), there are few sure-fire ways to check a patient for signs of COPD. Today, checking a FEV1/FVC level and considering risk factors is the most agreed-upon method of diagnosing COPD, but there is certainly potential for improvement.

COPD, being a leading cause of death, cannot be taken lightly. There is a need for more stringent definitions & requirements for a COPD diagnosis to avoid misdiagnosis and mistreatment of patients. Because of the chronic nature of COPD, perhaps there should be more emphasis placed on primary-care physicians in terms of monitoring a patient’s history, risk factors, and complaints over time so as to better differentiate COPD from other respiratory diseases. This is to say that an individual presenting to the emergency department with unexplained shortness of breath and being diagnosed with COPD is not the most viable nor the safest practice.

The Molecular Basis

Currently, there are many well-supported correlations made that lead to an understanding of COPD on the tissue & cellular levels. For example, over-activity of the inflammatory response and reactive oxygen species are known to be involved, as well as enzymes such as alpha-1-antitrypsin. However, future work needs a focus on the molecular level for a better understanding of COPD so that, ultimately, better treatments and management options are available.

Treatment and Management

The symptoms of COPD are caused by irreversible lung tissue damage, which is, expectedly, difficult or impossible to truly treat. The better management of COPD patients, however, is an area that could be significantly improved within the near future. Again, it is important to have clearer and more precise criteria for identification and diagnosis of COPD so that management can start sooner. The effects of cigarette smoking, especially those related to COPD, need to be more effectively presented to people – everyone, at every age – and especially to those that begin to manifest symptoms of COPD. The cessation of smoking is futile in terms of recovering damaged lung tissue, but it is certainly a great step closer to a longer life when it comes to COPD management.

COPD Exacerbations

It should be noted that most deaths associated with COPD are due to COPD exacerbations, which are episodes of severe symptoms, which typically require hospitalization. Whereas COPD is not understood to a great extent currently, the causes of COPD exacerbations and the factors that determine their severity are understood to a lesser extent. This is especially concerning, given the fatality of these exacerbations. However, exacerbations are inherently more difficult to study, given their often random occurrences. This means that, in terms of exacerbations, there needs to be research on the causes of COPD exacerbations on a molecular level, so that possible treatments can be developed to lessen the severity of exacerbations in a hospital or at an at-home setting.

5 Replies to “Conclusions and Proposals for Future Work”

  1. Hey Besher,

    I was wondering, given that the main cause of the symptoms is accumulation of lung and tissue damage, if there was anyway to preemptively treat the disease. Obviously this would be difficult to do in individuals who develop the disease environmentally, but I feel like there is an opportunity to prevent some of the symptoms in individuals with the mutation in Alpha-1 antitrypsin. If we screened people at birth for this mutation, do you think it would be possible to supplement with recombinant versions of this enzyme to try to prevent any lung damage from accumulating from the start?

    1. Hey Tommy, that’s an excellent point you bring up – and I’ll be sure to add it to the Treatment page. There is, in fact, a concentrate of the human enzyme that can be provided intravenously. The most commonly-used and studied is called Prolastin, which can be administered weekly. According to the NIH, there is “an overall death rate 1.5 times higher for those who did not receive augmentation therapy”, which is certainly significant, in my opinion. The research on this course of treatment is a little sparse, and I can’t find anything on long-term Prolastin treatment on patients before they exhibit signs of COPD, so I can’t say confidently that it may prevent (or greatly lessen) the severity of the disease in patients with A1AT deficiency, but I think it has potential. Hopefully there will be studies done soon!

  2. Besher – Nice job! I have a broad question and then some “future” ideas that I wanted to run by you.

    So your title page mentions the rise in COPD worldwide. I was wondering if you’d be able to tease out the public health/epidemiology behind that – Is it on the rise in particular pockets of the world (e.g. developed vs non developed countries)? What’s the deal in the US – I feel like I have read that smoking is on the decline, so why is COPD on the rise? Might it have something to do with aging Baby Boomers who grew up in a time with different attitudes towards smoking (most of this is based on my perceptions of smoking as the media portrays it…)? Is there any hard data that helps track its rise?

    You emphasized smoking very heavily – is there any data to distinguish between smoking versus second hand smoke exposure? What about e-cigarettes or vaporized nicotine? Is there a specific disease causing agent that has been identified?

    In terms of treatment, it seems pretty grave in that the lungs just stop working. Has there been any research into stem cell therapies or regenerative medicine? Lung transplants? Or is the majority of the future going to be public awareness and anti-smoking campaigns?

    Thanks!

    1. Hey Zach,
      In terms of prevalence, there is a 2004 article titled ‘The burden and impact of COPD in Asia and Africa’ that was very helpful with the epidemiology of COPD. According to studies done by WHO and the World Bank, COPD mortality is highest in the Western Pacific and lowest in Africa currently (they do say that this may be a reflection of Africa’s high young population and low old population). However, there is also a general decrease in the incidence of cigarette smoking in developed countries and a general increase in developing countries, and the authors expect that COPD will be on the rise in Africa.
      I expect your theory of Baby Boomers and their attitude on smoking does hold water, but I could not find studies to back that up, unfortunately. The diagnosis of COPD is most commonly given to those above the age of 45, which does mean that the majority of those with the diagnosis are at least a generation old, which does support your claim.
      In terms of smoking, every article I came across did note that second-hand smoking is something to avoid as well. The authors would not say this outright, but I’m sure that smoking a cigarette will expose an individual to much more of the irritants and ROS’s than exposure to second-hand smoke, but it is not insignificant nonetheless.
      A study was conducted and published in the CHEST journal (“The Official Publication of the American College of Chest Physicians”) on the effects of e-cigarette smoking, which claims “Results showed that smoking the device for just five minutes caused an increase in impedance, peripheral airway flow resistance, and oxidative stress in the lungs of healthy smokers”. E-cigarettes often use a nicotine cartridge, and so the vaporized nicotine is just as harmful as it is in cigarettes, but because e-cigarettes don’t burn, the harmful smoke is absent, which does make them slightly better.
      Stem cell research has been undergone, but there have been very few that were approved for clinical trials. Some have shown higher FVC ratings so far, but many are inconclusive or in different phases (you can see for yourself at https://www.clinicaltrials.gov/). Lung transplants have been efficacious for patients with severe symptoms. Typically, the patients have to be under the age of 65, and they usually receive only 1 new lobe, but the results are still worthwhile. I’ll make sure to add that to the Treatments page! And as I’m sure you noticed, I was big on the smoking cessation bit, as are all of the articles I came across while researching COPD. It is the most important measure that can be taken to prevent the disease and cannot be taken lightly.

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