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ERS Chiesi Rapport

Even during 2022, Chiesi´s Nordic Medical Respiratory Team will provide you with digital report from congresses and scientific meetings to highlight the latest scientific findings and treatment guidelines updates.

First off is the latest ERS Satellites symposium covering asthma, COPD, environment & climate change, amongst other, will take place digitally on February 24th.

Mechanisms that underpin symptom control and exacerbation risk in asthma


The asthma session started off with Associate Professor David J Jackson from King`s College London talking about mechanisms linked to symptom control and exacerbation risk in asthma. He showed that the link between eosinophilic inflammation and asthma has been known for more than 100 years and how recent research has provided further evidence that blood eosinophil counts and exhaled nitric oxide relate to both exacerbation risk and symptom control in asthma.

Today, it is well established that increased T2 inflammation is the key risk factor for asthma exacerbations. On the other hand, respiratory virus infection is the most common trigger of an asthma exacerbation. Jackson presented evidence for mechanisms linking these two facts, i.e. a combination of an impaired anti-viral interferon response and an inappropriate T2 inflammatory response to virus. A study performed by Jackson and colleagues in 2014 showed increased viral replication following experimental rhinovirus infection in subjects with asthma, representing in vivo evidence for an impaired antiviral response in these subjects. In contrast, rhinovirus infection induced type 2 cytokines and airway eosinophilia in the same asthmatics.

In line with this, other studies have shown that 1) the anti-viral interferon response in bronchial epithelial cells is diminished in the presence of IL-4 and IL-13, 2) that type I interferon restricts type 2 immunopathology through the regulation of group 2 innate lymphoid cells and 3) that targeting IL-4/IL-13 or the IL-5/eosinophilic pathway reduces exacerbations in the presence of T2 inflammation. Hence, anti-T2 therapies may work by preventing virus induced T2 inflammation and/or augmenting anti-viral immune responses.

Even though for many patients, asthma symptoms correlate with T2 inflammation and improve with ICS / T2 biologics, this is not the case for all. Towards the end of the lecture, Jackson discussed possible mechanisms that underpin symptom control in the absence of T2 inflammation. Overall, he concluded that the discordance between T2 inflammation and symptoms may be partly explained by pulmonary and extrapulmonary co-morbidities driving respiratory symptoms, such as obesity, anxiety, breathing pattern disorder and severe reflux.

Ingvild Bjellmo Johnsen
Medical Advisor

ERS clinical practice guidelines on asthma diagnosis in adults


The second lecture of the asthma session was given by Professor Renaud Louis from the University of Liège. He took us through the ERS Guidelines for Asthma Diagnosis in Adults worked out by an ERS task force set up in 2018. The task force, which included not only chest physicians but also general practitioners, respiratory nurses, and patient representatives, aimed at developing an evidence-based pragmatic clinical guideline by adopting the GRADE methodological approach using PICO (Patient Investigation Comparison Outcome).

The 8 PICOs chosen as measurements for potential help in the diagnose of asthma in adults with episodic
/chronic suggestive symptoms were the following:
1) airway obstruction measure by spirometry
2) PEF variability testing
3) fractional exhaled nitric oxide (FeNO)
4) blood eosinophil count
5) total serum IgE
6) combining FeNO, blood eosinophils and IgE
7) bronchial challenge testing
8) sGaw and RV/TLC by body plethysmography

The main recommendations to the questions addressed above were:
1) Spirometry should be performed to detect airway obstruction as part of the diagnostic work-up of adults with suspected asthma. An FEV1/FVC < LNN or < 75%, higher than the commonly used 70% threshold, should be considered supportive of asthma, and should prompt further testing. Importantly, a normal spirometry does not exclude asthma.

2) PEF variability should not be recorded as the primary test to make a diagnosis of asthma (PEF may be considered if no other lung function test is available including spirometry and bronchial challenge testing and should be monitored over a two week period and variation of 20% considered supportive of asthma).
3) In patients suspected of asthma, in whom the diagnosis is not established by the initial spirometry combined with reversibility testing, FeNO should be measured as part of the diagnostic work up of adults.

4) Blood eosinophil count should not be measured to make a diagnosis of asthma (but can contribute to phenotyping).
5) Serum total IgE should not be measured to make a diagnosis of asthma (but can contribute to phenotyping).
6) Combining FeNO, blood eosinophil count and total serum IgE is not recommended to make a diagnosis of asthma.
7) Bronchial challenge should be performed in secondary care to make a diagnosis of asthma when the diagnosis was not previously established in primary care. A provocative concentration of metacholine (PC20-M) or histamine (PC20-H) < 8 mg/ml in steroid naive patients and < 16 mg/ml in patients receiving regular inhaled corticosteroids supports a diagnosis of asthma.
8) Measuring sGAw and RV/TLC by whole body plethysmography in secondary care is not recommended to make a asthma diagnosis when diagnosis was not previously established.

In a summary of the guidelines presented, the task force highlights the critical importance of using spirometry in the diagnostic path while recognising that the reversibility criterion, though being meaningful, has a limited sensitivity to confirm diagnosis in most of the cases. When spirometry and bronchodilation test fail to confirm the diagnosis, the next step may rely on measuring fraction exhaled nitric oxide (FeNO), recording peak flow variability (PEF) or performing bronchial challenge depending on local resources, the latter offering the greatest robustness to ascertain the diagnosis. Beyond the diagnosis itself the task force recognise the interest of inflammatory phenotyping even in the mildest form of the disease.

Ingvild Bjellmo Johnsen
Medical Manager

How to manage a patient with asthma


In this interactive presentation of a patient case, we were demonstrated how to apply the current GINA recommendations for treatment of asthma. It was underlined that any initial treatment needs to be followed up first after three to six months, as symptoms are consequences of the underlying inflammation, following a certain time course in treatment response.

While night symptoms, FEV1 and PEF can improve within days or weeks, the use of SABA or the presence of airway hyperresponsiveness will first respond after years of treatment (Woodcock AJ, Clin Exp All Rev 2001; 1:62 and Bateman EJ, Asthma 2007;44:667). We were also introduced to the mechanism of synergistic effects of a combination treatment with ICS/ LABA (Barnes PJ, European Respiratory Journal 2002 19: 182-191): ICS suppress the chronic inflammation of asthma and reduce airway hyperresponsiveness. LABA has bronchodilator action, inhibit mast cell mediator release, plasma exudation and may reduce sensory nerve activation. Corticosteroids increase the expression of β2-receptors by increasing gene transcription. Experimentally this protects against the loss of β2-receptors in response to long-term exposure to β2-agonists. This is important in preventing loss of β-agonist effects on the non-bronchodilator actions of LABA.

Importantly, if a patient does not gain control when treated, the diagnosis of asthma must be re-confirmed. On the other hand, if good control was achieved, a careful step down of treatment is indicated to avoid over-treatment.

In general, asthma treatment needs to be personalised for every patient. Different treatment options were presented, including single maintenance and reliever therapy, and the addition of LAMA such as tiotropium or a triple combination with ICS/LABA/LAMA. In severe asthma requiring step 5 treatment, phenotyping using biomarkers of the underlying inflammation is crucial, to be able to choose the right treatment option, eg different monoclonal antibodies interfering with Type 2 inflammation.

Considering the COVID-19 pandemic, GINA concludes that people with asthma do not have an increased risk for COVID-19, severe COVID-19 or COVID-19 related deaths. Patients should be advised to continue taking their prescribed medications. Vaccines are safe in people with allergies. Based on risks and benefits, GINA recommends COVID-19 vaccination to people with asthma, and booster shots if offered.

Barbara Fuchs
Medical Advisor

Horizon scanning: what may be coming to practice soon


In this presentation, we had a peek on the most recent trends and evidence for upcoming treatment approaches of asthma.

The importance of a personalised management approach was underlined that involves all aspects of an individuum, and different concepts introduced.

To identify treatable traits from the three different dimensions “pulmonary”, “extrapulmonary” and “risk factor/behaviour” can improve care outcomes importantly. Common treatable traits include eg. airflow limitation, airway inflammation, mucus hypersecretion, obesity, gastroesophageal reflux disease, anxiety/depression, and non-adherence to treatment, among others. Comprehensive multi-
disciplinary management approaches will also cover comorbidities that potentially can make asthma worse, such as nasal polyposis or anxiety.

Another upcoming trend which needs to be validated in the clinics first is “risk profiling” (Coulliard et al , Thorax 2022 Feb;77(2):199-202), where the risk of exacerbations can be estimated by taking into consideration the presence of risk factors, blood eosinophil counts and FeNO measurements. Other studies have identified clusters of patients experiencing of exacerbations as being “moderately active, obese and distressed” and “inactive, obese and distressed” (Freitas et al. ERJ 2021 Jan 21;57(1):2000240.)

During the lecture, asthma remission was introduced as a treatment goal opposed to disease control, and the treat-to-target approach was introduced which is familiar from the area of rheumatology. In future, early intervention of asthma to prevent worsening of disease could be a concept. We closed the presentation by having a look on potential benefits digital health can add to asthma therapy.

Barbara Fuchs
Medical Manager


Causal pathways and mechanisms for respiratory health effects


Professor of Public Health Jaakkola at University of Oulu, Finland initiated the session with an overview of impact and causal pathways and mechanisms of the environment and climate changes on health effects, including those on respiratory diseases. Of today, it is a fact that human activities cause global warming, which is expected to reach 1.5°C in the near future. It is evident to most that the increasing global temperature can lead to an elevated incidence of extreme weather events like droughts, fires and floods. These changes can further increase the amount of dust storms, air pollutions and indoor mold problems, which are known environmental factors that worsen symptoms of many respiratory diseases.

Professor Jaakkola provided a three-armed framework on respiratory health effects caused
by climate changes:
1) Direct environmental effects (via extreme weather, heatwaves, air pollution)
2) Effects on natural biophysical systems (via ocean temperature increase and pH change, soil health, biodiversity, etc.)
3) Effects on social, infrastructural and economic conditions (based on the same factors as above)

As an interesting and maybe even surprising example of direct health effects caused by climate change Jaakkola presented a study by Simo Näyhä published in Journal of Circumpolar Health in 2005. Here, Simo showed that small but sudden changes in local climate and temperature had a measurable impact on mortality rates. Simo even suggest that each location on the planet has an optimal temperature, which the local population is adapted for. Interestingly, the optimal temperature can vary from 14°C to 22°C between Oulu and Athens, respectively.

As an example of effects on natural biophysical systems Jaakkola stated that climate changes are observed to affect the pollen season, which if leading to either a prolonged exposure or sudden drastic increase in pollen will affect many individuals with respiratory diseases, in particular those with asthma and allergies.

Finally, Jaakkola highlighted a study from Schleussner and colleagues published in PNAS in 2016 showing that effects on social and economic conditions caused by climate-related disasters enhance the risk of armed conflicts.

Nicolai Krogh
Medical Science Liaison


Horizon scanning and next steps
– Environmental pollution and climate change


Beside of being Professor in Environmental Epidemiology at University of Copenhagen, Denmark Prof. Andersen is also a chair member of the ERS Environment and Health Committee. As the last presenter in this session, she focused on air pollution and climate change, which is closely linked through burning of fossil fuels producing carbon and particle emission that is the major source of outdoor air pollution but also driver of global warming. In Europe, the health burden of air pollution is enormous with up to 370,000 related deaths and millions of individuals suffering from associated diseases such as asthma, COPD, pneumonia, etc.

Respiratory disease patients are notably susceptible to air pollutants, which are threatening with lifelong burdens. As long-term exposure in children supresses the immune system, impair lung growth and thus lung function the risk of developing asthma or other airways disorders is increased. In adults, long-term exposure increases risk of asthma, COPD, lung cancer, etc. In respiratory disease patients, short-term exposure can trigger symptom worsening and thus the need for medication or even hospitalization.

In a recent article from 2021, published in the European Respiratory Journal, Prof. Andersen and colleagues point out that the current accepted EU air-pollution-limit-values give little, if any, protection of our health – there are no safe levels of these pollutants, she says. Thus, the authors are recommending the EU to align with the WHO Air Quality Guidelines announced in 2021. The presenter stressed the importance of this as WHO has warned that climate change poses potentially the greatest threat to global health in this century. But she could happily remind us that COP26 in Glasgow held in 2021 was the first Climate Change Conference considering the impact of climate change on health. Europe aims to be the first climate-neutral continent by 2050 with net-zero greenhouse emissions and to cut emissions to 55% of 1990 levels by 2030.

Regarding the effect of climate change on health issues more research is needed. In particular, a holistic approach considering exposure to multiple air pollutants, pollen, etc. – the so called “exposome” will be crucial.

Nicolai Krogh
Medical Science Liaison

State of the art in diagnosis of COPD:
assessment of a patient with COPD and co-exiting conditions


Dr Han started her presentation with a review of the GOLD guideline and a closer look on how it frames comorbidities.

Some comorbidities are more common in COPD and there are probably some shared mechanism or risk factors that make these comorbidities more common. Additionally, some comorbidities may not be more prevalent, but their presence may impact the course or the treatment of COPD.

How common are comorbidities in COPD?
98% of patients with COPD suffer from
≥1 comorbidity.

There is a wide variety of comorbidities and they shift with the disease stage. In GOLD stages 1 and 2, the cause of death in 22% of patients is cardiovascular disease and 18% die of lung cancer. In GOLD stage 3-4 patients, respiratory disease is the dominant cause of death.

Dr Han made a deep dive in different groups of comorbidities.

COPD and Cardiovascular Disease
Patients with COPD are in risk for all sorts of cardiovascular diseases. Impaired lung function itself is an independent risk factor for cardiovascular mortality. For 90 days after a COPD exacerbation patients with high risk of ischemic heart disease have an increased risk for a cardiovascular event. This should be taken into consideration when a patient is presenting with dyspnea. As a recommendation a validated cardiovascular risk calculator should be used (age, gender, cholesterol, blood pressure smoking history and diabetes). Prevalence of systolic and diastolic heart failure in COPD patients is high, ranging between 20-70%. Diastolic dysfunction may be as prevalentas 60-90% and is thought to be related to hyperinflation of the lungs and this may impair cardiac filling. There is some evidence suggesting that some of the mechanisms of inflammation may contribute to myocardial fibrosis, whicht can further contribute to diastolic dysfunction. Presence of diastolic dysfunction has also been associated with hospitalisations for COPD exacerbations and longer stays in hospital.

COPD and Metabolic syndrome and diabetes
Metabolic syndrome (central obesity, hypertension, dyslipidemia and hyperglycemia) and diabetes are more frequent in COPD. The prevalence of diabetes in COPD is ~30% and it affects COPD prognosis i.e. patients have greater risk of hospitalisation and mortality when both diseases are present. Recommendation for diabetes screening in patients with COPD follows general population guidance.

COPD and osteoporosis
The prevalence of osteoporosis is 2-5 times higher in COPD patients and they are at risk for vertebral fractures. Osteoporosis is associated with emphysema, low BMI and low-fat free mass. Screening of osteoporosis in COPD patients follows the same recommendations as for general population.

COPD and Gastroesophageal reflux (GERD)
GERD is an independent risk factor for exacerbations and is associated with worse health status.
Proton pump inhibitors may decrease the risk of exacerbations.

– habitual snoring
– witnessed apnoea, gasping or choking during sleep
– diagnosed hypertension

Dr Han referred to a study (Marin JM et al AMJCCM 2010; 182:325-331), which suggested that patients who had both COPD and sleep apnoea have improved survival and exacerbation free survival when they were treated with CPAP.

COPD and depression
It is well known that many COPD patients have anxiety and depression, particularly patients who have more severe illness. This is associated with poor prognosis. COPD patients are 1.9 times more likely to commit suicide than people without COPD. It is recommended that all patients should be screened for depression during routine visits.

There is a vicious circle between symptoms, disturbed sleep and depression in COPD. Over 70% of COPD patients report nocturnal awakening and there are multiple mechanisms that may contribute to poor sleep including age, medications, comorbidities, wheezing and cough. Also psychological distress related to COPD may contribute in this. Sleep disturbance is predictive of COPD exacerbations and all-cause mortality.

COPD and lung cancer risk
COPD patients who have emphysema have increased risk for lung cancer. US Preventive Services Task Force has recommended annual low dose CT for lung cancer screening for adults 50-80 years old who are at high risk of lung cancer and have at least 20 pack-year smoking history.

Pekka Ojasalo
Medical Advisor

State of the art in diagnosis of COPD:
assessment of a patient with COPD and co-exiting conditions


In his presentation Prof. Wilkinson wanted to share some of the new insights about the role of microbiome in controlling the nature of inflammation in COPD and how treatment interacts with that. The disease burden of COPD remains great despite current therapies. Part of the problem is that there are no modifying treatments which could make enormous difference to the trajectory of the illness. There is still a developing understanding of the mechanisms which drive disease progression, particularly the disease aetiology and risk of exacerbations. In recent years there have been real advances by using the biological tools that are now available. The airway itself is not a benign or passive environment and is constantly being challenged by the infectious agents. It has its own microbiome, which in some cases can be beneficial and in others less so. In his presentation Prof. Wilkinson aimed to explore the role of this phenomenon in the context of this disease and how the treatments that are currently used can influence the microbiome.

The current treatment approach is blunt in managing exacerbations. Current treatment paradigm highlights self-diagnose and self- management, i.e. patients are advised to monitor their symptoms and make their own decision when to use rescue medication, such as antibiotics and steroids. The concept of a precision medicine approach is thus very limited. This often leads to over-treatment, late-treatment and there is a risk for overuse of antibiotics. This in turn leads to treatment failure, because right treatments have not been used in the right endotype or type of exacerbation.

It is known that the lung is not a sterile environment. A close relationship between bacterial colonisation and lung function changes has been shown.

What is a microbiome and why it is important to health? It is a rich polymicrobial community and plays a vital role in a number of biological processes. In terms of amount of genetic diversity and DNA, there is far more microbial diversity in the human body than our own genetic material. Thus, it has a very fundamental role in our health and well-being. The microbiome is essential to the common function of all our organs. It has a broad role in the lung and in the gut competitively excluding r pathogens. It has a role in development and maintenance of host defences. It has a role in maintaining health of cells in providing vital nutrients and modulates inflammation. This is well studied in the gut but may have a key role also in the lung.

By understanding more about the microbiome context in lung diseases we may understand more about the maintenance of a healthy environment.

The advances in sequencing technology and other platform technologies have driven the understanding of the microbiome. 16s ribosomal RNA-sequencing allows sequencing the genes that are expressed in bacteria, which vary between different species. It is possible to describe the nature (diversity, abundance) of the microbiota which exists in the lung from the biological samples e.g. sputum.

Microbiome is a very dynamic phenomenon, particularly in the lung. Breathing in cigarette smoke and pollution, eating and drinking, and medication intake can affect the microbiome itself.

Microbiome is quite distinct in different disease states. Several studies have established that microbiome of COPD, asthma, cystic fibrosis and ILD are quite different from each other and understanding these differences is important – when do they develop and how could they be modulated? This may give some insights into the role of microbiome particularly in COPD.

What can change this diverse environment? If a selection pressure is added in the lung by antibiotics, immune or inflammatory impact, the microbial environment becomes much less diverse.

Prof Wilkinson’s AERIS study looked at the diversity of bacterial presence in the microbiota of the airway. In the study they found that when COPD progresses from moderate to severe stage, there was a change in the microbial composition, i.e. loss of diversity which is extended in severe disease. As disease progresses particular bacterial groups, such as proteobacteria are extended.

There is a clear relationship between the microbiome and the patternof inflammation. Abnormal microbiome associates with poor outcome e.g., proteobacterial dominance is associated with increased mortality.

There is concern about steroid use in COPD driven largely by the relationships between the high-dose steroids and the risks of pneumonia. There are also associations between the use of OCS and poor outcomes of certain exacerbation types. Meta-analysis data have shown, that patients who have low eosinophil count and receive prednisolone are more likely to be proteobacteria dominant and have higher level of OCS treatment failure compared to those patients who have high eosinophil counts. ICS use is associated with higher abundance of proteobacteria. There is at least an associative relationship between the use of steroids and a more dysbiotic environment. There are number of mechanisms by which steroids can affect microbial environment.

There are different groups of patients that respond quite differently to the use of steroids. Patients with proteobacteria-dominant microbiota can be quite vulnerable to steroid effects and they might see a rise in bacterial load. Other patients with more benign bacteria have eosinophilic phenotype and may benefit more from the use of steroids. Further research is needed.

Antibiotics might have a significant effect on healthy microbiome. This has been studied most widely in the gut but there is certainly important impact in the lung as well. Using antibiotics may worsen microbial dysbiosis and reduce the diversity of these populations. Recurrent exacerbations and the frequent us of antiobiotics increase the rate of progression to a dysbiotic microbiome.

What could be done differently? Laboratory tests are available for estimating the nature of microbial dysbiosis in the patients. This may help to target therapies more effectively.

Key messages of Prof Wilkinson’s presentation:

– Diverse and balanced microbiome in lung and gut is vital for health
– Microbial dysbiosis occurs in COPD and is asso ciated with loss of bacterial diversity, inflamma- tion and poor outcomes
– Microbial dysbiosis can be accentuated by indiscriminate use of corticosteroids and antibiotics
– Further understanding of microbial-host interactions are needed
– Assessing the microbiota and maintaining its health/restoring its balance offers new opportunities to treat COPD

Pekka Ojasalo
Medical Advisor

How to manage a patient with COPD


The presentation by Dr Franssen pictured the challenges in identifying and choosing treatment options for COPD patients. In this interactive session, he presented two patient cases from his clinic, one patient experiencing a high degree of dyspnoea, but only few exacerbations, and the other being a frequent exacerbator with massive impact on health-related quality of life. He asked the audience for advice to find the best treatment option. It became evident that there is not always an easy answer to this task.

– Dr Franssen highlighted the clinical challenges, such as
conflicting priorities of care (address obesity or
prioritise smoking cessation with the risk of
gaining more weight?)
– should massive medication be stepped down if the patient is still symptomatic?
– can pulmonary rehabilitation be offered if the patient is still smoking?
– the difficulty to evaluate ICS efficacy and
adverse events in individual patients. Should ICS
treatment be continued based on a single biomarker assessment? Are we then treating a lab value rather than a patient?
– Consider extrapulmonary features of the disease,
such as anxiety/depression, and other comorbidities

Dr Franssen both referred to the GOLD recommendations and the ERS guideline for ICS withdrawal in COPD (Chalmers et al, Eur Resp J 2021), but reminded the audience that these recommendations can give suggestions, but the treatment of each and every patient needs to be individualised. COPD remains a disease with very high burden for the patient, and therapy and management of the disease does not stop when the level of maximal pharmacotherapy has been reached. Dr Franssen ended his talk saying: “You can always do more for your patient.”

Barbara Fuchs
Medical Manager

Horizon scanning: What needs to happen with COPD?
Identification of early COPD disease: how to change the lung function trajectories?


The last lecture of the COPD session was given by Professor Erik Melèn from Karolinska Institutet who presented a horizon scanning of lung function trajectories for identification of early COPD. He started his talk by proposing that pulmonary physicians might need to look back to look forward when it comes to COPD.

From childhood to adulthood, we know that low lung function trajectory is influenced by several factors including genetics, preterm birth, early life environmental exposures, lower respiratory tract infections and childhood persistent asthma. Melén presented results from a study of different lung function trajectories from childhood to adulthood, showing that individuals with the trajectories “persistently low lung function”, “below average lung function” and “early below average, accelerated decline” represented 75 % of COPD cases at 53 years of age (Bui et al., 2018). Among the individuals with the trajectory “early below average, accelerated decline” almost 50 % had COPD at the age of 53. These findings suggest that early life factors including allergic disease, lung infections, parental asthma and maternal smoking influences unfavourable lung function trajectories.

Melén asked if these trajectories can be changed and if that is a way to prevent COPD? Results from the BAMSE cohort show that the trajectory characterized by lung function failure is influenced by preterm birth, early bronchitis/pneumonia, sensitization, and childhood asthma. Melén pointed out that there is a potential for lung function catch-up. However, apart from avoiding exposures, early life infections and pneumonia, more research is needed to understand this important area. Moreover, results from the BAMSE cohort reveal that among young adults aged 21-24 years, 5,5 % have chronic bronchitis and 2 % have irreversible airflow limitation according to COPD-criteria. Both conditions were associated with cough, phlegm, recurrent airway infections and respiratory symptoms. Also, looking at exposure, a close correlation was found between these conditions and air pollution exposure, RSV bronchiolitis/pneumonia and active smoking.

Looking at childhood asthma, a study published by McGeachie et al. showed that 11% of subjects with asthma at age 5-6 years had COPD according to spirometry at the age of 30. Another study published by Tai et al. demonstrated that among children with severe asthma, 44 % had COPD by the age of 50. Moreover, the CADSET (Chronic Airway Disease Early Stratification) study looking at the prevalence of the obstructive phenotype (FEV1/FVC<LLN) from early childhood (<5 years) to young adulthood (24 years) in almost 50 000 subjects showed that 5-10 % were classified of having an obstructive phenotype with no clear age trend.

Finally, Melén introduced a new concept called the GETomics, which is a proposed holistic strategy that considers all gene (G) – environment (E) interactions that an individual may encounter through the life spam (T) to better understand the pathogenesis of COPD.

Melén summarised the lecture by stating that pathophysiology of COPD starts early in life, and that COPD in young individuals < 50 years of age does exist. Childhood asthma is a major risk factor of COPD, especially severe asthma, which might be considered as a pre-COPD phenotype. Furthermore, Melén suggested that it might be time to revisit the ACOS concept, also in children. Changing trajectories and preventing COPD will likely be a multifaceted effort, including the catch-up vs growth failure vs decline. COPD phenotyping beyond spirometry is needed requiring integration of clinical data omics and imaging. Hopefully we can soon apply a precision medicine approach to provide the right treatment and/or intervention for the right patient.

Ingvild Bjellmo Johnsen
Medical Advisor