Talk:Chronic obstructive pulmonary disease
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Looking for newer sources
[edit]This PubMed link should give you a list of about 198 review articles that were published in the core clinical journals during the last five years. I think that would make a decent jumping-off place for updating this article.
@Jfdwolff, @Colin, @TylerDurden8823, anyone else: Would you like to look through these and see if any of them seem to be especially useful? Alternatively, there might be some value in finding a recent med school textbook, and using that for basic information. WhatamIdoing (talk) 06:13, 26 May 2021 (UTC)
- PMID 33146552 caught my eye in that list. It's the GOLD Science Committee report on how COVID-19 interacts with COPD. WhatamIdoing (talk) 06:14, 26 May 2021 (UTC)
- The 2021 GOLD Report would seem to be a good place to start and a good source. From reading the introduction, and contents list, this seems like an ideal up-to-date consensus document with a broad coverage of the topic. -- Colin°Talk 08:47, 26 May 2021 (UTC)
- PMID 32745458 "Chronic Obstructive Pulmonary Disease"
- PMID 31553837 "Update on clinical aspects of chronic obstructive pulmonary disease"
- PMID 31553836 "Update on the Pathogenesis of Chronic Obstructive Pulmonary Disease"
- PMID 30806700 "Diagnosis and Outpatient Management of Chronic Obstructive Pulmonary Disease: A Review"
- PMID 30286833 "COPD Guidelines: A Review of the 2018 GOLD Report" (more for information).
It seems we are already using the GOLD reports of various vintages and formats (summary, or full). It would be good to consolidate those with the current 2021 report and to introduce then a citation format that cites the specific page, section or chapter in the huge main report document. It would be good also to remove some of the weaker sources, such as fact sheets. There are quite a few Google Books citations used to support a single factoid, which seems rather odd. In fact, there are really too many individual sources here (200+), often supporting a single fact. Within the domain of "diagnosis, management, and prevention" I don't currently see much reason to deviate from using the GOLD report, where other experts have reviewed the literature, including reviews, systematic and otherwise, and their reports are up-to-date and global in outlook. There seems a risk with alternatives that we end up describing US or UK healthcare, for example, without explicitly saying so. Or we describe what is merely the opinions of the review authors, but doesn't reflect any consensus. Are there some other consensus documents that are up-to-date (Cochrane, NICE, SIGN, etc?). Many sources are 10 or more years old. -- Colin°Talk 22:12, 5 June 2021 (UTC)
- This NICE guideline was last updated in 2019 (And: "We checked this guideline in March 2020. We found no new evidence that affects the recommendations in this guideline.") Alexbrn (talk) 06:47, 6 June 2021 (UTC)
- NICE guidelines are often an excellent basis for an article. Maybe it'd be worth looking for how many citations could just be replaced with either the GOLD report or the NICE guideline? WhatamIdoing (talk) 04:15, 7 June 2021 (UTC)
- There is also a lot of material at American Thoracic Society's COPD page.
- The European Respiratory Society White book chapter on COPD. (this is dated 2013, so perhaps not so useful)
- CDC resources for clinicians has links to useful stuff. -- Colin°Talk 15:57, 7 June 2021 (UTC)
- There is a 2021 Annual Review of Medicine article, Advances in Chronic Obstructive Pulmonary Disease (10.1146/annurev-med-080919-112707) which is available through the WIkipedia Library. Among other things it summarizes materials from GOLD. MaryMO (AR) (talk) 18:13, 1 September 2021 (UTC)
Epidemiology
[edit]The Epidemiology section could make use of PMID 32800187 "Epidemiology of Chronic Obstructive Pulmonary Disease". There are some fascinating statistics at British Lung Foundation: Chronic obstructive pulmonary disease (COPD) statistics but this appears to be a primary source (see methodology). The NICE guideline references a couple of facts from it and perhaps we can find another secondary source to use more. I wonder if that web page could be an external link, since it contains far more accessible information than we could use. However, apart from the chart of global deaths per country, it is fairly UK-centric. -- Colin°Talk 19:18, 9 June 2021 (UTC)
Actually, I've gone off PMID 32800187 because it made a serious error. It cites PMID 28822787 saying "COPD affected an estimated 299 million people in 2015, which was an increase from 174 million or 44% since 1990". But that source (Global Burden of Disease Study 2015) says "From 1990 to 2015, the prevalence of COPD increased by 44·2% to 174·5 million individuals" (which would put the 1990 figure at 121 million). So I don't know where they got the 299 million figure from. It is interesting that that study mentions they made a major change in their definition and estimation methods which previously put the estimate for 2013 at 329 million (which our article currently states). That's a heck of a difference. Perhaps the review authors were so shocked by the smaller number that they thought it was a delta, rather than the actual figure.
The other paper that the review mentions is PMID 26755942, which is also of 2015 vintage, and estimates the figures in 1990 were 227.3 million, increasing to 384 million in 2010, an increase of 68.9%, and corresponding to a prevalence of 11.7%. It is these higher figures that the GOLD report uses. So unless we have strong reasons to prefer the lower Global Burden of Disease Study 2015 figures, I guess we should use the GOLD ones, but take the numbers with a pinch of salt.
This all makes me rather suspicious of the article text which describes a decrease in deaths from 3.1 to 2.9 million between 1990 and 2010 and then an increase back to 3.1 million by 2012. It turns out that latter text claiming a "rose again" was added independently and so represents the personal opinion of the editor. The literature makes it very clear that it is hard to compare one study with another, so editors comparing one year with another are on dodgy ground. What about the first "decrease" citing PMID 23245604. That paper does not discuss a decrease in COPD deaths. It does, however, have a huge table of deaths for various diseases, with figures for 1990 and 2010 and a %△. The 1990 figures are 3099·0 thousands and those for 2010 are 2899·9 thousands, which matches the numbers we give. However, these are estimates, and the confidence interval for the 1990 figures are (2914·2–3338·6) and those for the 2010 figures are (2669·3–3245·8). That's a range each of 424 and 576 respectively and an overlap of 332. Which means it is quite likely there was no change at all and this is just noise. Both trends that the article describe are not only original research but very likely a mirage. The GOLD report says "Globally, there are around three million deaths annually", which frankly is about as precise as we should be. -- Colin°Talk 21:17, 9 June 2021 (UTC)
I plan to replace most of the epidemiology section. The sources are very old and the material added in a random fashion over the years, making points that really should be coming from fewer sources. Some of the statements are just wrongly worded or oddly put. For example "This is most likely due to rates of smoking in women and men becoming more similar" -- but one recent study says "in 2015, 1 in every 4 men and 1 in every 20 women in the world smoke daily" which is about as far away from "similar" as it is possible to get. And "COPD is more common in older people" is an odd way of describing an age-related disease. A number of sources are research papers. I'm going to use the review I mentioned above, even though it got one of the numbers wrong, I'll double check it, along with the Gold report.
An older version of the WHO fact sheet said "The disease now affects men and women almost equally" and this translated to our lead saying "Males and females are affected equally commonly", which is a bit different. However, their data for 2000, 2010, 2015 and 2019 show consistently that men account for a third more deaths than women. The PMID 26755942 study has prevalence figures for 30+ age group of 14.3% (13.3–15.3) for men and 7.6% (7.0–8.2) for women, which is a factor of 2, not "almost equally" or "equally commonly". This remains true even when one groups the data by WHO region, by urban/rural or by income. The current WHO fact sheet does not mention sex other than to say both are affected. The GOLD report merely states that the prevalence is "appreciably higher... in men compared to women". Perhaps this vagueness comes from their commentary in the report about the wide variation in figures due not only from "differences in survey methods, diagnostic criteria, and analytical approaches" but also "widespread under-recognition and under-diagnosis of COPD...reduces the accuracy of mortality data". The report mentions that WHO publish mortality statistics for selected causes of death but their "data must be interpreted with caution because of the inconsistent use of COPD terminology." One problem is that the ICD-10 has a "broad category of 'COPD and allied conditions' (ICD-10 codes J42-46)". -- Colin°Talk 15:32, 19 June 2021 (UTC)
Risk of Death
[edit]The article says that in those with COPD "Stopping smoking decreases the risk of death by 18%". Which would be very nice, but without some qualification is a bit daft. I looked up the source here, which is a good but old (2012) review in The Lancet. It says "The first step must be smoking cessation. This intervention lessens the decline of FEV1 by about 35 mL per year, which slows disease progression and lowers mortality by 18%." It isn't clear if this is e.g., annual mortality or mortality at some period after intervention or diagnosis. So I looked up the source: The Effects of a Smoking Cessation Intervention on 14.5-Year Mortality. Even the title makes it clear this is looking at mortality at 14.5 years and also that it is examining "a smoking cessation intervention", which is not the same thing as "stopping smoking". The study had three large groups. One had "usual care" and the other two had an intervention consisting of "a strong physician message and 12 two-hour group sessions, using behavior modification and nicotine gum" over 10 weeks. One of the intervention groups also used a ipratropium inhaler and the other had a placebo inhaler.
What is notable is that most of the participants did not die of COPD. 33% died of lung cancer, 22% had a cardiovascular disease death, and 21% had cancer of organs other than the lung. Only 7.8% died of "respiratory disease other than cancer". The ipratropium had no effect. When comparing the intervention with usual care, the only significant improvement was of "deaths from respiratory diseases not related to lung cancer". The two treatment groups had 15 and 14 such deaths vs 28 in the other care group. Overall, "The hazard ratio for mortality in the usual care group was 1.18 (95% CI, 1.02 to 1.37) compared with the special intervention group." I think that is where the 18% figure is coming from, but I'm not confident in my statistics here. But important is that it is having a smoking cessation intervention that gives this particular number, not whether you actually stop smoking. It was also only significant for those under 45 years old and those with a heavy 40-a-day habit or worse, and in those with moderate COPD rather than low or high FEV1 values.
So the study then examined the participants who successfully quit for a sustained period, those who intermittently quit, and those who continued smoking. Of those in the intervention groups, only 22% were sustained quitters, 29% intermittent quitters and 49% continued smoking. The numbers for the usual care group were 5.4%, 23% and 71%. The degree of quitting was strongly and significantly related to mortality: 6 per 1000 person-years, 8 per 1000 person-years and 11 per 1000 person-years respectively. This time smoking habit did not make a significant difference to death due to "respiratory deaths not related to lung cancer" -- it was the other deaths that were avoided.
There are studies that the Lancet review cite that demonstrate clearly that stopping smoking reduces the decline in lung function. Which is very important for quality of life and disability. But it seems that in terms of death, stopping smoking didn't reduce the risk of dying of COPD, but from the other things associated with smoking. That study was from 2005. I wonder if there is a newer one, cited by newer reviews, that we can use. If anyone thinks my interpretation of the stats is wrong, please let me know. -- Colin°Talk 20:05, 19 June 2021 (UTC)
COPD and eosinophils count
[edit]in treatment modalities 2400:C600:342A:6581:1:0:7588:9138 (talk) 08:45, 18 February 2023 (UTC)
MEDRS?
[edit]For the record, an edit of mine was removed due to WP:MEDRS. However, if you look at the research paper carefully, in fact it also included a review of others' research efforts, citing at least six other papers in its discussion part:
Alveolar lavage using antibiotics based on the bronchoscope technique has been widely applied in clinic... which can effectively increase the treatment effective rate of COPD patients complicated with pneumonia, and reduce the inflammatory response (10). Fortún et al (11) treated the COPD patients complicated with type II respiratory failure using alveolar lavage combined with mechanical ventilation, and the results showed that... improved. Gasiuniene et al (12) studied the curative effect of bronchoalveolar lavage on COPD patients... found that sputum suction and lavage via fiber bronchoscope can improve the symptoms, increase the cure rate and shorten the length of hospital stay... Studies have found that bronchoalveolar lavage can effectively remove the lung mucus and ... (15,16)... the application of bronchoalveolar lavage in removing the airway and lung mucus can significantly increase the cure rate of COPD complicated with pneumonia (17)...
So I believe it is a peer reviewed, reliable, third-party published secondary source. Anyway, I'm not going to revive my original edit. — Preceding unsigned comment added by Dustfreeworld (talk • contribs) 17:27, 10 April 2023 (UTC)
- With a second look, I believe I was probably wrong in saying that it's a secondary source. I might have misunderstood what the authors meant. It seems that the citations didn't directly support BAL as a treatment for COPD (though they might support symptom improvements with BAL). Being too impulsive when edits were reverted is really no good. Hope I'm more thoughtful now :). It's not uncommon for BAL being used for treatment of conditions besides pulmonary alveolar proteinosis (e.g., pneumonia, pneumoconiosis and COPD) in some parts of the world though[1][2][3][4][5][6][7][8][9][10]. Since it's a "relatively" safe procedure, BAL may still worth more weight in the article ... (should have posted this earlier, just too busy). — Preceding unsigned comment added by Dustfreeworld (talk • contribs) 09:43, 28 May 2023 (UTC)
types and phenotypes
[edit]- The two most common types of COPD are emphysema and chronic bronchitis and have been the two classic COPD phenotypes.
Is there a meaningful difference between the two parts of this sentence? —Tamfang (talk) 22:31, 29 November 2023 (UTC)
- It doesn't seem like it. I would go with:
- The two most common phenotypes of COPD are emphysema and chronic bronchitis.
- Reconrabbit (talk) 19:18, 30 November 2023 (UTC)
- Have added to from same ref- meaning is possibly clearer with reading further down.--Iztwoz (talk) 21:17, 30 November 2023 (UTC)
- The addition is clarifying, but the sentence in question still seems to be repeating itself here, unless the concern is with the phrase "classic". Reconrabbit (talk) 21:21, 30 November 2023 (UTC)
- I have just written a new Talk on this topic, and it might interest you. I do not believe that the first part of the sentence is redundant, rather inaccurate. I think a false assumption was made based on the cited study regarding COPD imaging. You could read my argument and reply so we may correct the Wiki article if enough people agree to it.
- What I can say as answer to your question is that, yes, there is a meaningful difference between the two parts. Type and Phenotype are two different terms regarding diseases; the former describes categories, classes, etc; the latter means the varying "appearances" (varieties) of a certain characteristic or disease, resulting from differing genotypes (genes) and epigenetic factors. Different phenotypes could be the sorting factor for a disease categorization, which could make the aforementioned part redundant. But this is not the problem in this case, since I find that the first part is straight-up incorrect. Θεμιστοκλής Χατζής (talk) 21:00, 20 September 2024 (UTC)
- The addition is clarifying, but the sentence in question still seems to be repeating itself here, unless the concern is with the phrase "classic". Reconrabbit (talk) 21:21, 30 November 2023 (UTC)
- Have added to from same ref- meaning is possibly clearer with reading further down.--Iztwoz (talk) 21:17, 30 November 2023 (UTC)
Suggestion for a correction
[edit]I am a nursing student. I am doing some research on COPD for a personal project and I decided to visit Wikipedia to find ideas for things I could add, while cross-examining the details with other sources, mostly some books collected from my university. In the second paragraph of the first section of the article I ran across this statement: [...] The two most common types of COPD are emphysema and chronic bronchitis and have been the two classic COPD phenotypes. However, this basic dogma has been challenged as varying degrees of co-existing emphysema, chronic bronchitis, and potentially significant vascular diseases have all been acknowledged in those with COPD, giving rise to the classification of other phenotypes or subtypes. From what I already know, there is only a four-class classification for COPD, which mostly relates to the exacerbation and worsening of the disease and the emergence of dyspnea in relation to movement/exercise. Emphysema and chronic bronchitis are the two most basic pathophysiological characteristics of the disease (alongside the non-mentioned small airway disease), and are present alongside each other from the very onset of it. There is no such thing as two (sub)types, one characterized by emphysema only and the other by chronic bronchitis only.
To confirm whether the information on the Wiki article is correct of not, I decided to look at the cited paper (10 - Role of medical and molecular imaging in COPD). In the section "Background" the following is stated, from which I believe the aforementioned "two-type" deduction was made: The natural history of COPD is characterized by an irreversibly progressive decline in lung function, with the pathophysiology resulting in airway obstruction characterized by either the loss alveolar gas exchange units and elasticity or the development of muco-fibrotic airway remodeling. These paradigms have served as the basis for the two classic COPD phenotypes: emphysema and chronic bronchitis. However, this basic dogma has been challenged in recent years as varying degrees of co-existing emphysema, chronic bronchitis, and potentially significant vascular pathologies have been appreciated in patients with COPD.
While sharing the common terminal phenotype of irreversible airflow limitation, emphysema and chronic bronchitis are fundamentally different diseases and are suspected to have unique biomolecular mechanisms underpinning their pathogenesis.
The mentioned dogma refers to emphysema and chronic bronchitis being considered the two basic phenotypes of COPD, which is based on knowledge regarding its by-far-known mechanism, the paradigm (irreversible progressive decline... airway remodeling.). The mention of the basic dogma being challenged has to do with the latest findings of potentially significant vascular pathologies co-existing alongside the two basic phenotypes, all of which can appear in varying degrees (of exacerbation, I assume). Therefore, the deduction written in the Wikipedia article must be wrong.
While the second quoted paragraph says that the two characteristics are fundamentally different diseases, that does not mean they cannot co-exist in COPD as pathophysiological entities, only that they are physiologically independent. Nevertheless, I believe this might be what solidified to the Wiki writer that the two entities do not normally co-exist in COPD. Admittedly, I do question the report of the pathophysiology resulting in airway obstruction characterized by either the loss alveolar gas exchange units and elasticity or the development of muco-fibrotic airway remodeling, since it implies a mutually exclusive relationship between loss of alveolar gas exchange units and elasticity (emphysema) and muco-fibrotic airway remodeling (chronic bronchitis). It could be an error in syntax and/or grammar, but I do not know.
Since I am only a student, and I might have assumed something by fault, I need other people's opinion on this. Whether it be from people inside the medical field or just anyone following my argumentation process, I am open to any answer. Closing, I also need to admit that I haven't read the full study and I might be missing some important detail. I'll return to my project now, thank you for your time. Θεμιστοκλής Χατζής (talk) 20:40, 20 September 2024 (UTC)
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