COPD and asthma are two different diseases. The diagnosis of COPD is based on postbronchodialtor data (spirometry data: post bronchodilator ratio between the first second expiratory volume and forced vital capacity is low than 0.70).

Thanks Prof. Roth. The problem is that of an overlap in smoking asthmatics and those with COPD and a good bronchodilator response. This makes you wonder if they are two diseases in terms of management???

COPD and ASTHMA as per DUTCH HYPOTHESIS is a continuum of same disease though many controversies already on the list....asthma primarily involves medium sized and upper airways to start with whereas COPD primarily involves small airways. There are many inflammatory mediators common in both asthma and COPD though eosinophil plays a significant role in asthma but no role in COPD. There are some common genetic sharings in asthma and COPD.

Asthma is not fully reversible where as COPD is almost reversible. The only reversible component in COPD is airway vagal tone.

Asthma is diagnosed mainly by clinical history and family history where as diagnosis of COPD is based on spirometric evaluation.

Inhaled corticosteroids are mainstay in asthma treatment whereas in COPD they are used only when there is increased risk factors for exacerbation and there is more than 2 past exacerbations in the year before. Otherwise treatment are more or less same.

Asthma usually donot cause cor-pulmonale it may mimick PAH but COPD frequently cause cor-pulmonale.

Comorbidities of asthma and COPD are different.

Hence asthma and COPD are no-longer continuum of same disease process.

Yes Arnab. While what you note is absolutely correct but the distinction gets hazy in COPD with hyper-responsive airways or asthma with fixed obstruction and severe asthma. Neutrophilic asthma is another area of confusion. There is a relative steroid resistance in acute exacerbations of asthma while hyper-responsive COPD might respond to steroids. There are differences but they get imperceptibly hazy in many situations and hence the question.

Oh, yes. There are only in some cases when we are able absolutely correct distinct COPD and asthma... and after inflammation ( long time) fibrosis, or any type of restrictive lung function problem with obstructiv ventillation results.... And after obstruction: bronchiectasy... And what is the correct diagnosis???

Indeed, this is an ancient dilemma. Are these two conditions the same bird with different feathers (in other words different phenotypes) - according to the Dutch theory or totally different conditions - according to the British theory , Asthma being eosinophilic inflammation and COPD neutrophilic inflammation . Perhaps this question will be solved when the secrets of the human genome will be revealed. This unfortunately does not seem to be very close. In Tristan Del Cuncha there are around 40% asthmatics ( advise to read the amazing report of Prof Noah Zamel ) yet to the best of my knowledge - the asthma gene has not been identified.

Despite the many similarities and admitted overlap : COPD with asthmatic component, asthma that lost reversibility and turned into COPD with neutrophilic inflammation, smoking asthmatics and coexistence of the two conditions .

It is important to try to distinguish though as the therapeutic approaches are not identical, i.e. the inhaled steroids are advised early in asthma and late ( or not at all according to Prof Sammy Suissa) in COPD

I agree with just about everything stated above, and also feel that these are two different diseases , but as the "devil's advocate " I could argue it's still possible that all the differences represent different phenotypic presentation of the same condition. But than - it's semantics, isn't it ?

As for bronchial biopsies - I think rarely done for this indication outside a research project. However , Induced sputum may point to eosinophilic versus neutrophilic inflammation

Thanks Drs Roth and Priel. I totally agree with the points raised. COPD and mild asthma are distinctly different but the distinction gets hazy i severe asthma where you can have similar cellular and biomarker response. The inflammation is neutrophilic and sputum examination may not reveal anything different. Same is true of asthma in smokers..

While there is a Th1 response in COPD and a TH2 response in mild asthma, that in severe asthma is also TH1.

TNF alpha, IL-8 and reactive oxidant species are not known to play a major role in mild asthmatics, they are seen in both COPD as well as severe asthma and the lines of distinction get hazier.

While HAT activity and HDAC activity is bronchial biopsies of smoking asthmatics actually mirror those of COPD. Same is true of what we term as neutrophilic asthma.

And not to be left behind are those COPD patients who have a reversible component of airway obstruction with documented eosinophilic inflammation as well as steroid response.

While I would loved a rigid wall between the two, the overlap simply doesn't allow one to be erected.

I was at an Asthma meeting recently and in a debate someone metioned disagreements in the definition of difficult and severe asthma. In my opinion the issue has to do with the disease definitions of COPD and asthma and their purpose or usefulness. There are patients who fit neatly into a diagnosis of COPD or asthma and they are usually not difficult to manage.

By definition, the two diseases are distinct entities, the challenge lies in the patients with airflow obstruction who are not clearly COPD or asthma or may have a mixture of features present in both conditions.diseases. My problem with choosing the best treatment for these patients is that I am not sure the large trials adequately represent this group of patients, and I am a bit wary of subgroup analyses and meta-analyses.

(A similar problem exists with patient who have DPLD/ILD that is difficult to define).

In these situations, i feel "phenotyping" the patients in different domains and treating according to the dominant phenotype(s) is more useful than the exact diagnosis.

(Regarding biopsies, the experience from ILD has shown that tissue can be heterogenous and what you find may depend on where you take your biopsy). This is not an excuse for not making an exhaustive attempt to get the diagnosis right. As seen in studies patients who have "difficult to treat asthma", "difficult asthma" or "severe asthma", a percentage (usually greater than 10%) turn out to have another diagnosis.

To answer the question - i feel the two are different diseases, but the patients without a distinct diagnosis exist along with a continuum (typical case is symptoms suggestive of asthma, but fixed and apparently irreversible airflow obstruction, and increased markers of eosinophilic inflammation) When a patient's illness turns out to be more complex than we thought, we should be content to use descriptive terms until we are more confident of the disease diagnosis. It may hark back to the days of "cardiac asthma", "bronchial asthma", "chronic bronchitis", and "emphysema". These "labels" are still present in the ICD-10. http://apps.who.int/classifications/icd10/browse/2010/en

I also forgot to say that your opinion may depend on whether you are a patient, a physician, a statistician/coder, a researcher, the insurance company, the welfare officer etc etc. And also to say thank you for all the contributions

Bronchial asthma by definition is a reversible airway disease where as COP is not

There are phenotypic and perhaps pathogenic overlap between asthma in adults and COPD. There was a really nice pro-con in the blue journal a few years back discussing the same disease different disease hypotheses, well worth a read:

1. Kraft M. Asthma and chronic obstructive pulmonary disease exhibit common origins in any country! Am J Respir Crit Care Med 2006;174:238–240.

2. Barnes PJ. Against the Dutch hypothesis: asthma and chronic obstructive pulmonary disease are distinct diseases. Am J Respir Crit Care Med 2006;174:240–243

Me I favour the dutch hypothesis if I was forced to choose but as always there is right on both sides.

While both of these entities are characterized by airflow obstruction, the history, risk factors, and underlying pathophysiology of these 2 entities are different. While current therapies, particularly bronchodilators, treat both of these conditions, we shall see in years to come that targeted therapies based on endotype and mechanism, will differ for asthma and COPD.

Is this question valid in paediatric age group we see lot of cases of asthma to me both are different diseases

In 10- 15% of adult cases there is an overlap of asthma and COPD.

Inflammation is different; obstruction is persistent in COPD and variable, or completely reversible in COPD. Treatment have many similarities but with different outcomes.

Asthma is the most prevalent chronic disease in children. There is no COPD in infants.

There are totally different diseases in terms of pathogenesis, inflammation, risk factors (i.e. for COPD smoking, for asthma atopy/AHR), lung function, reversibility, symptoms (chronic and progressively worsening in COPD vs sporadic in asthma), epidemiology etc etc. However, in a proportion around 10% there is a coexistence (overlap of the 2 diseases) and also there is a progression of asthmatic smokers to COPD. A big question unanswered yet, is whether asthma in COPD represents a COPD phenotype or a COPD comorbidity.

We are always making the same question again and again. Are "x" asthma phenotype and "y" COPD phenotype the same disease? Do they "just look like" each other, but are quite different? If you had asthma and have smoked, what makes you now wheeze is Asthma or COPD? Always? Or for some patients the answer is Asthma and for others COPD? I feel we are just making the wrong question. I think the real question is: which pathological mechanisms do each "asthma" phenotype and each "COPD" share? Which are unique to each condition? How can we use this knowledge to improve the treatment of individual patients?

Trying to separate COPD from asthma may be sometimes irrelevant in daily clinical practice. In our experience (allergic part of US (Southeastern)), after separting out emphysematous COPD (which seems to behave differently), other COPD phenotypes with airway predomiment pathology seem to behave with much overlap similar to asthma. There is a large number of patients with chronic bronchitc COPD who have high IgE, multiple RAST positivity and sinus diseases. At least as of now, after differentiating these non-emphysematous COPD from pure emphysematous COPD, more practical decision will depend on usage of ICS anti-inflammatory. For example, what is the right dose of ICS? If you have non-emphysematous COPD patients with documented allergy, then would you more likely push up the ICS to greather than 500 MCG dose fluticasone equivalent because you may be treating an asthmatic who happened to be smoking? I think this could be a wonderful substudy to TORCH in the future....

Hello, by other hand the answer could be in our genetic charge, in our genes, which are saying how we are going to answer in the future... For me, If a person has asthma probably will develop COPD during his/her advanced old age if they have diferent polymorphisms for example in antioxidative enzymes (GSTM1, GSTP1, GSTT1, mEPHx), even we could considered several process like autophagy and apoptosis in her/his neutrophils, because and the end the immune cells like eosinophils in asthma and neutrophils in COPD are playing and important role together with oxidative stress... definitly is a complex definition and they are multifactorial diseases.We had found some preliminary results about that in Venezuelan population.

Here I'm going to share an abstract from a team,they focused in describe diferent topic, that could be usefull or interesting to read...

and a link, of Course, from a book published in ScienceDirect, Edited by:

Peter J. Barnes, Jeffrey M. Drazen, Stephen Rennard and Neil C. Thomson

ISBN: 978-0-12-079028-9

Article: Biomarkers in asthma and COPD

Alexis García, Dolores Moreno, Jenny Garmendia, Juan B. De Sanctis

[hide abstract]

ABSTRACT: In the recent years, a large number of potential biomarkers for asthma and Chronic Obstructive Pulmonary Disease (COPD) have been described. Biomarkers derive from a variety of sources (bronchioalveolar lavage fluid, sputum, exhaled breath, and blood), provide complementary information to ascertain disease diagnosis, stage, activity/progression and/or treatment responses. The present review highlights the current literature and patents in the field with potential increase in disease control and therapeutic effectiveness to be granted in the near future.

http://www.sciencedirect.com/science/book/9780120790289#ancPA3

Definitions of asthma and COPD are not static and have evolved. Thus, in one sense they are mostly different because the definitions make them so, and there is overlap because the definitions are still a little ambiguous. As we move towards molecular endotypes and more precise definitions, the overlaps will keep diminishing

Asthma can be totally reversible, where as there is disruption of Bronchial structure in COPD. Though the features with which the patient presents are similar Asthma & COPD are two different phenomenon(theoretically). There is an emerging concept of Asthma COPD Overlap syndrome, where one can find symptoms of both Asthma & COPD in a patient