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Take a look at a selection of our recent media coverage:

Lung progenitor cell transplant may provide a cure for COPD, study suggests

14th September 2023

Using lung progenitor cell transplantation in patients with chronic obstructive pulmonary disease (COPD) appears to improve symptoms and could lead to a cure, according to a study presented at the recent European Respiratory Society (ERS) International Congress 2023 in Milan, Italy.

It has been previously shown that P63+ progenitor cells, which are used by the body to repair and replace damaged tissue, are able to induce lung epithelium regeneration in animal models.

Consequently, in this first-in-human phase 1 clinical trial (abstract OA4297), researchers set out to investigate the efficacy and safety of taking autologous P63+ progenitor cells transplanted into the lungs of patients with COPD.

They demonstrated that the use of P63+ progenitor cells in those with COPD enabled patients to breathe better, walk further and have improved quality of life. This is the first time researchers have shown it‘s possible to repair damaged lung tissue in patients with COPD using their own lung cells.

The trial included 17 COPD patients with a diffusing capacity of the lungs (DLCO) of less than 80% of the predicted value and three control patients. Individuals were autologously transplanted with the P63+ progenitor cells through bronchoscopy, followed by subsequent assessment for both safety and efficacy within 24 weeks.

The cell treatment was well tolerated by all patients and following transplantation, the median DLCO of treated patients increased from a baseline value of 30.00% to 39.70% after 12 weeks and still further to 40.30% after 24 weeks.

When it came to quality of life, the average St George’s Respiratory Questionnaire score of those receiving cell therapy group decreased from 51.3% at baseline to 44.2% after treatment. The median six-minute-walk distance increased from 410m to 447m at 24 weeks.

In addition, two patients with mild emphysema showed resolution of the lesions at 24 weeks by CT imaging.

Progenitor cell transplant offers better quality of life

Professor Wei Zuo, chief scientist of the study and professor in the school of medicine at Tongji University, Shanghai, China, told the congress: ‘P63+ progenitor cells are known for their ability to regenerate the tissues of the airways, and previously we and other scientists have shown in animal experiments that they can repair the damaged epithelial tissue in the alveoli.‘

He added: ‘We found that P63+ progenitor cell transplantation, not only improved the lung
function of patients with COPD
, but also relieved their symptoms, such as shortness of breath, loss
of exercise ability and persistent coughing. This means that the patients could live a better life, and
usually with longer life expectancy.

‘If emphysema progresses, it increases the risk of death. In this trial, we found that P63+ progenitor cell transplantation could repair mild emphysema, making the lung damage disappear. However, we
cannot repair severe emphysema yet.‘

Commenting on the ‘encouraging‘ results, Professor Omar Usmani, head of the European Respiratory Society group on airway disease and professor of respiratory medicine at Imperial College London, UK, added: ‘COPD is in desperate need of new and more effective treatments, so if these results can be confirmed in subsequent clinical trials it will be very exciting. It is also very encouraging that two patients with emphysema responded so well.

‘A limitation of this study is that the uptake of the progenitor cells when they were transplanted back into the patients is uncontrolled. So we do not know whether the lungs of some patients responded better to the transplantation than other. We hope this information may become apparent in future studies.‘

The researchers are planning a phase II trial of the treatment, which will evaluate its efficacy in a
larger group of patients.

European Respiratory Society issues consensus statement on climate change and respiratory health

11th September 2023

Guidance on how global warming can be addressed in clinical practice has been outlined by the European Respiratory Society (ERS) in its latest consensus statement on climate change and respiratory health.

Published in the European Respiratory Journal, the statement describes climate change as ‘an unfolding major planetary and health crisis’, and a major threat to those with common lung conditions.

This, it says, is linked to the frequent and extreme weather events, prolonged aeroallergen seasons and poorer air quality associated with climate change, which can lead directly to a worsening of health and an increased risk of death.

Traditionally, clinicians have been involved in climate change adaptation strategies such as identifying vulnerable groups and providing advice on how they can protect themselves during heatwaves, for example.

However, the ERS says this clinical role has now expanded to focus on both human and planetary health, which includes contributing to the reduction in greenhouse gas emissions.

According to the ERS, subsequent changes to clinical practice could therefore include promoting green prescriptions such as inhalers; focusing efforts on smoking eradication; and encouraging patients, where appropriate, to engage with nature, take active modes of transport and make more sustainable food choices.

Professor Zorana Jovanovic Andersen, chair of the ERS Environment and Health Committee and professor of environmental epidemiology at the University of Copenhagen, who was one of the authors, said: ‘As respiratory doctors and nurses, we need to be aware of these new risks and do all we can to help alleviate patients’ suffering. We also need to explain the risks to our patients so they can protect themselves from adverse effects of climate change.‘

Climate change and lung health

The consensus statement also highlights that climate change will have a disproportionately greater adverse effect on individuals living with respiratory diseases such as asthma and chronic obstructive pulmonary disease (COPD).

It outlines some of the health risks of climate change such as a decline in lung function, increases in allergic responses and/or new cases of chronic (asthma, COPD, lung cancer) or infectious (pneumonia, influenza, tuberculosis, Covid-19) respiratory diseases.

It also identifies a higher risk of exacerbations for existing respiratory diseases, increased use of medication, emergency department visits, hospitalisations and death.

The fact that children are more susceptible to the impact of climate change on lung health is also highlighted, including the fact that the prevention of chronic respiratory disease should start as early as possible as many chronic lung diseases in adults have childhood origins.

The burden of global warming

Several previous reviews have provided extensive summaries of the different mechanisms by which climate change affects respiratory health, as well as outlining adaptation strategies. The latest statement provides an overview of all major pathways linking climate change with lung health.

While it summarises all of the available evidence, the authors also recognise some gaps in current knowledge. For instance, there is the need for further research to fully map the burden of climate change on respiratory diseases under different global warming scenarios and to understand underlying biological mechanisms, as well as identifying pathways of adaptation that can be translated into public health policies.

Professor Jovanovic Andersen, added: ‘Climate change affects everyone’s health, but arguably, respiratory patients are among the most vulnerable. These are people who already experience breathing difficulties and they are far more sensitive to our changing climate. Their symptoms will become worse, and for some this will be fatal.

‘Air pollution is already damaging our lungs. Now the effects of climate change are becoming a major threat to respiratory patients.’

Indeed, the deleterious respiratory effects of the particulate matter contained within air pollution, are already known to provide a mechanism through which lung cancer can develop among individuals who have never smoked.

Study suggests lower vitamin K levels linked to reduced lung function

14th August 2023

Patients who have low vitamin K levels have a reduced ventilatory capacity and are more likely to self-report asthma, COPD or wheezing, according to a study by researchers from Copenhagen University Hospital and the University of Copenhagen.

The study, which was published in the journal ERJ Open Research, set out to assess whether lower vitamin K status was associated with lung function and lung disease/symptoms. The researchers focused on the measurement of dephosphorylated-uncarboxylated MGP (dp-ucMGP), which serves as an inverse plasma biomarker for vitamin K status.

The team recruited members of the general population and invited them to a health examination to complete questionnaires and undergo spirometry, together with measurement of plasma dp-ucMGP. Lung function assessments were the forced expiratory volume during the first second (FEV1) and forced vital capacity (FVC). FEV1/FVC-ratio was calculated as the ratio between these two measurements.

In the questionnaires, researchers asked participants whether they had ever been diagnosed with either asthma or COPD, or whether they had experienced wheezing during the last 12 months. They then used multivariable logistic regression to assess the associations between dp-ucMGP and the dichotomous variables, COPD, asthma and wheezing.

Vitamin K status and lung function

A total of 4,092 individuals aged 24-77 years were included in the analysis.

Lower vitamin K status, reflected by higher dp-ucMGP levels, was associated with lower FEV1 and FVC. However, dp-ucMGP was not associated with the FEV1/FVC-ratio. A lower status was significantly associated with COPD (Odds ratio, OR = 2.24, 95% CI 1.53 – 3.27), wheezing (OR = 1.81 95% CI 1.44 – 2.28) and asthma (OR = 1.44 95% CI 1.12 – 1.83).

Lead author of the study, Dr Torkil Jespersen, said: ‘We already know that vitamin K has an important role in the blood, and research is beginning to show that it’s also important in heart and bone health, but there’s been very little research looking at vitamin K and the lungs.

‘To our knowledge, this is the first study on vitamin K and lung function in a large general population. Our results suggest that [it] could play a part in keeping our lungs healthy.‘

The vitamin is found in leafy green vegetables, vegetable oils and cereal grains. It plays a role in blood clotting, although, clinically, vitamin K antagonists are used as anticoagulants to control bleeding.

Capnography machine learning model provides high diagnostic accuracy for COPD

15th June 2023

Using capnography breath data, a machine learning algorithm diagnosed chronic obstructive pulmonary disease (COPD) with an accuracy of 91%.

In the study, published in Respiratory Research, UK researchers used the N-Tidal device and applied machine learning techniques to capnography data to help distinguish the CO2 recordings (i.e. capnograms) of patients with and without COPD.

The team utilised capnography data from four clinical studies and developed machine learning algorithms to discriminate COPD from non-COPD, which comprised a group of patients who were either healthy or who had other conditions including asthma, heart failure, pneumonia, breathing pattern disorder and motor neurone disease.

The team developed three machine learning models and the predictability for COPD was assessed using receiver operator characteristic (ROC) curves and the subsequent estimates of sensitivity, specificity negative and positive predictive values.

Capnography machine learning accuracy

A total of 88,186 capnograms were collected from 295 patients, with each patient providing an average of 299 capnograms over 179 days.

The highest accuracy (91.3%) was provided by an XGBoost model with a corresponding sensitivity of 91.5% and a specificity of 91.4% for the diagnosis of COPD. Even on an unseen test data set, the XGBoost model still had an accuracy of 90%.

According to the manufacturer of the N-Tidal device, TidalSense, it takes under five minutes from the start of the breath test to diagnosis.

Based on the findings of the current study, the researchers concluded that the ability of the N-Tidal capnography device to accurately diagnose COPD in near-real-time lends support to its future use in a clinical setting.

COPD diagnostics in context

COPD led to 3.23 million deaths in 2019 and was the third leading cause of global deaths. Spirometry is generally considered to the be gold standard diagnostic tool for COPD, and its use is on the rise, yet it is also one of the major causes for misdiagnosis. Capnography is a widely used technique that could be used to diagnose COPD.

Diagnostic spirometry for COPD on the rise

8th June 2023

Diagnostic spirometry is increasingly used to confirm the presence of chronic obstructive pulmonary disease (COPD) but there are still existing barriers to more widespread use, according to a recent analysis.

Published in the journal NPJ Primary Care Respiratory Medicine, Swedish researchers examined whether the proportion of patients with diagnostic spirometry had increased over time. The team originally explored spirometry use in 2005 but re-assessed the level of use following the introduction of national guidelines in 2014. In the current study, they also set out to determine any factors associated with omitted or incorrectly interpreted spirometry.  

Using data from medical reviews and a questionnaire from primary and secondary care patients diagnosed with COPD between 2004 and 2010, the researchers compared the findings from a cohort diagnosed between 2000 and 2003. 

Changes in use of diagnostic spirometry

Among 703 patients with a COPD diagnosis between 2004 and 2010, 88% of these had diagnostic spirometry, compared with 59% (p < 0.001) in the previous cohort. Furthermore, the correct interpretation of spirometry results also increased between the two periods (75% vs 82%; p = 0.010).

In further analysis, it became clear that factors associated with not having diagnostic spirometry were: current smoking (Odds ratio, OR = 2.21, 95% CI 1.36 – 3.60), low educational level (OR = 1.81, 1.09 – 3.02) and being managed in primary care (OR = 2.28, 95% CI 1.02 – 5.14). The authors speculated that the lower use of spirometry in current smokers was largely because physicians probably felt the diagnosis was more likely and hence did not require confirmation.

While greater use of diagnostic spirometry was encouraging, the authors suggested that there was still a need for continuous medical educational activities to increase diagnostic accuracy.

Spirometry in context

The use of diagnostic spirometry has been advocated as a means to identify COPD in those with airflow obstruction and respiratory symptoms. However, spirometry is under-used in practice, with a real-world study finding that data from the technique was only used in 43.5% of nearly 60,000 COPD patients.

In fact, not using diagnostic spirometry potentially means that patients could be either under- or over-diagnosed with the condition. For example, it has been suggested that approximately 70% of COPD worldwide may be under-diagnosed and 30-60% of patients over-diagnosed. 

An inadequate assessment with diagnostic spirometry has important implications for patient management. For example, a late COPD diagnosis, can result in a higher exacerbation rate, increased comorbidities and costs compared with an early diagnosis.

Breathlessness patients should have diagnosis and care plan within six months, says NHS England

25th May 2023

Most patients presenting with breathlessness should have a diagnosis and comprehensive treatment plan in place with six months, a support tool published by NHS England to reduce variation in care says.

Breathlessness is associated with high use of healthcare services accounting for 4% of GP consultations and 5% of emergency department attendances, NHS England said.

Yet despite the burden to the patient and the NHS, delays to diagnosis and misdiagnosis are common, the toolkit notes.

This includes 58% of patients with COPD who present with respiratory symptoms for over five years before diagnosis, as well as 41% of patients with heart failure.

A timely approach

Patients with chronic breathlessness are likely to need multiple investigations and should be provided with self-management advice, have lifestyle issues addressed and support for mental health from the first presentation, the guidance states.

Timeliness is key with a proactive approach to reassessment rather than waiting for patients to keep highlighting their breathlessness, it says, and in a third of patients the cause will be multifactorial.

The guidance sets out diagnostic pathway for initial investigations of chronic breathlessness lasting more than eight weeks including ECG, spirometry and FeNO with suggestions for further tests should be diagnosis be unclear.

Referral to respiratory physician or cardiologist is the third step should other investigations provide no explanation, the pathway says.

‘If there is no obvious cause(s) for breathlessness after robust investigation, fitness and lifestyle factors should be addressed,’ the toolkit continues. ‘Consider referral for therapeutic interventions for alcohol reduction, weight management, physical activity improvement and psychosocial support.’

It notes the guidance is not intended to override clinical judgment in individual cases.

Some COPD patients waiting a decade

In its annual report on COPD care, Asthma and Lung UK said almost a quarter of patients wait five year or more before their condition is diagnosed and 12% of 6,500 patients surveyed had waited more than a decade. 

Some community diagnostic centres have been piloting the use of a pre-diagnosis breathlessness pathway, the charity said, but this approach now needs to be rolled out nationally as a matter of urgency.

The goal would be for any patients presenting with breathlessness with no obvious diagnosis to be referred to a diagnostic hub to have an assessment by heart, respiratory and mental health experts before onward specialist referral and treatment where necessary. 

Dr Daryl Freeman, Primary Care Respiratory Society committee member and associate clinical director at Norfolk Community Health & Care said: ‘The NHSE breathlessness pathway is an opportunity to fine tune primary care diagnosis of breathlessness and look at how they can develop their PCN hublets or refer into community based diagnostic hubs if they exist.

‘The algorithm is useful I feel and is particularly useful for allied health professionals looking after patients with new onset breathlessness.’

This story was originally published by our sister publication Pulse.

Exacerbations reduced by dupilumab in COPD patients with type 2 inflammation

24th May 2023

The rate of exacerbations in COPD patients with type 2 inflammation is lowered by treatment with dupilumab, according to the findings of a recent randomised, placebo trial.

Patients with chronic obstructive pulmonary disease (COPD) and type 2 inflammation experience a lower annualised rate of moderate to severe disease exacerbations when dupilumab is added to standard triple therapy, the BOREAS clinical trial group found.

Published in the New England Journal of Medicine, the study looked at COPD patients with type 2 inflammation, based on an elevated eosinophil count (≥300 cells/µL), who were in receipt of standard triple therapy. They were randomised them to either dupilumab 300 mg or placebo, given subcutaneously once every two weeks. 

The primary endpoint was the annualised rate of moderate or severe exacerbations of COPD. Secondary outcomes included the change in the prebronchodilator FEV1 and the St. George’s Respiratory Questionnaire (SGRQ) for which lower scores indicated a better quality of life. In addition, the Evaluating Respiratory Symptoms in COPD (E-RS–COPD) scale was used, with, again, lower scores indicative of less severe symptoms.

Exacerbation rates and use of dupilumab

A total of 939 patients were included and randomised to either dupilumab (468) or placebo. The mean baseline absolute blood eosinophil count was 401. 

The annualised rate of moderate or severe exacerbations was 0.78 (95% CI 0.64 – 0.93) for those given dupilumab and 1.10 (95% CI 0.93 to 1.30) with placebo (rate ratio, RR = 0.70, 95% CI 0.58 to 0.86, p < 0.001).

For the secondary outcomes, the prebronchodilator FEV1 increased from baseline to week 12 by a mean of 160 ml with dupilumab and 77 ml with placebo (p < 0.001) and this difference was sustained through to week 52. Similarly, both the SGRQ and E-RS–COPD scores were significantly lower in those receiving dupilumab at week 52.

The authors concluded that the use of dupilumab in COPD patients with a type 2 inflammation phenotype, experience a lower annualised rate of moderate to severe exacerbations, improved quality of life and better lung function.

COPD exacerbations in context

COPD exacerbations are linked to an accelerated decline in lung function, especially in patients with eosinophil counts greater than 350 cells/µL and not using inhaled corticosteroids.

Type 2 inflammation is present in a sub-set of COPD patients, with one study finding a prevalence of 37%, and such individuals show a better response to systemic corticosteroids such as prednisolone. Type 2 inflammation is characterised by increased eosinophil counts together with elevated levels of various interleukins including interleukin-5, interleukin-4 and interleukin-13.

Monoclonal antibody treatment targeting interleukin-5 with a view to reducing disease exacerbations has, to date, produced mixed results. For instance, use of benralizumab was not associated with a lower annualised rate of COPD exacerbations. In contrast, treatment with mepolizumab, did lower the annual rate of moderate or severe exacerbations. An alternative, yet untested therapeutic approach, is the use of dupilumab, which blocks two other interleukins elevated in those with the type 2 inflammation phenotype, namely, interleukin-4 and 13.

Altering the trajectory of COPD exacerbations

11th May 2023

The King’s Centre for Lung Health aims to eliminate lung disease through a better understanding of diagnostics, prevention and treatment. Here, the Centre’s director Dr Mona Bafadhel discusses these lofty ambitions and her research and practice in COPD.

Dr Mona Bafadhel is the chair of respiratory medicine at King’s College London and director of the King’s Centre for Lung Health. Launched in June 2022, the Centre’s vision is to become a hub of world-class excellence for understanding respiratory disease, focusing on innovative and inclusive research to tackle unmet global need.

This new initiative, described by Dr Bafadhel as “very exciting” and bringing with it “lots of opportunities”, is a collaboration between multiple NHS trusts in the locality, as well as its charity partner Asthma and Lung UK.

With a large population of patients and strong “cohesion and collegiality across the associated groups from the basic scientists all the way through to clinicians, nurses, pharmacists, the palliative care team”, Dr Bafadhel hopes it will lead to lots of new insights about respiratory lung disease.

What lung diseases are being investigated at the Centre?

We’re covering the common and the uncommon lung diseases – we have very big clinical research excellence in asthma, we’re going to set up some COPD research and we have a very big presence in physiology. There’s also work being done in sleep and ventilation, cancer, of course, and infection. Pleural-based and interstitial lung disease is also a focus area. We’re covering a lot of ground.

We’re also interested in the life course, so we’re looking to share our knowledge with colleagues from early in utero and paediatrics as well, and we will be working with our imaging colleagues too. It’s a wide breadth of different disciplines coming together for the different disease states that we’re looking at.

What is your own clinical area of interest?

My main interest is in COPD, particularly COPD exacerbations. COPD probably affects one in 10 of the adult population in the UK and it’s not just a smoking disease. We’re learning a lot about these exacerbations, so these episodes or crisis moments where patients feel worse. There’s a COPD patient having one of these crisis attacks probably once every 20 seconds in this country alone, so it’s a huge health burden and a distressing time for patients. My main interest and focus for the last 15 or so years of research has been looking to try and improve how we understand these episodes and how we treat them better.

COPD is almost an umbrella term for chronic bronchitis and emphysema. The majority of COPD is caused by smoking, but we’re now recognising that the effects of air pollution – the effects of early exposure in your life – and the effects of infection may also lead to obstructive lung disease. It’s diagnosed by a classic symptom history of cough, breathlessness, sputum production and it’s confirmed by spirometry – the lung function test that we can do in community and in hospital. It’s often diagnosed later on in life, but I suspect we’re missing lots of early cases because people attribute their breathlessness to getting older or getting unfitter.

Exacerbation episodes are the greatest burden, they’re associated with worsening quality of life, worsening lung function, increased risk of needing to go to hospital and an increased risk of dying. It’s one of the greatest needs in respiratory medicine.

Can you tell us about your research on eosinophils in COPD?

I could talk about COPD and eosinophils for a very long time! The eosinophil is an immune cell that everyone has, and it was largely known to be related to allergy, asthma and parasitic infections where you’d have a higher eosinophil blood count. We never really thought about the importance of eosinophil in COPD. In my research about 15 years ago, I was able to show that eosinophil in the airway correlated to eosinophil in the blood and, importantly, the eosinophil in the blood is a very good surrogate marker for telling you that you have a particular type of airway inflammation. What’s important about that? Well, we know from asthma studies that this particular airway inflammation – T2 high inflammation – indicates that someone will have the best response to inhaled corticosteroids, oral corticosteroids or monoclonal antibodies, for example.

We saw that it had exacerbations so there was a group of people who had this eosinophilic-type exacerbation and who had a better response to prednisolone. We did some proof-of-concept studies looking at that and the blood was the easiest way to test it. We’ve subsequently shown that the blood eosinophil was related to who was going to have the best response to inhaled corticosteroids in COPD and that work has been able to influence clinical guideline practice such that now, looking at the eosinophil when you’re starting to think about inhaled steroids in patients with COPD is indicated from a global point of view.

What does the eosinophil do?

We’re not really sure yet. It’s a tough old cell, it does lots of different things and I think what we’re slowly trying to find out is how it links to what’s going on in the airway, what’s going on in the blood and how it’s affecting other organs. There are two schools of thought, one who think it actually does something and one who think it’s just a bystander. I’m in the former group, I think they do something important. We’ll try to tease it out in the next few years, I hope.

For an acute exacerbation event, I think there’s potential to look at the eosinophil count at the acute time in a point-of-care analysis. We’ve just done a study about that – it’s currently in preparation for manuscript and peer review – and really it does look like you can use a point of care analysis to tell you that someone may not need steroids. And, of course, oral steroids themselves have side effects so we’re trying to be much more personalised and precise in treatments. We’re not fully there yet, but I don’t think it’ll be too long before things change in clinical practice – the next five or 10 years, I suspect.

Is there a role for monoclonal antibodies in COPD?

The studies didn’t reach their primary endpoints, so they weren’t positive in the first go for using monoclonal antibodies. The two monoclonal antibodies that have been tested with COPD so far have been mepolizumab or benralizumab and they’re not licensed yet. When people have delved down into the characteristics a bit more, there probably is a subgroup that do best, and that’ll be the group that have higher eosinophils and more exacerbations.

The trials are being redone; I know the benralizumab study is being repeated for monoclonal antibodies in COPD – that’s the RESOLUTE study. And we also have the dupilumab studies being done in COPD, so we’ve got a few more trials that will hopefully come out in the next 12-18 months that will give us more insight into whether there is a role for monoclonal antibodies in COPD. I would hope that there might be, but it’s going to be in a subgroup, it’s not going to be for everyone.

The King’s Centre for Lung Health is involved in shaping how the studies are reported and how they get started so it’s very exciting for us.

What other areas of research are you exploring?

We’re currently doing an early phase study looking at the use of a monoclonal antibodies at the acute exacerbation stage. If these are positive then we’ll go on to work on the bigger trials. We’re also looking at research trying to understand the cardiovascular risk for patients with COPD, there’s work looking at readmissions in people with COPD and we’re interested in the immunology and the response people have with infections such as viruses.

We’re also interested in looking at the effect or hormones in COPD, particularly the menopause in women. There are oestrogen receptors are present in the lining of the lungs and, if there are receptors there, it must mean that oestrogen is probably playing a role and doing something. The interest has been sparked because we’ve learnt that women have a quicker loss of lung function when exposed to cigarette smoke and they’re often more severe in their disease categories when they’re diagnosed with asthma and COPD. The menopausal effect is something that we need to consider a little bit more when we’re doing our clinical trials, our basic science experiments and when we’re recruiting our patients.

What are your hopes for lung disease research in the future?

I’d like us to be able to diagnose lung disease earlier. Ultimately, I’d like us to prevent it from happening. I think that requires us to understand how it happens, what the exposures are and what the interactions are at the immune level. Earlier diagnosis will be key to influence starting treatment earlier to be able to alter disease trajectory. That’s one really key aspect. Of course, what I’d really like us to do is prevent these exacerbations from happening completely, so almost have the ability for the human response to be able to manage when you have a lung disease. There are colleagues at Imperial, for example, who are looking at early COPD cohorts, so I think we’ll get lots more information on this as that data comes out.

The Covid-19 pandemic showed us that we’re now understanding how important our lungs are. We all recognise that symptoms of cough or breathlessness aren’t normal and so many of us are empowered now to go and say, ‘I’m not feeling right, we need to do some tests.’ That’s a step forward and, of course, we’re recognising the impact of viruses on lungs whether you’ve got healthy lungs or unhealthy lungs. With time, I’d like to see the next five or 10 years really transform lung health and the health of our patients.

Abdominal and general obesity linked with asthma and COPD in women

10th May 2023

An analysis suggests that both abdominal and general obesity are independently associated with asthma and COPD in women but not men.

There are several recognised co-morbidities associated with obesity including hypertension and asthma. In addition, the accumulation of more fat mass, is strongly associated with functional limitation among those with COPD. Moreover, other data suggest a positive association between abdominal obesity (AO) and asthma. This association appears to apply equally to both sexes. But whether abdominal or general obesity has a stronger association with either asthma or COPD is unclear.

The Respiratory Health in Northern Europe (RHINE) III study explored the independent association of abdominal and general obesity with asthma and COPD. In addition, the researchers examined any sex-related differences in these associations. In a cross-sectional study, the team used self-measured waist circumference (WC) as an index of AO. General obesity (GO) was a BMI ≥ 30.0 kg/m2. For the purposes of the analysis, a WC > 102 cm in males and ≥88 cm in females defined AO. Participants completed several questionnaires asking about respiratory symptoms and directly about a diagnosis of asthma and COPD.

Abdominal obesity and asthma or COPD

The study included data from a total of 12,290 participants of whom, 34.7% had AO and 6.7% GO. Abdominal obesity independently associated with the presence of wheeze (adjusted odds ratio, aOR = 1.40, 95% CI 1.24 – 1.58). This independent relationship was also present for GO (aOR = 1.96, 95% CI 1.70 – 2.27). There was a significant association between asthma and both AO and GO. In contrast, the association was only significant between COPD and GO (aOR = 2.14, 95% CI 1.54 – 2.99).

In relation to sex-related differences, asthma significantly associated with both AO (OR = 1.56) and GO in women (OR = 1.95) but not in men. This association also applied for COPD.

Reduced human beta-defensin-2 levels associated with COPD exacerbations

14th April 2023

Lowered levels of human beta-defensin-2 levels have been linked to exacerbations in patients with chronic obstructive pulmonary disease

Chinese researchers have identified that lower levels of human beta-defensin-2 are significantly associated with an increased risk of a disease exacerbation in patients with chronic obstructive pulmonary disease (COPD).

Human beta-defensin 2 (hBD-2) has antimicrobial activity and is elevated in distal airways of COPD patients and may be involved in pathogenesis of the disease. Moreover, hBD2 has been shown to be reduced in the central airways of current smokers with COPD. Since human beta-defensin-2 levels are reduced in smokers with COPD, in the current study, researchers speculated on the association between hBD2 levels and disease exacerbations in COPD. In trying to establish the nature of the relationship between hBD2 and disease exacerbations, the researchers recruited patients with COPD and compared sputum levels with healthy controls. Levels of hBD2 were measured at baseline in the two groups and then after 12 and 24 months and compared. In a further analysis, researchers also compared human beta-defensin-2 levels among COPD patients who either had, or did not have, at least one symptom aggravation or disease exacerbation, over the next 2 years.

Human beta-defensin-2 levels and COPD exacerbations

A total of 203 COPD patients with a mean baseline age of 64.7 years (82% male) were compared to 51 controls who were younger (mean age = 59.5 years).

At baseline, there were no significant differences in the sputum and serum hBD-2 levels between COPD and control patients, although levels were actually slightly lower among COPD patients (2152.5 vs 1716.9 pg/mL, p = 0.057). However, when turning to COPD patients who had at least one symptom aggravation over the next 2 years, hBD2 levels were significantly lower in those who experienced an exacerbation (p = 0.001). Interestingly, sputum hBD-2 levels were not significantly different between COPD patients without an exacerbation and health controls (p = 0.626).

Using regression analysis, the researchers showed that low hBD-2 level (< 1000 pg/mL) was significantly associated with exacerbations and patients with such levels more likely to experience exacerbations over the next 12 months (p = 0.001).

They concluded that the risk of exacerbations in patients with COPD are more likely to occur when they had lower sputum hBD-2 levels, adding that these findings had important implications for future therapies for COPD.

Citation
Feng S et al. Low human beta-defensin-2 levels in the sputum of COPD patients are associated with the risk of exacerbations. BMC Pulm Med 2023

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