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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.
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.
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.
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.
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.
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.
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.
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 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.
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.
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.
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.
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.
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.
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.
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.
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.
10th May 2023
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.
14th April 2023
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
Danish researchers have found that use of drugs affecting the renin-angiotensin-system (RAS) is associated with a lower risk of both acute exacerbations and death in patients with chronic obstructive pulmonary disease (COPD).
COPD remains a major public health problem with one analysis finding that globally in 2019, there were 212.3 million cases and which accounted for 3.3 million deaths. In addition, COPD is characterised not only by local pulmonary, but also by systemic inflammation which promotes the development of extra-pulmonary and cardiovascular co-morbidities. Although traditionally used in the management of hypertension, there is emerging evidence that RAS inhibitors such as angiotensin converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARBs) also have potential benefits in COPD patients. In fact, evidence from a retrospective analysis suggest that RAS inhibitors have dual cardiopulmonary protective properties, reducing the risk of myocardial infarction as well as COPD-related hospitalisation.
In the current study, the Danish researchers hypothesised that the use of RAS inhibitors could reduce the incidence of acute exacerbations of COPD as well as mortality in those with severe disease. Adopting a propensity-score matching approach, the team matched COPD patients prescribed a RAS drug with a similar cohort of COPD patients given bendroflumethiazide as an active comparator. The primary outcome was severe acute exacerbations of COPD within 12 months after study entry or death in the same period.
RAS inhibitor use and COPD outcomes
A total of 3029 patients with a median age of 72 years (69.1% female) and prescribed either an ACEi or ARB and propensity matched to a similar number prescribed bendroflumethiazide.
The use of either an ACEi or ARB was associated with a 14% lower risk of exacerbations or death compared to those using bendroflumethiazide (hazard ratio, HR = 0.86, 95% CI 0.78 – 0.95). This reduced risk was also evident in a sensitivity analysis of the propensity-score-matched population (HR = 0.89, 95% CI 0.83 – 0.94) and in an adjusted Cox proportional hazards model (HR = 0.93, 95% CI 0.89- 0.98).
The authors concluded that use of RAS inhibitor treatment lowered the risk of both acute exacerbations and death in those with COPD. However, they added the caveat that while there is a biologically plausible explanation for this finding, randomised controlled trials were needed to confirm this effect, given the observational nature of their study.
Citation
Vilstrup F et al. Renin-angiotensin-system inhibitors and the risk of exacerbations in chronic obstructive pulmonary disease: a nationwide registry study. BMJ Open Respir Res 2023
17th March 2023
Abnormal spirometry, defined as either airflow obstruction (AFO) or preserved ratio impaired spirometry, has been identified in just over a third of patients deemed at high risk of developing COPD because of a smoking history of at least 10 pack-years according to an analysis of data from the COPDgene study.
Chronic obstructive pulmonary disease (COPD) is an increasingly important cause of morbidity, disability, and mortality worldwide with data from 2019, estimating that globally, 391·9 million people aged 30-79 years had COPD. Nevertheless, COPD often goes undetected and one study of the general population, revealed how of 95,288 screened individuals, 3699 (11%) met the COPD criteria yet 2903 (78%) of these were undiagnosed yet 71% were symptomatic. However, the prevalence of undiagnosed COPD among heavy smokers, i.e., those who are at a high risk of developing the disease is less clear and was the overall objective of the current study, where researchers assessed the extent of abnormal spirometry, based on AFO and preserved ratio impaired spirometry, among a cohort of heavy smokers.
The team included individuals with a ≥10 pack-years of smoking and for whom there was no self-reported or physician diagnosed COPD, asthma or other related disease. In addition, a subgroup of patients were followed-up for a period of 5 years.
Abnormal spirometry findings
A total of 5,055 individuals without known obstructive lung disease were enrolled in the study, ranging in age from 56 to 61. Abnormal spirometry, based on AFO and preserved ratio impaired spirometry was seen in 21 % and in 13.6% of participants respectively.
Factors such as age, pack-years, current smoking and a history of acute bronchitis were all significantly and positively associated with AFO. In contrast, body mass index, female gender and Black ethnicity, were inversely, but significantly associated with AFO.
In a subgroup of 2,800 participants who had 5 years of follow-up, 19% had an incident diagnosis of COPD and factors significantly associated with the diagnosis included a MMRC > 2 (dyspnoea score) and the presence of a chronic, productive cough.
The authors concluded that there was a high prevalence of undiagnosed COPD in at-risk individuals and that the associated factors could be used to identify those at risk for enable earlier diagnosis and treatment of the disease.
Citation
Trab TV et al. Prevalence of abnormal spirometry in individuals with a smoking history and no known obstructive lung disease. Respir Med 2023
19th February 2023
A study analysing hospital admissions for both chronic obstructive pulmonary disease (COPD) and asthma from 1999 to 2020, has revealed a significant increase for both conditions despite a considerable increase in prescribed treatments for these diseases.
Both COPD and asthma are common respiratory diseases. In a recent global systematic review it was estimated that some 391·9 million people had COPD in 2019 and the World Health Organization (WHO) estimates than in 2019, there were 3.23 million global deaths from COPD. Asthma also affects a huge number of people and WHO estimated that in 2019, the disease affected some 262 million people across the world and led to 455,000 deaths. With both diseases leading to a considerable number of deaths, in the present study, a team of Saudi Arabian researchers examined the trends in hospital admissions and which could result in death, for both COPD and asthma between 1999 and 2020. The researchers extracted information from the hospital episode statistics database in England and the corresponding database was Wales. In addition to hospital admissions data, the team also collected information on COPD and asthma-related medicines prescribed between 2004 and 2020.
Hospital admissions for COPD and asthma
The total annual number of admissions for the two conditions rose by 82.2% between 1999 and 2020 which represented a 59.1% increase in the hospital admission rate over this period of time (p < 0.05).
The most common reason for COPD admission (38.7%) was in combination with an acute lower respiratory tract infection and which increased by 198.5% between 1999 and 2020. In contrast, acute exacerbations of COPD alone, accounted for a quarter of admissions (25.5%) and this rate had actually reduced by 4.8% between 1999 and 2020. As with COPD, asthma additions also increased by 46.1% over the 21-year period.
Just over a third (34.7%) of COPD and asthma admissions occurred in those age 75 years and older with just under a quarter (23.5%) in those aged 15 – 59 years. Interestingly, slightly more than half (53.8%) of admissions for both conditions occurred in women.
When looking at prescriptions, the researched observed a 42.2% increase the absolute number of COPD and asthma-related dispensed medicines between 2004 and 2020, which represented a 27.2% increase between the two periods of time (p < 0.05).
The authors concluded that while the data showed a clear rise in hospital admissions for both conditions the reasons behind these increases were unclear and they called for further research to try and better understand the factors responsible for these higher rates.
Citation
Alwafi H et al. Trends in hospital admissions and prescribing due to chronic obstructive pulmonary disease and asthma in England and Wales between 1999 and 2020: an ecological study. BMC Pulm Med 2023
16th February 2023
While prior work has revealed a heightened capsaicin cough reflex sensitivity in those with COPD, Japanese researchers have observed the opposite and found that this reduced sensitivity is associated with an increased risk of both an acute exacerbation or community-acquired pneumonia requiring hospitalisation.
According to the World Health Organisation, COPD was the third highest global cause of death in 2020. Moreover, community-acquired pneumonia (CAP) can often co-exists in patients hospitalised with an acute exacerbation of COPD. Typically patients with COPD experience cough, sputum and dyspnoea and it is know that the presence of both cough and sputum production are associated with frequent disease exacerbations leading to hospitalisation. Previous studies in animals, suggest that patients with COPD have a heightened response to stimulation with capsaicin, leading to a greater number of coughs. Such heightened responses have an important role in helping to protect the airways from particles although other work has identified a reduced capsaicin cough response in those with recurrent pneumonia.
In the present study, the Japanese team speculated that among those with COPD, rather than being more sensitive, as seen in previous work, the capsaicin cough reflex sensitivity would actually be lower due to the fact that many exacerbations occur alongside a co-existent CAP infection. The team prospectively recruited COPD patients and performed a number of baseline tests that included various lung and cardiac function tests, blood eosinophil counts as well as the capsaicin cough reflex sensitivity. These patients were then monitored over the next 12 months for cases of an acute exacerbation or CAP infections leading to hospitalisation.
Capsaicin cough reflex sensitivity and COPD exacerbations
A total of 68 patients with a mean age of 74 years (85.3% male) were included in the study and during the 12 month follow-up, 8 patients (3 with an exacerbation of COPD and 5 with CAP) were hospitalised.
Capsaicin cough reflex sensitivity scores were lower among those hospitalised and using multivariate regression analysis, the researchers identified that a decreased cough sensitivity was significantly associated with an acute exacerbation or CAP infection requiring hospitalisation (odds ratio, OR = 2.19, 95% CI 1.08 – 4.44, P = 0.029). In addition, an eosinophil count ≥300 µL was also significantly associated with hospitalisation (OR = 45.9, 95% CI 1.09 – 1934, P = 0.045).
The authors concluded that use of the capsaicin cough reflex sensitivity in those with COPD, may have a role in the prevention of severe acute exacerbations or pneumonia that require hospitalisation.
Citation
Kanemitsu Y et al. Decreased capsaicin cough reflex sensitivity predicts hospitalisation due to COPD. BMJ Open Respir Res 2023
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