COPD

COPD patients with high plasma immunoglobulin E are more likely to have exacerbations and die from any cause, based on a Danish population-cohort study.

The predictive power of IgE was independent from blood eosinophil level, hinting at different subsets of patients with COPD, lead author Yunus Çolak MD, PhD, of Copenhagen University Hospital, and colleagues reported.

“Additional biomarkers are necessary as blood eosinophils alone seem insufficient for risk stratification in COPD,” the investigators wrote in Annals of Allergy, Asthma & Immunology. “Since asthma and COPD share some pathophysiological mechanisms, a logical approach would be to investigate well-known biomarkers for asthma in COPD and vice versa.”

Dr. Çolak and colleagues cited previous research supporting this perspective. Specifically, IgE-targeting monoclonal antibodies have shown promise in patients with severe asthma and asthma-COPD overlap, whereas COPD with high IgE has been associated with a history of lung function decline and previous exacerbations.

The present study drew from a database of 46,598 adults enrolled in the Copenhagen General Population study. All participants underwent physical examination, completed a questionnaire, and provided blood for analysis. From this population, 1,559 individuals had COPD, among whom 446 had high plasma IgE (at least 76 IU/mL).

Over a median follow-up of 6.9 years in the COPD group, 224 severe exacerbations and 434 deaths of any cause occurred. Compared with COPD patients who had normal plasma IgE, those with high IgE were 43% more likely to have severe exacerbation (hazard ratio, 1.43; 95% confidence interval, 1.07-1.89) and 30% more likely to die of any cause (HR, 1.30; 95% CI, 1.06-1.62). These risks were similar when excluding patients with IgE of 700 IU/mL or higher.

“These findings suggest that plasma IgE concentration may be a potential prognostic biomarker and treatment target for a subset of COPD patient,” wrote Dr. Çolak and colleagues.

The above risks increased moderately when the high IgE group was trimmed to include only those with low eosinophils (less than 300 cells/mcL); in this subgroup, risk of exacerbation was increased 62% (HR, 1.62; 95% CI, 1.17-2.24), while risk of all-cause mortality was increased 47% (HR, 1.47; 95% CI, 1.14-1.88).

“We were not able to show that individuals with higher blood eosinophils further stratified by IgE had higher risk of severe exacerbation or all-cause mortality,” the investigators wrote, although they noted “the relatively low statistical power in stratified analysis,” considering the wide confidence intervals observed.

­­­­“Thus, we should be careful with interpreting the results in relation to blood eosinophils and IgE combined,” they suggested. “However, we believe that the mechanisms driving exacerbations through plasma IgE are different from those driving blood eosinophils, and we believe that plasma IgE may be a marker for a subset of COPD patients similar to blood eosinophils, which is compatible with the heterogeneity of patients with COPD.”

According to principal author Shoaib Afzal, MD, PhD, of Copenhagen University Hospital, the findings are “probably no surprise for practitioners that often observe overlap between asthma and COPD pathology.”

As smoking prevalence goes down in many countries, relatively more never-smokers are being diagnosed with COPD, Dr. Afzal said in a written comment, “which means that asthma as a risk factor for COPD is gaining importance.”

While patients with asthma can be treated with IgE-targeting omalizumab, a trial evaluating the same biologic for COPD patients with high IgE was withdrawn because of a lack of recruitment; however, Dr. Afzal suggested that this should not be the end of the story, since these new data imply that more patients could benefit than previously recognized.

“Our observational study has generated a hypothesis that needs to be tested by pulmonologists in randomized interventions trials designed with updated inclusion criteria,” he said.

Such trials are needed, Dr. Afzal went on, because they could help unlock the “huge” potential benefit that may come from characterizing COPD patients beyond “exposures, symptoms, and spirometry.”

“Sadly, the progress in establishing biomarkers in COPD for improving risk stratification and treatment allocation have been rather disappointing in the last decades, with the exception of small successes with eosinophils and perhaps FeNO,” Dr. Afzal said.

courtesy of Temple University

Nathaniel Marchetti, DO, professor of thoracic medicine and surgery at Temple University and medical director of the respiratory ICU at Temple University Hospital, both in Philadelphia, said the study by Dr. Afzal and colleagues is noteworthy because “biomarkers for COPD are desperately needed to help risk stratify patients for exacerbation risk and risk of disease progression and even mortality.”

In a written comment, Dr. Marchetti agreed with Dr. Afzal that the findings “open the possibility for interventional trials targeting IgE,” which could one day reshape the way patients with COPD are treated.

“I think that biomarkers will become vital in caring for patients with COPD in the future,” Dr. Marchetti said. “There will be medications that will be used to target different pathways of inflammation that drive disease progression and exacerbations. Biomarkers will be important in driving personalized medicine in COPD. We already know the disease seems to vary greatly from patient to patient.”

The study was supported by The Capital Region of Copenhagen, The Danish Lung Foundation, The Velux Foundation, and others. The investigators disclosed relationships with Boehringer Ingelheim, AstraZeneca, Sanofi Genzyme, and others. Dr. Marchetti disclosed no conflicts of interest.

COPD patients with high plasma immunoglobulin E are more likely to have exacerbations and die from any cause, based on a Danish population-cohort study.

The predictive power of IgE was independent from blood eosinophil level, hinting at different subsets of patients with COPD, lead author Yunus Çolak MD, PhD, of Copenhagen University Hospital, and colleagues reported.

“Additional biomarkers are necessary as blood eosinophils alone seem insufficient for risk stratification in COPD,” the investigators wrote in Annals of Allergy, Asthma & Immunology. “Since asthma and COPD share some pathophysiological mechanisms, a logical approach would be to investigate well-known biomarkers for asthma in COPD and vice versa.”

Dr. Çolak and colleagues cited previous research supporting this perspective. Specifically, IgE-targeting monoclonal antibodies have shown promise in patients with severe asthma and asthma-COPD overlap, whereas COPD with high IgE has been associated with a history of lung function decline and previous exacerbations.

The present study drew from a database of 46,598 adults enrolled in the Copenhagen General Population study. All participants underwent physical examination, completed a questionnaire, and provided blood for analysis. From this population, 1,559 individuals had COPD, among whom 446 had high plasma IgE (at least 76 IU/mL).

Over a median follow-up of 6.9 years in the COPD group, 224 severe exacerbations and 434 deaths of any cause occurred. Compared with COPD patients who had normal plasma IgE, those with high IgE were 43% more likely to have severe exacerbation (hazard ratio, 1.43; 95% confidence interval, 1.07-1.89) and 30% more likely to die of any cause (HR, 1.30; 95% CI, 1.06-1.62). These risks were similar when excluding patients with IgE of 700 IU/mL or higher.

“These findings suggest that plasma IgE concentration may be a potential prognostic biomarker and treatment target for a subset of COPD patient,” wrote Dr. Çolak and colleagues.

The above risks increased moderately when the high IgE group was trimmed to include only those with low eosinophils (less than 300 cells/mcL); in this subgroup, risk of exacerbation was increased 62% (HR, 1.62; 95% CI, 1.17-2.24), while risk of all-cause mortality was increased 47% (HR, 1.47; 95% CI, 1.14-1.88).

“We were not able to show that individuals with higher blood eosinophils further stratified by IgE had higher risk of severe exacerbation or all-cause mortality,” the investigators wrote, although they noted “the relatively low statistical power in stratified analysis,” considering the wide confidence intervals observed.

­­­­“Thus, we should be careful with interpreting the results in relation to blood eosinophils and IgE combined,” they suggested. “However, we believe that the mechanisms driving exacerbations through plasma IgE are different from those driving blood eosinophils, and we believe that plasma IgE may be a marker for a subset of COPD patients similar to blood eosinophils, which is compatible with the heterogeneity of patients with COPD.”

According to principal author Shoaib Afzal, MD, PhD, of Copenhagen University Hospital, the findings are “probably no surprise for practitioners that often observe overlap between asthma and COPD pathology.”

As smoking prevalence goes down in many countries, relatively more never-smokers are being diagnosed with COPD, Dr. Afzal said in a written comment, “which means that asthma as a risk factor for COPD is gaining importance.”

While patients with asthma can be treated with IgE-targeting omalizumab, a trial evaluating the same biologic for COPD patients with high IgE was withdrawn because of a lack of recruitment; however, Dr. Afzal suggested that this should not be the end of the story, since these new data imply that more patients could benefit than previously recognized.

“Our observational study has generated a hypothesis that needs to be tested by pulmonologists in randomized interventions trials designed with updated inclusion criteria,” he said.

Such trials are needed, Dr. Afzal went on, because they could help unlock the “huge” potential benefit that may come from characterizing COPD patients beyond “exposures, symptoms, and spirometry.”

“Sadly, the progress in establishing biomarkers in COPD for improving risk stratification and treatment allocation have been rather disappointing in the last decades, with the exception of small successes with eosinophils and perhaps FeNO,” Dr. Afzal said.

courtesy of Temple University

Nathaniel Marchetti, DO, professor of thoracic medicine and surgery at Temple University and medical director of the respiratory ICU at Temple University Hospital, both in Philadelphia, said the study by Dr. Afzal and colleagues is noteworthy because “biomarkers for COPD are desperately needed to help risk stratify patients for exacerbation risk and risk of disease progression and even mortality.”

In a written comment, Dr. Marchetti agreed with Dr. Afzal that the findings “open the possibility for interventional trials targeting IgE,” which could one day reshape the way patients with COPD are treated.

“I think that biomarkers will become vital in caring for patients with COPD in the future,” Dr. Marchetti said. “There will be medications that will be used to target different pathways of inflammation that drive disease progression and exacerbations. Biomarkers will be important in driving personalized medicine in COPD. We already know the disease seems to vary greatly from patient to patient.”

The study was supported by The Capital Region of Copenhagen, The Danish Lung Foundation, The Velux Foundation, and others. The investigators disclosed relationships with Boehringer Ingelheim, AstraZeneca, Sanofi Genzyme, and others. Dr. Marchetti disclosed no conflicts of interest.

COPD patients with high plasma immunoglobulin E are more likely to have exacerbations and die from any cause, based on a Danish population-cohort study.

The predictive power of IgE was independent from blood eosinophil level, hinting at different subsets of patients with COPD, lead author Yunus Çolak MD, PhD, of Copenhagen University Hospital, and colleagues reported.

“Additional biomarkers are necessary as blood eosinophils alone seem insufficient for risk stratification in COPD,” the investigators wrote in Annals of Allergy, Asthma & Immunology. “Since asthma and COPD share some pathophysiological mechanisms, a logical approach would be to investigate well-known biomarkers for asthma in COPD and vice versa.”

Dr. Çolak and colleagues cited previous research supporting this perspective. Specifically, IgE-targeting monoclonal antibodies have shown promise in patients with severe asthma and asthma-COPD overlap, whereas COPD with high IgE has been associated with a history of lung function decline and previous exacerbations.

The present study drew from a database of 46,598 adults enrolled in the Copenhagen General Population study. All participants underwent physical examination, completed a questionnaire, and provided blood for analysis. From this population, 1,559 individuals had COPD, among whom 446 had high plasma IgE (at least 76 IU/mL).

Over a median follow-up of 6.9 years in the COPD group, 224 severe exacerbations and 434 deaths of any cause occurred. Compared with COPD patients who had normal plasma IgE, those with high IgE were 43% more likely to have severe exacerbation (hazard ratio, 1.43; 95% confidence interval, 1.07-1.89) and 30% more likely to die of any cause (HR, 1.30; 95% CI, 1.06-1.62). These risks were similar when excluding patients with IgE of 700 IU/mL or higher.

“These findings suggest that plasma IgE concentration may be a potential prognostic biomarker and treatment target for a subset of COPD patient,” wrote Dr. Çolak and colleagues.

The above risks increased moderately when the high IgE group was trimmed to include only those with low eosinophils (less than 300 cells/mcL); in this subgroup, risk of exacerbation was increased 62% (HR, 1.62; 95% CI, 1.17-2.24), while risk of all-cause mortality was increased 47% (HR, 1.47; 95% CI, 1.14-1.88).

“We were not able to show that individuals with higher blood eosinophils further stratified by IgE had higher risk of severe exacerbation or all-cause mortality,” the investigators wrote, although they noted “the relatively low statistical power in stratified analysis,” considering the wide confidence intervals observed.

­­­­“Thus, we should be careful with interpreting the results in relation to blood eosinophils and IgE combined,” they suggested. “However, we believe that the mechanisms driving exacerbations through plasma IgE are different from those driving blood eosinophils, and we believe that plasma IgE may be a marker for a subset of COPD patients similar to blood eosinophils, which is compatible with the heterogeneity of patients with COPD.”

According to principal author Shoaib Afzal, MD, PhD, of Copenhagen University Hospital, the findings are “probably no surprise for practitioners that often observe overlap between asthma and COPD pathology.”

As smoking prevalence goes down in many countries, relatively more never-smokers are being diagnosed with COPD, Dr. Afzal said in a written comment, “which means that asthma as a risk factor for COPD is gaining importance.”

While patients with asthma can be treated with IgE-targeting omalizumab, a trial evaluating the same biologic for COPD patients with high IgE was withdrawn because of a lack of recruitment; however, Dr. Afzal suggested that this should not be the end of the story, since these new data imply that more patients could benefit than previously recognized.

“Our observational study has generated a hypothesis that needs to be tested by pulmonologists in randomized interventions trials designed with updated inclusion criteria,” he said.

Such trials are needed, Dr. Afzal went on, because they could help unlock the “huge” potential benefit that may come from characterizing COPD patients beyond “exposures, symptoms, and spirometry.”

“Sadly, the progress in establishing biomarkers in COPD for improving risk stratification and treatment allocation have been rather disappointing in the last decades, with the exception of small successes with eosinophils and perhaps FeNO,” Dr. Afzal said.

courtesy of Temple University

Nathaniel Marchetti, DO, professor of thoracic medicine and surgery at Temple University and medical director of the respiratory ICU at Temple University Hospital, both in Philadelphia, said the study by Dr. Afzal and colleagues is noteworthy because “biomarkers for COPD are desperately needed to help risk stratify patients for exacerbation risk and risk of disease progression and even mortality.”

In a written comment, Dr. Marchetti agreed with Dr. Afzal that the findings “open the possibility for interventional trials targeting IgE,” which could one day reshape the way patients with COPD are treated.

“I think that biomarkers will become vital in caring for patients with COPD in the future,” Dr. Marchetti said. “There will be medications that will be used to target different pathways of inflammation that drive disease progression and exacerbations. Biomarkers will be important in driving personalized medicine in COPD. We already know the disease seems to vary greatly from patient to patient.”

The study was supported by The Capital Region of Copenhagen, The Danish Lung Foundation, The Velux Foundation, and others. The investigators disclosed relationships with Boehringer Ingelheim, AstraZeneca, Sanofi Genzyme, and others. Dr. Marchetti disclosed no conflicts of interest.

Anand S. Iyer, MD, MSPH, frequently hears his patients with chronic obstructive pulmonary disease (COPD) express fear and hopelessness and describe panic and other symptoms of anxiety. He sees anxiety affect the course of COPD, worsening symptoms and outcomes.

“I had questions about what we are doing [to help patients], so I began looking into the role of palliative care to help patients assess and manage these complex emotional and psychological symptoms,” said Dr. Iyer, assistant professor in the division of pulmonology, allergy, and critical care medicine at the University of Alabama at Birmingham.

His research is now focused on the integration of palliative care principles in COPD care. For Dr. Iyer and others engaged in research and/or patient care, finding ways of identifying and managing anxiety in patients with COPD – and other chronic lung diseases – is a calling of growing urgency.

More has been published about anxiety in patients with COPD than in other pulmonary conditions – and in COPD, anxiety has long been established as a prevalent comorbidity. Prevalence rates vary from about 1 in 4, to 1 in 2 or higher, depending on the instruments used and whether clinical DSM-based diagnoses are made, Dr. Iyer said.

A 2013 systematic review of 10 studies that utilized clinical interviews based on DSM criteria, for instance, found a prevalence of clinical anxiety of 10%-55% among inpatients and 13%-46% among outpatients with COPD. The results were similar, investigators said, to studies using self-report screening tools (Respiratory Care 2013;58[5]:858-66).

In the 16 years since an ACCP workshop panel on anxiety and depression in COPD reported higher prevalence rates than for other chronic diseases and detailed a host of problems and research needs (CHEST. 2008;134;43S-56), investigators have more fully documented links to COPD outcomes, showing, for instance, that anxiety predicts exacerbations, hospitalizations, poorer adherence to therapies, poorer quality of life and higher mortality.

Dr. Iyer and other experts say anxiety is still too often a neglected comorbidity. “It’s still underdiagnosed and therefore undertreated,” said Nick Hanania, MD, MS, professor of medicine and director of the Airways Clinical Research Center at Baylor College of Medicine, Houston.

The literature on optimal approaches for management remains limited, and the role of pharmacotherapy for anxiety (and depression) in the context of COPD has not been well investigated. But there have been some advances: Screening tools have been further studied, questionnaires specific to COPD have been developed, and pulmonary rehabilitation (PR) and cognitive behavioral therapy (CBT) have both been shown to be effective in decreasing anxiety.

Researchers and academic clinicians are talking, meanwhile, about how to have to important conversations about anxiety with patients who have COPD and other chronic lung conditions, and how improve care in the face of significant health system challenges.
 

Understanding anxiety in COPD

Anxiety is often intertwined with dyspnea in a bidirectional and complex relationship, but anxiety in COPD is not always acute or limited to times of acute exacerbations.

“There’s not only the acute experience of shortness of breath or a lung change episode, but there’s an anticipation that can occur, psychologically and socially,” said Lauren Garvin, PhD, of the department of psychiatry at the University of Iowa, Iowa City. Patients worry, “what if I’m short of breath in a particular situation? What if my devices fail when I’m out somewhere?”

Patients are often living “in a state of heightened surveillance of the body,” she noted, which can be exhausting and can impact functioning.

It’s also important to appreciate that anxiety is “a continuum of experience,” said Karin Hoth, PhD, associate professor of psychiatry at the medical school, whose research includes projects focusing on psychological adjustment in COPD.

“Research historically categorizes anxiety as ‘have or don’t have.’ But there’s a continuum of experience that we’re moving toward understanding and recognizing in research,” she said. “Anxiety is part of a patient’s whole experience, no matter where one falls on the continuum.”

Female sex, current smoking, greater airflow restrictions – and in some studies, younger age – have all been associated with a greater risk of anxiety in COPD. (It may well be that women receive more attention, leaving men with higher rates of undiagnosed anxiety, Dr. Hoth said.)

Dr. Iyer stresses the complex relationship between smoking – the No. 1 cause of COPD – and anxiety. Smoking has been associated in multiple studies with an increased risk of anxiety (Brain and Behavior. 2013;3[3]:302-26), he said. (A study led by Dr. Iyer found a similar frequency of anxiety symptoms in smokers with and without COPD [Journal of Psychosomatic Research. 2019;118:18-26].)

Some patients with COPD and anxiety may smoke in order to ease their anxiety, he said, making management of anxiety an important part of the smoking cessation desired for COPD improvement.

COPD medications such as bronchodilators may cause transient symptoms of anxiety, but these are rare and short-lived, Dr. Iyer said.
 

Screening tools and conversations

“It’s not just us not thinking about anxiety that’s the problem, it’s also patients thinking that it’s just the disease [causing their anxiety symptoms],” said Dr. Hanania, a member of the 2006 ACCP panel and an author of numerous papers on COPD and anxiety and depression. “There’s quite a bit of overlap between COPD symptoms and anxiety and depression symptoms, and unless you use structured questionnaires, you may not pick it up,” he said.

Screening tools include the Generalized Anxiety Disorder 7-item (GAD-7) scale, the PHQ-9 for depression and anxiety, and the longer Primary Care Evaluation of Mental Disorders (PRIME-MD). The Hospital Anxiety and Depression Scale (HADS), Dr. Iyer noted, has been well validated for use in ambulatory settings.

Validated screening tools specific to anxiety in COPD are also now an option. Abebaw M. Yohannes, PhD, MSc, FCCP, professor in the department of physical therapy at Azuza Pacific University in Orange, Calif., and the author of numerous studies on COPD and anxiety, developed one of these tools – the 10-item Anxiety Inventory for Respiratory Disease (AIR) scale – out of concern that other surveys contain overlapping somatic symptoms (Chest. 2013;144[5]:1587-96).

“We removed the physical symptoms [of anxiety] that often manifest in patients with COPD,” he said.

Dr. Iyer said screening tools can effectively “highlight which person might be dealing with high levels of anxiety symptoms that might meet a threshold of clinical significance and require collaborative or interprofessional management,” including with psychologists and psychiatrists.

They can also open the door to conversation with patients. “I’ll often bluntly ask, do you feel anxious? Do you feel scared, or hopeless about what the future holds for you?,” he said. “Anxiety about the future plays a big role, and helping patients navigate the illness and understand early how it might look … can ease the level of anxiety.”

Asking patients about their experiences in managing their symptoms and about their psychological and emotional well-being can help to normalize anxiety – and it can be therapeutic, said Dr. Hoth and Dr. Garvin. Asking “how it’s going with the things that really matter in [their] life” is often a good question, they said.

Patients “won’t be offended if you ask,” said Dr. Hoth. “They view their mood and [whole] well-being as part of their medical condition.”

Time is a challenge, she said, but “conversation can be done little by little, as part of a philosophy of engaging the patient around their whole functioning, even if there’s not [a need or] a route to refer just then.”

Such early and integrated conversation borrows from the palliative care model. “Palliative care is a specialty, but it can also be an approach to care,” Dr. Iyer said. He is leading a National Institutes of Health–funded study on nurse-coach–led early palliative care for older adults with COPD and wants to see training opportunities for pulmonologists to learn basic palliative care skills that would equip them to better guide management of mild-moderate anxiety and other complex symptoms.
 

Pulmonary rehabilitation

For many patients with COPD who have anxiety and/or depressive symptoms, referral for nonpharmacologic therapies such as psychotherapy, cognitive-behavioral therapy (CBT), and pulmonary rehabilitation (PR) is “one of the best things you can do,” Dr. Iyer said.

“If patients haven’t done pulmonary rehabilitation, get them in. And if they have done it before, get them back into it again,” he emphasized. “Accredited programs give a holistic approach to improving your strength, your breathlessness, your mindset and understanding of your breathlessness, and your own levels of security.”

Studies addressing the impact of PR and CBT on anxiety have been mostly small and observational but have yielded encouraging findings. A 2017 review reported that PR and CBT were effective in the treatment of anxiety and dyspnea, in the short term, in the majority of 47 studies (JAMA. 2017;18[12]:1096.e1-1096.e17). And a 2019 systematic review and meta-analysis focused on PR reported that, across 11 studies comprising 734 patients, PR conferred significant benefits for anxiety and depression compared with usual care (CHEST. 2019;156[1]:80-91).

Dr. Yohannes, Dr. Hanania, and colleagues recently reported on 734 patients with clinically stable COPD who completed a community-based 8-week PR program of 2 hours a week: 1 hour of exercise and 1 hour of education, the latter of which covered anxiety, panic management, and relaxation.

Patients who had severe dyspnea and comorbid anxiety and depression prior to PR – one-third of the group compared with 20% having anxiety alone and 5% having depression alone – had the most significant improvements in dyspnea scores and anxiety and depression scores (Respir Med. Apr 9. doi: 10.1016/j.rmed.2022.106850.)

The problem is, pulmonary rehabilitation is under-reimbursed and not widely accessible. It’s logistically challenging for patients to attend therapy 2-3 times a week. And according to a recently published study by Dr. Yohannes, Dr. Hanania, and colleagues, patients with more anxiety and dyspnea may be at higher risk of dropping out (Respir Med. 2022 Jan 20. doi: 10.1016/j.rmed.2022.10674). Moreover, Dr. Iyer said, there is a shortage of programs that are accredited.

Telehealth may help on some of these fronts. The efficacy of real-time video PR for COPD is being investigated in a randomized NIH trial (now in the recruitment phase) led by pulmonologist Surya P. Bhatt, MD, also at the University of Alabama at Birmingham.

Researchers also need to investigate issues of sustainability – to learn what “works best in the long run,” Dr. Iyer said.

Dr. Yohannes and Dr. Hanania are encouraged by a recent finding that patients with COPD who completed 8 weeks of PR maintained improvements in anxiety and quality-of-life scores at 2 years. (Improvements in dyspnea and other outcomes did not persist.) (CHEST. 2021;159[3]:967-74). Prospective studies contrasting maintenance programs with no maintenance following PR, are needed, they wrote.
 

Understanding psychological interventions

Dr. Hoth and Dr. Garvin advise their pulmonologist colleagues to feel as confident as possible in describing for patients what CBT and other psychological therapies entail.

“A person [with COPD] who is experiencing something on the continuum of anxiety might be really turning inward and [assessing] unwanted internal experiences” and accompanying thoughts, sensations, emotional impacts and behaviors, Dr. Garvin said.

Among the goals, she said, are to “make shifts around those internal experiences that might invoke some more tolerance or that might shift their relationship with the experiences, or even with the diagnosis itself and all the uncertainties it carries.”

Psychological therapies can involve social support, or “breath and grounding work,” she said. “There are lots of different approaches from different providers.”

Dr. Yohannes advocates incorporating principles of CBT into PR. “In the absence of one-on-one or group [stand-alone] CBT … the principles are worth incorporating as part of the education piece [of PR],” he said. “CBT helps patients to refocus their attention. … and gives them self-confidence to engage in exercise and to function a bit more in their daily activities.”

None of those interviewed for this story reported having any relevant conflicts of interest.

Anand S. Iyer, MD, MSPH, frequently hears his patients with chronic obstructive pulmonary disease (COPD) express fear and hopelessness and describe panic and other symptoms of anxiety. He sees anxiety affect the course of COPD, worsening symptoms and outcomes.

“I had questions about what we are doing [to help patients], so I began looking into the role of palliative care to help patients assess and manage these complex emotional and psychological symptoms,” said Dr. Iyer, assistant professor in the division of pulmonology, allergy, and critical care medicine at the University of Alabama at Birmingham.

His research is now focused on the integration of palliative care principles in COPD care. For Dr. Iyer and others engaged in research and/or patient care, finding ways of identifying and managing anxiety in patients with COPD – and other chronic lung diseases – is a calling of growing urgency.

More has been published about anxiety in patients with COPD than in other pulmonary conditions – and in COPD, anxiety has long been established as a prevalent comorbidity. Prevalence rates vary from about 1 in 4, to 1 in 2 or higher, depending on the instruments used and whether clinical DSM-based diagnoses are made, Dr. Iyer said.

A 2013 systematic review of 10 studies that utilized clinical interviews based on DSM criteria, for instance, found a prevalence of clinical anxiety of 10%-55% among inpatients and 13%-46% among outpatients with COPD. The results were similar, investigators said, to studies using self-report screening tools (Respiratory Care 2013;58[5]:858-66).

In the 16 years since an ACCP workshop panel on anxiety and depression in COPD reported higher prevalence rates than for other chronic diseases and detailed a host of problems and research needs (CHEST. 2008;134;43S-56), investigators have more fully documented links to COPD outcomes, showing, for instance, that anxiety predicts exacerbations, hospitalizations, poorer adherence to therapies, poorer quality of life and higher mortality.

Dr. Iyer and other experts say anxiety is still too often a neglected comorbidity. “It’s still underdiagnosed and therefore undertreated,” said Nick Hanania, MD, MS, professor of medicine and director of the Airways Clinical Research Center at Baylor College of Medicine, Houston.

The literature on optimal approaches for management remains limited, and the role of pharmacotherapy for anxiety (and depression) in the context of COPD has not been well investigated. But there have been some advances: Screening tools have been further studied, questionnaires specific to COPD have been developed, and pulmonary rehabilitation (PR) and cognitive behavioral therapy (CBT) have both been shown to be effective in decreasing anxiety.

Researchers and academic clinicians are talking, meanwhile, about how to have to important conversations about anxiety with patients who have COPD and other chronic lung conditions, and how improve care in the face of significant health system challenges.
 

Understanding anxiety in COPD

Anxiety is often intertwined with dyspnea in a bidirectional and complex relationship, but anxiety in COPD is not always acute or limited to times of acute exacerbations.

“There’s not only the acute experience of shortness of breath or a lung change episode, but there’s an anticipation that can occur, psychologically and socially,” said Lauren Garvin, PhD, of the department of psychiatry at the University of Iowa, Iowa City. Patients worry, “what if I’m short of breath in a particular situation? What if my devices fail when I’m out somewhere?”

Patients are often living “in a state of heightened surveillance of the body,” she noted, which can be exhausting and can impact functioning.

It’s also important to appreciate that anxiety is “a continuum of experience,” said Karin Hoth, PhD, associate professor of psychiatry at the medical school, whose research includes projects focusing on psychological adjustment in COPD.

“Research historically categorizes anxiety as ‘have or don’t have.’ But there’s a continuum of experience that we’re moving toward understanding and recognizing in research,” she said. “Anxiety is part of a patient’s whole experience, no matter where one falls on the continuum.”

Female sex, current smoking, greater airflow restrictions – and in some studies, younger age – have all been associated with a greater risk of anxiety in COPD. (It may well be that women receive more attention, leaving men with higher rates of undiagnosed anxiety, Dr. Hoth said.)

Dr. Iyer stresses the complex relationship between smoking – the No. 1 cause of COPD – and anxiety. Smoking has been associated in multiple studies with an increased risk of anxiety (Brain and Behavior. 2013;3[3]:302-26), he said. (A study led by Dr. Iyer found a similar frequency of anxiety symptoms in smokers with and without COPD [Journal of Psychosomatic Research. 2019;118:18-26].)

Some patients with COPD and anxiety may smoke in order to ease their anxiety, he said, making management of anxiety an important part of the smoking cessation desired for COPD improvement.

COPD medications such as bronchodilators may cause transient symptoms of anxiety, but these are rare and short-lived, Dr. Iyer said.
 

Screening tools and conversations

“It’s not just us not thinking about anxiety that’s the problem, it’s also patients thinking that it’s just the disease [causing their anxiety symptoms],” said Dr. Hanania, a member of the 2006 ACCP panel and an author of numerous papers on COPD and anxiety and depression. “There’s quite a bit of overlap between COPD symptoms and anxiety and depression symptoms, and unless you use structured questionnaires, you may not pick it up,” he said.

Screening tools include the Generalized Anxiety Disorder 7-item (GAD-7) scale, the PHQ-9 for depression and anxiety, and the longer Primary Care Evaluation of Mental Disorders (PRIME-MD). The Hospital Anxiety and Depression Scale (HADS), Dr. Iyer noted, has been well validated for use in ambulatory settings.

Validated screening tools specific to anxiety in COPD are also now an option. Abebaw M. Yohannes, PhD, MSc, FCCP, professor in the department of physical therapy at Azuza Pacific University in Orange, Calif., and the author of numerous studies on COPD and anxiety, developed one of these tools – the 10-item Anxiety Inventory for Respiratory Disease (AIR) scale – out of concern that other surveys contain overlapping somatic symptoms (Chest. 2013;144[5]:1587-96).

“We removed the physical symptoms [of anxiety] that often manifest in patients with COPD,” he said.

Dr. Iyer said screening tools can effectively “highlight which person might be dealing with high levels of anxiety symptoms that might meet a threshold of clinical significance and require collaborative or interprofessional management,” including with psychologists and psychiatrists.

They can also open the door to conversation with patients. “I’ll often bluntly ask, do you feel anxious? Do you feel scared, or hopeless about what the future holds for you?,” he said. “Anxiety about the future plays a big role, and helping patients navigate the illness and understand early how it might look … can ease the level of anxiety.”

Asking patients about their experiences in managing their symptoms and about their psychological and emotional well-being can help to normalize anxiety – and it can be therapeutic, said Dr. Hoth and Dr. Garvin. Asking “how it’s going with the things that really matter in [their] life” is often a good question, they said.

Patients “won’t be offended if you ask,” said Dr. Hoth. “They view their mood and [whole] well-being as part of their medical condition.”

Time is a challenge, she said, but “conversation can be done little by little, as part of a philosophy of engaging the patient around their whole functioning, even if there’s not [a need or] a route to refer just then.”

Such early and integrated conversation borrows from the palliative care model. “Palliative care is a specialty, but it can also be an approach to care,” Dr. Iyer said. He is leading a National Institutes of Health–funded study on nurse-coach–led early palliative care for older adults with COPD and wants to see training opportunities for pulmonologists to learn basic palliative care skills that would equip them to better guide management of mild-moderate anxiety and other complex symptoms.
 

Pulmonary rehabilitation

For many patients with COPD who have anxiety and/or depressive symptoms, referral for nonpharmacologic therapies such as psychotherapy, cognitive-behavioral therapy (CBT), and pulmonary rehabilitation (PR) is “one of the best things you can do,” Dr. Iyer said.

“If patients haven’t done pulmonary rehabilitation, get them in. And if they have done it before, get them back into it again,” he emphasized. “Accredited programs give a holistic approach to improving your strength, your breathlessness, your mindset and understanding of your breathlessness, and your own levels of security.”

Studies addressing the impact of PR and CBT on anxiety have been mostly small and observational but have yielded encouraging findings. A 2017 review reported that PR and CBT were effective in the treatment of anxiety and dyspnea, in the short term, in the majority of 47 studies (JAMA. 2017;18[12]:1096.e1-1096.e17). And a 2019 systematic review and meta-analysis focused on PR reported that, across 11 studies comprising 734 patients, PR conferred significant benefits for anxiety and depression compared with usual care (CHEST. 2019;156[1]:80-91).

Dr. Yohannes, Dr. Hanania, and colleagues recently reported on 734 patients with clinically stable COPD who completed a community-based 8-week PR program of 2 hours a week: 1 hour of exercise and 1 hour of education, the latter of which covered anxiety, panic management, and relaxation.

Patients who had severe dyspnea and comorbid anxiety and depression prior to PR – one-third of the group compared with 20% having anxiety alone and 5% having depression alone – had the most significant improvements in dyspnea scores and anxiety and depression scores (Respir Med. Apr 9. doi: 10.1016/j.rmed.2022.106850.)

The problem is, pulmonary rehabilitation is under-reimbursed and not widely accessible. It’s logistically challenging for patients to attend therapy 2-3 times a week. And according to a recently published study by Dr. Yohannes, Dr. Hanania, and colleagues, patients with more anxiety and dyspnea may be at higher risk of dropping out (Respir Med. 2022 Jan 20. doi: 10.1016/j.rmed.2022.10674). Moreover, Dr. Iyer said, there is a shortage of programs that are accredited.

Telehealth may help on some of these fronts. The efficacy of real-time video PR for COPD is being investigated in a randomized NIH trial (now in the recruitment phase) led by pulmonologist Surya P. Bhatt, MD, also at the University of Alabama at Birmingham.

Researchers also need to investigate issues of sustainability – to learn what “works best in the long run,” Dr. Iyer said.

Dr. Yohannes and Dr. Hanania are encouraged by a recent finding that patients with COPD who completed 8 weeks of PR maintained improvements in anxiety and quality-of-life scores at 2 years. (Improvements in dyspnea and other outcomes did not persist.) (CHEST. 2021;159[3]:967-74). Prospective studies contrasting maintenance programs with no maintenance following PR, are needed, they wrote.
 

Understanding psychological interventions

Dr. Hoth and Dr. Garvin advise their pulmonologist colleagues to feel as confident as possible in describing for patients what CBT and other psychological therapies entail.

“A person [with COPD] who is experiencing something on the continuum of anxiety might be really turning inward and [assessing] unwanted internal experiences” and accompanying thoughts, sensations, emotional impacts and behaviors, Dr. Garvin said.

Among the goals, she said, are to “make shifts around those internal experiences that might invoke some more tolerance or that might shift their relationship with the experiences, or even with the diagnosis itself and all the uncertainties it carries.”

Psychological therapies can involve social support, or “breath and grounding work,” she said. “There are lots of different approaches from different providers.”

Dr. Yohannes advocates incorporating principles of CBT into PR. “In the absence of one-on-one or group [stand-alone] CBT … the principles are worth incorporating as part of the education piece [of PR],” he said. “CBT helps patients to refocus their attention. … and gives them self-confidence to engage in exercise and to function a bit more in their daily activities.”

None of those interviewed for this story reported having any relevant conflicts of interest.

Anand S. Iyer, MD, MSPH, frequently hears his patients with chronic obstructive pulmonary disease (COPD) express fear and hopelessness and describe panic and other symptoms of anxiety. He sees anxiety affect the course of COPD, worsening symptoms and outcomes.

“I had questions about what we are doing [to help patients], so I began looking into the role of palliative care to help patients assess and manage these complex emotional and psychological symptoms,” said Dr. Iyer, assistant professor in the division of pulmonology, allergy, and critical care medicine at the University of Alabama at Birmingham.

His research is now focused on the integration of palliative care principles in COPD care. For Dr. Iyer and others engaged in research and/or patient care, finding ways of identifying and managing anxiety in patients with COPD – and other chronic lung diseases – is a calling of growing urgency.

More has been published about anxiety in patients with COPD than in other pulmonary conditions – and in COPD, anxiety has long been established as a prevalent comorbidity. Prevalence rates vary from about 1 in 4, to 1 in 2 or higher, depending on the instruments used and whether clinical DSM-based diagnoses are made, Dr. Iyer said.

A 2013 systematic review of 10 studies that utilized clinical interviews based on DSM criteria, for instance, found a prevalence of clinical anxiety of 10%-55% among inpatients and 13%-46% among outpatients with COPD. The results were similar, investigators said, to studies using self-report screening tools (Respiratory Care 2013;58[5]:858-66).

In the 16 years since an ACCP workshop panel on anxiety and depression in COPD reported higher prevalence rates than for other chronic diseases and detailed a host of problems and research needs (CHEST. 2008;134;43S-56), investigators have more fully documented links to COPD outcomes, showing, for instance, that anxiety predicts exacerbations, hospitalizations, poorer adherence to therapies, poorer quality of life and higher mortality.

Dr. Iyer and other experts say anxiety is still too often a neglected comorbidity. “It’s still underdiagnosed and therefore undertreated,” said Nick Hanania, MD, MS, professor of medicine and director of the Airways Clinical Research Center at Baylor College of Medicine, Houston.

The literature on optimal approaches for management remains limited, and the role of pharmacotherapy for anxiety (and depression) in the context of COPD has not been well investigated. But there have been some advances: Screening tools have been further studied, questionnaires specific to COPD have been developed, and pulmonary rehabilitation (PR) and cognitive behavioral therapy (CBT) have both been shown to be effective in decreasing anxiety.

Researchers and academic clinicians are talking, meanwhile, about how to have to important conversations about anxiety with patients who have COPD and other chronic lung conditions, and how improve care in the face of significant health system challenges.
 

Understanding anxiety in COPD

Anxiety is often intertwined with dyspnea in a bidirectional and complex relationship, but anxiety in COPD is not always acute or limited to times of acute exacerbations.

“There’s not only the acute experience of shortness of breath or a lung change episode, but there’s an anticipation that can occur, psychologically and socially,” said Lauren Garvin, PhD, of the department of psychiatry at the University of Iowa, Iowa City. Patients worry, “what if I’m short of breath in a particular situation? What if my devices fail when I’m out somewhere?”

Patients are often living “in a state of heightened surveillance of the body,” she noted, which can be exhausting and can impact functioning.

It’s also important to appreciate that anxiety is “a continuum of experience,” said Karin Hoth, PhD, associate professor of psychiatry at the medical school, whose research includes projects focusing on psychological adjustment in COPD.

“Research historically categorizes anxiety as ‘have or don’t have.’ But there’s a continuum of experience that we’re moving toward understanding and recognizing in research,” she said. “Anxiety is part of a patient’s whole experience, no matter where one falls on the continuum.”

Female sex, current smoking, greater airflow restrictions – and in some studies, younger age – have all been associated with a greater risk of anxiety in COPD. (It may well be that women receive more attention, leaving men with higher rates of undiagnosed anxiety, Dr. Hoth said.)

Dr. Iyer stresses the complex relationship between smoking – the No. 1 cause of COPD – and anxiety. Smoking has been associated in multiple studies with an increased risk of anxiety (Brain and Behavior. 2013;3[3]:302-26), he said. (A study led by Dr. Iyer found a similar frequency of anxiety symptoms in smokers with and without COPD [Journal of Psychosomatic Research. 2019;118:18-26].)

Some patients with COPD and anxiety may smoke in order to ease their anxiety, he said, making management of anxiety an important part of the smoking cessation desired for COPD improvement.

COPD medications such as bronchodilators may cause transient symptoms of anxiety, but these are rare and short-lived, Dr. Iyer said.
 

Screening tools and conversations

“It’s not just us not thinking about anxiety that’s the problem, it’s also patients thinking that it’s just the disease [causing their anxiety symptoms],” said Dr. Hanania, a member of the 2006 ACCP panel and an author of numerous papers on COPD and anxiety and depression. “There’s quite a bit of overlap between COPD symptoms and anxiety and depression symptoms, and unless you use structured questionnaires, you may not pick it up,” he said.

Screening tools include the Generalized Anxiety Disorder 7-item (GAD-7) scale, the PHQ-9 for depression and anxiety, and the longer Primary Care Evaluation of Mental Disorders (PRIME-MD). The Hospital Anxiety and Depression Scale (HADS), Dr. Iyer noted, has been well validated for use in ambulatory settings.

Validated screening tools specific to anxiety in COPD are also now an option. Abebaw M. Yohannes, PhD, MSc, FCCP, professor in the department of physical therapy at Azuza Pacific University in Orange, Calif., and the author of numerous studies on COPD and anxiety, developed one of these tools – the 10-item Anxiety Inventory for Respiratory Disease (AIR) scale – out of concern that other surveys contain overlapping somatic symptoms (Chest. 2013;144[5]:1587-96).

“We removed the physical symptoms [of anxiety] that often manifest in patients with COPD,” he said.

Dr. Iyer said screening tools can effectively “highlight which person might be dealing with high levels of anxiety symptoms that might meet a threshold of clinical significance and require collaborative or interprofessional management,” including with psychologists and psychiatrists.

They can also open the door to conversation with patients. “I’ll often bluntly ask, do you feel anxious? Do you feel scared, or hopeless about what the future holds for you?,” he said. “Anxiety about the future plays a big role, and helping patients navigate the illness and understand early how it might look … can ease the level of anxiety.”

Asking patients about their experiences in managing their symptoms and about their psychological and emotional well-being can help to normalize anxiety – and it can be therapeutic, said Dr. Hoth and Dr. Garvin. Asking “how it’s going with the things that really matter in [their] life” is often a good question, they said.

Patients “won’t be offended if you ask,” said Dr. Hoth. “They view their mood and [whole] well-being as part of their medical condition.”

Time is a challenge, she said, but “conversation can be done little by little, as part of a philosophy of engaging the patient around their whole functioning, even if there’s not [a need or] a route to refer just then.”

Such early and integrated conversation borrows from the palliative care model. “Palliative care is a specialty, but it can also be an approach to care,” Dr. Iyer said. He is leading a National Institutes of Health–funded study on nurse-coach–led early palliative care for older adults with COPD and wants to see training opportunities for pulmonologists to learn basic palliative care skills that would equip them to better guide management of mild-moderate anxiety and other complex symptoms.
 

Pulmonary rehabilitation

For many patients with COPD who have anxiety and/or depressive symptoms, referral for nonpharmacologic therapies such as psychotherapy, cognitive-behavioral therapy (CBT), and pulmonary rehabilitation (PR) is “one of the best things you can do,” Dr. Iyer said.

“If patients haven’t done pulmonary rehabilitation, get them in. And if they have done it before, get them back into it again,” he emphasized. “Accredited programs give a holistic approach to improving your strength, your breathlessness, your mindset and understanding of your breathlessness, and your own levels of security.”

Studies addressing the impact of PR and CBT on anxiety have been mostly small and observational but have yielded encouraging findings. A 2017 review reported that PR and CBT were effective in the treatment of anxiety and dyspnea, in the short term, in the majority of 47 studies (JAMA. 2017;18[12]:1096.e1-1096.e17). And a 2019 systematic review and meta-analysis focused on PR reported that, across 11 studies comprising 734 patients, PR conferred significant benefits for anxiety and depression compared with usual care (CHEST. 2019;156[1]:80-91).

Dr. Yohannes, Dr. Hanania, and colleagues recently reported on 734 patients with clinically stable COPD who completed a community-based 8-week PR program of 2 hours a week: 1 hour of exercise and 1 hour of education, the latter of which covered anxiety, panic management, and relaxation.

Patients who had severe dyspnea and comorbid anxiety and depression prior to PR – one-third of the group compared with 20% having anxiety alone and 5% having depression alone – had the most significant improvements in dyspnea scores and anxiety and depression scores (Respir Med. Apr 9. doi: 10.1016/j.rmed.2022.106850.)

The problem is, pulmonary rehabilitation is under-reimbursed and not widely accessible. It’s logistically challenging for patients to attend therapy 2-3 times a week. And according to a recently published study by Dr. Yohannes, Dr. Hanania, and colleagues, patients with more anxiety and dyspnea may be at higher risk of dropping out (Respir Med. 2022 Jan 20. doi: 10.1016/j.rmed.2022.10674). Moreover, Dr. Iyer said, there is a shortage of programs that are accredited.

Telehealth may help on some of these fronts. The efficacy of real-time video PR for COPD is being investigated in a randomized NIH trial (now in the recruitment phase) led by pulmonologist Surya P. Bhatt, MD, also at the University of Alabama at Birmingham.

Researchers also need to investigate issues of sustainability – to learn what “works best in the long run,” Dr. Iyer said.

Dr. Yohannes and Dr. Hanania are encouraged by a recent finding that patients with COPD who completed 8 weeks of PR maintained improvements in anxiety and quality-of-life scores at 2 years. (Improvements in dyspnea and other outcomes did not persist.) (CHEST. 2021;159[3]:967-74). Prospective studies contrasting maintenance programs with no maintenance following PR, are needed, they wrote.
 

Understanding psychological interventions

Dr. Hoth and Dr. Garvin advise their pulmonologist colleagues to feel as confident as possible in describing for patients what CBT and other psychological therapies entail.

“A person [with COPD] who is experiencing something on the continuum of anxiety might be really turning inward and [assessing] unwanted internal experiences” and accompanying thoughts, sensations, emotional impacts and behaviors, Dr. Garvin said.

Among the goals, she said, are to “make shifts around those internal experiences that might invoke some more tolerance or that might shift their relationship with the experiences, or even with the diagnosis itself and all the uncertainties it carries.”

Psychological therapies can involve social support, or “breath and grounding work,” she said. “There are lots of different approaches from different providers.”

Dr. Yohannes advocates incorporating principles of CBT into PR. “In the absence of one-on-one or group [stand-alone] CBT … the principles are worth incorporating as part of the education piece [of PR],” he said. “CBT helps patients to refocus their attention. … and gives them self-confidence to engage in exercise and to function a bit more in their daily activities.”

None of those interviewed for this story reported having any relevant conflicts of interest.

Chronic obstructive pulmonary disease (COPD) was among the significant predictors of hospital readmission in older adults with fractures, based on data from nearly 400 individuals.

Fractures in the elderly remain a major health concern, and readmissions are common; however, “The predictive factors for hospital readmission of elderly people with fractures are multifactorial and complex,” Lara Cristina da Cunha Guimarães, MSN, of State School of Public Health Candido Santiago, State Department of Health of Goiás (Brazil), and colleagues wrote.

Previous research suggests that readmissions risk may be greater in patients with preadmission conditions including pulmonary and cardiac disease, history of stroke and other neurological conditions, and other factors associated with aging in general, they said.

In a study published in the journal Injury , the researchers reviewed data from 376 adults aged 60 years and older in a trauma referral hospital in Brazil who had suffered fractures and were hospitalized between Sept. 1, 2016, and Feb. 28, 2017. The primary outcome was readmission up to one year after discharge from the initial hospitalization for fracture.

Approximately half of the patients experienced femur fractures (53.2%), and the most frequent cause was falling from standing height (72.9%). The overall incidence of readmission was 20.7%. A total of 30.5% of readmissions were related to the fracture, and surgical-site infections were the most common cause of fracture-related complications.

More than half (58.3%) of the readmissions were related to clinical complications.

In a multivariate analysis, several clinical factors not related to fractures were independently associated with readmission, including a previous diagnosis of COPD, age between 60 and 69 years, a fracture of the femur, and delirium at the time of the first hospitalization for fracture.

Pneumonia was the most frequent cause of clinical complications, reflecting data from other recent studies, the researchers noted. “Elderly people with COPD are more susceptible to infections, such as pneumonia, which was a cause of frequent readmissions in the population studied. The presence of COPD can contribute to imbalance in the pulmonary microbiome, mucus production and persistent inflammation of the airways, and structural damage, which increases exposure of the pulmonary mucosa to pathogens.” COPD also can be associated with cardiovascular, mental, and musculoskeletal diseases that can further complicate and delay recovery from fractures.

The study findings were limited by the potential for incomplete information in medical records. However, the results indicate a range of causes and conditions associated with hospital readmission after fractures in older adults, they said. Recognizing these factors can guide plans for transitions from hospital to home care to reduce complications and readmissions.

The study received no outside funding. The researchers had no financial conflicts to disclose.

Chronic obstructive pulmonary disease (COPD) was among the significant predictors of hospital readmission in older adults with fractures, based on data from nearly 400 individuals.

Fractures in the elderly remain a major health concern, and readmissions are common; however, “The predictive factors for hospital readmission of elderly people with fractures are multifactorial and complex,” Lara Cristina da Cunha Guimarães, MSN, of State School of Public Health Candido Santiago, State Department of Health of Goiás (Brazil), and colleagues wrote.

Previous research suggests that readmissions risk may be greater in patients with preadmission conditions including pulmonary and cardiac disease, history of stroke and other neurological conditions, and other factors associated with aging in general, they said.

In a study published in the journal Injury , the researchers reviewed data from 376 adults aged 60 years and older in a trauma referral hospital in Brazil who had suffered fractures and were hospitalized between Sept. 1, 2016, and Feb. 28, 2017. The primary outcome was readmission up to one year after discharge from the initial hospitalization for fracture.

Approximately half of the patients experienced femur fractures (53.2%), and the most frequent cause was falling from standing height (72.9%). The overall incidence of readmission was 20.7%. A total of 30.5% of readmissions were related to the fracture, and surgical-site infections were the most common cause of fracture-related complications.

More than half (58.3%) of the readmissions were related to clinical complications.

In a multivariate analysis, several clinical factors not related to fractures were independently associated with readmission, including a previous diagnosis of COPD, age between 60 and 69 years, a fracture of the femur, and delirium at the time of the first hospitalization for fracture.

Pneumonia was the most frequent cause of clinical complications, reflecting data from other recent studies, the researchers noted. “Elderly people with COPD are more susceptible to infections, such as pneumonia, which was a cause of frequent readmissions in the population studied. The presence of COPD can contribute to imbalance in the pulmonary microbiome, mucus production and persistent inflammation of the airways, and structural damage, which increases exposure of the pulmonary mucosa to pathogens.” COPD also can be associated with cardiovascular, mental, and musculoskeletal diseases that can further complicate and delay recovery from fractures.

The study findings were limited by the potential for incomplete information in medical records. However, the results indicate a range of causes and conditions associated with hospital readmission after fractures in older adults, they said. Recognizing these factors can guide plans for transitions from hospital to home care to reduce complications and readmissions.

The study received no outside funding. The researchers had no financial conflicts to disclose.

Chronic obstructive pulmonary disease (COPD) was among the significant predictors of hospital readmission in older adults with fractures, based on data from nearly 400 individuals.

Fractures in the elderly remain a major health concern, and readmissions are common; however, “The predictive factors for hospital readmission of elderly people with fractures are multifactorial and complex,” Lara Cristina da Cunha Guimarães, MSN, of State School of Public Health Candido Santiago, State Department of Health of Goiás (Brazil), and colleagues wrote.

Previous research suggests that readmissions risk may be greater in patients with preadmission conditions including pulmonary and cardiac disease, history of stroke and other neurological conditions, and other factors associated with aging in general, they said.

In a study published in the journal Injury , the researchers reviewed data from 376 adults aged 60 years and older in a trauma referral hospital in Brazil who had suffered fractures and were hospitalized between Sept. 1, 2016, and Feb. 28, 2017. The primary outcome was readmission up to one year after discharge from the initial hospitalization for fracture.

Approximately half of the patients experienced femur fractures (53.2%), and the most frequent cause was falling from standing height (72.9%). The overall incidence of readmission was 20.7%. A total of 30.5% of readmissions were related to the fracture, and surgical-site infections were the most common cause of fracture-related complications.

More than half (58.3%) of the readmissions were related to clinical complications.

In a multivariate analysis, several clinical factors not related to fractures were independently associated with readmission, including a previous diagnosis of COPD, age between 60 and 69 years, a fracture of the femur, and delirium at the time of the first hospitalization for fracture.

Pneumonia was the most frequent cause of clinical complications, reflecting data from other recent studies, the researchers noted. “Elderly people with COPD are more susceptible to infections, such as pneumonia, which was a cause of frequent readmissions in the population studied. The presence of COPD can contribute to imbalance in the pulmonary microbiome, mucus production and persistent inflammation of the airways, and structural damage, which increases exposure of the pulmonary mucosa to pathogens.” COPD also can be associated with cardiovascular, mental, and musculoskeletal diseases that can further complicate and delay recovery from fractures.

The study findings were limited by the potential for incomplete information in medical records. However, the results indicate a range of causes and conditions associated with hospital readmission after fractures in older adults, they said. Recognizing these factors can guide plans for transitions from hospital to home care to reduce complications and readmissions.

The study received no outside funding. The researchers had no financial conflicts to disclose.

Air pollution levels mediated the impact of temperature on oxygen saturation in adults with chronic obstructive pulmonary disease (COPD) based on data from 117 individuals.

COPD is attributed to environmental factors including air pollution, and air pollution has been linked to increased risk of hospitalization and mortality because of acute COPD exacerbation, wrote Huan Minh Tran, PhD, of Taipei (Taiwan) Medical University and colleagues. However, the effects of air pollution on climate-associated health outcomes in COPD have not been explored, they said.

In a study published in Science of The Total Environment the researchers identified 117 adult COPD patients at a single center in Taiwan. They measured lung function, 6-minute walking distance, oxygen desaturation, white blood cell count, and percent emphysema (defined as low attenuation area [LAA]) and linked them to 0- to 1-year, 0- to 3-year, and 0- to 5-year lags in exposures to relative humidity (RH), temperature, and air pollution. The mean age of the participants was 72.9 years; 93% were men.

Pollution was defined in terms of fine particulate matter (PM2.5).

Overall, an increase in RH by 1% was associated with increases in forced expiratory volume in 1 second (FEV₁), eosinophils, and lymphocytes.

A 1% increase in RH also was associated with a decrease in the total-lobe LAA.

As for temperature, an increase of 1° C was associated with decreased oxygen desaturation and with decreases in right-, left-, and upper-lobe LAA values.

When the researchers examined the impact of pollution, they found that a 1 mcg/m³ increase in PM2.5 was associated with a decrease in the FEV₁ as well as with an increase in oxygen desaturation. A 1 mcg/m³ increase in PM10 and PM2.5 was associated with increases in the total-, right-, left, and upper-lobe LAA; increases in lower-lobe LAA were associated with an increase in PM2.5 only.

“This is reasonable because PM2.5 can travel and deposit in distal parts of the lung, while PM10 is preferably deposited in the larger airways of the upper lung regions,” the researchers wrote in their discussion.

A one part per billion increase in nitrogen dioxide (NO₂) was associated with decreased FEV₁ and increased upper-lobe LAA.

“We observed that NO₂ fully mediated the association between RH and FEV₁, while PM2.5 fully mediated associations of temperature with oxygen saturation and emphysema severity in COPD patients,” the researchers added.

The study findings were limited by several factors including the relatively small and homogeneous male, Taiwanese population, which may limit generalizability, the researchers noted. Other limitations included the lack of control for factors such as body mass index, occupational exposure, comorbidities, medication use, and indoor air pollution, they said.

However, the results suggest that air pollution could have an effect on the established associations between climate and adverse health outcomes in COPD, and more research is needed. Climate change–related air pollution is an important public health issue, especially with regards to respiratory disease,” they concluded.

The study was supported by the Ministry of Science and Technology of Taiwan. The researchers had no financial conflicts to disclose.

Air pollution levels mediated the impact of temperature on oxygen saturation in adults with chronic obstructive pulmonary disease (COPD) based on data from 117 individuals.

COPD is attributed to environmental factors including air pollution, and air pollution has been linked to increased risk of hospitalization and mortality because of acute COPD exacerbation, wrote Huan Minh Tran, PhD, of Taipei (Taiwan) Medical University and colleagues. However, the effects of air pollution on climate-associated health outcomes in COPD have not been explored, they said.

In a study published in Science of The Total Environment the researchers identified 117 adult COPD patients at a single center in Taiwan. They measured lung function, 6-minute walking distance, oxygen desaturation, white blood cell count, and percent emphysema (defined as low attenuation area [LAA]) and linked them to 0- to 1-year, 0- to 3-year, and 0- to 5-year lags in exposures to relative humidity (RH), temperature, and air pollution. The mean age of the participants was 72.9 years; 93% were men.

Pollution was defined in terms of fine particulate matter (PM2.5).

Overall, an increase in RH by 1% was associated with increases in forced expiratory volume in 1 second (FEV₁), eosinophils, and lymphocytes.

A 1% increase in RH also was associated with a decrease in the total-lobe LAA.

As for temperature, an increase of 1° C was associated with decreased oxygen desaturation and with decreases in right-, left-, and upper-lobe LAA values.

When the researchers examined the impact of pollution, they found that a 1 mcg/m³ increase in PM2.5 was associated with a decrease in the FEV₁ as well as with an increase in oxygen desaturation. A 1 mcg/m³ increase in PM10 and PM2.5 was associated with increases in the total-, right-, left, and upper-lobe LAA; increases in lower-lobe LAA were associated with an increase in PM2.5 only.

“This is reasonable because PM2.5 can travel and deposit in distal parts of the lung, while PM10 is preferably deposited in the larger airways of the upper lung regions,” the researchers wrote in their discussion.

A one part per billion increase in nitrogen dioxide (NO₂) was associated with decreased FEV₁ and increased upper-lobe LAA.

“We observed that NO₂ fully mediated the association between RH and FEV₁, while PM2.5 fully mediated associations of temperature with oxygen saturation and emphysema severity in COPD patients,” the researchers added.

The study findings were limited by several factors including the relatively small and homogeneous male, Taiwanese population, which may limit generalizability, the researchers noted. Other limitations included the lack of control for factors such as body mass index, occupational exposure, comorbidities, medication use, and indoor air pollution, they said.

However, the results suggest that air pollution could have an effect on the established associations between climate and adverse health outcomes in COPD, and more research is needed. Climate change–related air pollution is an important public health issue, especially with regards to respiratory disease,” they concluded.

The study was supported by the Ministry of Science and Technology of Taiwan. The researchers had no financial conflicts to disclose.

Air pollution levels mediated the impact of temperature on oxygen saturation in adults with chronic obstructive pulmonary disease (COPD) based on data from 117 individuals.

COPD is attributed to environmental factors including air pollution, and air pollution has been linked to increased risk of hospitalization and mortality because of acute COPD exacerbation, wrote Huan Minh Tran, PhD, of Taipei (Taiwan) Medical University and colleagues. However, the effects of air pollution on climate-associated health outcomes in COPD have not been explored, they said.

In a study published in Science of The Total Environment the researchers identified 117 adult COPD patients at a single center in Taiwan. They measured lung function, 6-minute walking distance, oxygen desaturation, white blood cell count, and percent emphysema (defined as low attenuation area [LAA]) and linked them to 0- to 1-year, 0- to 3-year, and 0- to 5-year lags in exposures to relative humidity (RH), temperature, and air pollution. The mean age of the participants was 72.9 years; 93% were men.

Pollution was defined in terms of fine particulate matter (PM2.5).

Overall, an increase in RH by 1% was associated with increases in forced expiratory volume in 1 second (FEV₁), eosinophils, and lymphocytes.

A 1% increase in RH also was associated with a decrease in the total-lobe LAA.

As for temperature, an increase of 1° C was associated with decreased oxygen desaturation and with decreases in right-, left-, and upper-lobe LAA values.

When the researchers examined the impact of pollution, they found that a 1 mcg/m³ increase in PM2.5 was associated with a decrease in the FEV₁ as well as with an increase in oxygen desaturation. A 1 mcg/m³ increase in PM10 and PM2.5 was associated with increases in the total-, right-, left, and upper-lobe LAA; increases in lower-lobe LAA were associated with an increase in PM2.5 only.

“This is reasonable because PM2.5 can travel and deposit in distal parts of the lung, while PM10 is preferably deposited in the larger airways of the upper lung regions,” the researchers wrote in their discussion.

A one part per billion increase in nitrogen dioxide (NO₂) was associated with decreased FEV₁ and increased upper-lobe LAA.

“We observed that NO₂ fully mediated the association between RH and FEV₁, while PM2.5 fully mediated associations of temperature with oxygen saturation and emphysema severity in COPD patients,” the researchers added.

The study findings were limited by several factors including the relatively small and homogeneous male, Taiwanese population, which may limit generalizability, the researchers noted. Other limitations included the lack of control for factors such as body mass index, occupational exposure, comorbidities, medication use, and indoor air pollution, they said.

However, the results suggest that air pollution could have an effect on the established associations between climate and adverse health outcomes in COPD, and more research is needed. Climate change–related air pollution is an important public health issue, especially with regards to respiratory disease,” they concluded.

The study was supported by the Ministry of Science and Technology of Taiwan. The researchers had no financial conflicts to disclose.

Patients with chronic obstructive pulmonary disease (COPD) typically have emphysema, which involves destruction of alveoli and reduction of elasticity leading to airflow obstruction, air trapping, and hyperinflation. Over time, these changes cause low respiratory reserve volume and increased residual volume, which cause dyspnea.  

One of the newest treatment options for patients who have advanced COPD with severe emphysema is a minimally invasive procedure called bronchoscopic lung volume reduction (BLVR). Most recently, the FDA approved the use of endobronchial valves for this procedure, which are implanted in the airways of the lungs to reduce air trapping and hyperinflation. 

In certain patients, BLVR has been shown to improve lung function, facilitate easier breathing, enhance exercise tolerance, and lead to better quality of life. 

In this ReCAP, Dr. Javier Diaz-Mendoza, program director of the Interventional Pulmonology Fellowship at Henry Ford Health System in Detroit, discusses the benefits of BLVR in patients who have advanced COPD with emphysema. He discusses the procedure, patient outcomes, and which patients should be considered for BLVR.  

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Associate Professor of Medicine, Henry Ford Hospital, Wayne State University; Program Director, Interventional Pulmonology Fellowship, Henry Ford Health System, Detroit, MI

Javier Diaz-Mendoza, MD, FCCP, has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Ion Intuitive Serve(d) as a speaker or a member of a speakers bureau for: Association of Interventional Pulmonology Program Directors

Patients with chronic obstructive pulmonary disease (COPD) typically have emphysema, which involves destruction of alveoli and reduction of elasticity leading to airflow obstruction, air trapping, and hyperinflation. Over time, these changes cause low respiratory reserve volume and increased residual volume, which cause dyspnea.  

One of the newest treatment options for patients who have advanced COPD with severe emphysema is a minimally invasive procedure called bronchoscopic lung volume reduction (BLVR). Most recently, the FDA approved the use of endobronchial valves for this procedure, which are implanted in the airways of the lungs to reduce air trapping and hyperinflation. 

In certain patients, BLVR has been shown to improve lung function, facilitate easier breathing, enhance exercise tolerance, and lead to better quality of life. 

In this ReCAP, Dr. Javier Diaz-Mendoza, program director of the Interventional Pulmonology Fellowship at Henry Ford Health System in Detroit, discusses the benefits of BLVR in patients who have advanced COPD with emphysema. He discusses the procedure, patient outcomes, and which patients should be considered for BLVR.  

--

Associate Professor of Medicine, Henry Ford Hospital, Wayne State University; Program Director, Interventional Pulmonology Fellowship, Henry Ford Health System, Detroit, MI

Javier Diaz-Mendoza, MD, FCCP, has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Ion Intuitive Serve(d) as a speaker or a member of a speakers bureau for: Association of Interventional Pulmonology Program Directors

Patients with chronic obstructive pulmonary disease (COPD) typically have emphysema, which involves destruction of alveoli and reduction of elasticity leading to airflow obstruction, air trapping, and hyperinflation. Over time, these changes cause low respiratory reserve volume and increased residual volume, which cause dyspnea.  

One of the newest treatment options for patients who have advanced COPD with severe emphysema is a minimally invasive procedure called bronchoscopic lung volume reduction (BLVR). Most recently, the FDA approved the use of endobronchial valves for this procedure, which are implanted in the airways of the lungs to reduce air trapping and hyperinflation. 

In certain patients, BLVR has been shown to improve lung function, facilitate easier breathing, enhance exercise tolerance, and lead to better quality of life. 

In this ReCAP, Dr. Javier Diaz-Mendoza, program director of the Interventional Pulmonology Fellowship at Henry Ford Health System in Detroit, discusses the benefits of BLVR in patients who have advanced COPD with emphysema. He discusses the procedure, patient outcomes, and which patients should be considered for BLVR.  

--

Associate Professor of Medicine, Henry Ford Hospital, Wayne State University; Program Director, Interventional Pulmonology Fellowship, Henry Ford Health System, Detroit, MI

Javier Diaz-Mendoza, MD, FCCP, has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Ion Intuitive Serve(d) as a speaker or a member of a speakers bureau for: Association of Interventional Pulmonology Program Directors

Treatment with an interleukin-6 neutralizing antibody significantly reduced airway mucus hypersecretion (AMH) in chronic obstructive pulmonary disease (COPD), based on data from human and mouse cells in a human organoid model.

AMH plays a large part in aggravating airway obstruction in patients with COPD, Yuan-Yuan Wei, MD, of First Affiliated Hospital of Anhui Medical University, Hefei, China, and colleagues wrote.

Current pharmacotherapies relieve COPD symptoms and improve exercise tolerance, but have not proven effective for relieving the airflow limitations caused by mucus accumulation that “leads to irreversible structural damage and an unfavorable prognosis,” the researchers said. Although reducing AMH could help manage COPD, the molecular mechanisms of action have not been fully explored.

In a study published in Biomedicine & Pharmacotherapy , the researchers examined the relationship between IL-6 and AMH. Since IL-6 has been shown to cause overexpression of the mucin-type protein known as Muc5ac, they hypothesized that IL-6 antibodies (IL-6Ab) might block this protein elevation.

The researchers recruited 30 adults with COPD and 30 controls from a single center. Bronchial epithelial cells were isolated from the participants and measured the levels of Muc5ac protein and mRNA in the lung tissue. Compared with controls, COPD patients had elevated Muc5ac positively correlated with IL-6.

The researchers then created an organoid model of a trachea for COPD patients and controls. In the model, Muc5ac was similarly elevated in COPD patients, compared with controls. “Furthermore, IL-6 significantly induced excessive secretion of mucus in the organoid model of trachea in COPD patients as observed under electron microscope, and IL-6Ab attenuated these effects,” they noted.

IL-6 significantly increased both Muc5ac mRNA and protein expression in the organoid model of trachea (P < .0001 and P < .005, respectively), but both of these significantly decreased when treated with IL-6Ab (P < .0001 and P < .05, respectively).

The researchers also examined human and mouse cells to explore the mechanism of action of IL-6Ab. Using high-throughput sequencing, they found that the IL-6Ab induced nuclear translocation of the Nrt2 gene in COPD patients, and that this action promoted the effect of IL-6Ab on excessive mucus secretion.

The study findings were limited by the relatively small study population from a single center, the researchers noted.

However, the results support the potential of IL-6Ab as “a novel therapeutic strategy in the treatment of IL-6–induced hypersecretion of airway mucus so as to improve airflow limitations in COPD,” they concluded.

The study was supported by supported by the National Natural Science Foundation of China and the Scientific Research Project of Education Department of Anhui Province. The researchers had no financial conflicts to disclose.

Treatment with an interleukin-6 neutralizing antibody significantly reduced airway mucus hypersecretion (AMH) in chronic obstructive pulmonary disease (COPD), based on data from human and mouse cells in a human organoid model.

AMH plays a large part in aggravating airway obstruction in patients with COPD, Yuan-Yuan Wei, MD, of First Affiliated Hospital of Anhui Medical University, Hefei, China, and colleagues wrote.

Current pharmacotherapies relieve COPD symptoms and improve exercise tolerance, but have not proven effective for relieving the airflow limitations caused by mucus accumulation that “leads to irreversible structural damage and an unfavorable prognosis,” the researchers said. Although reducing AMH could help manage COPD, the molecular mechanisms of action have not been fully explored.

In a study published in Biomedicine & Pharmacotherapy , the researchers examined the relationship between IL-6 and AMH. Since IL-6 has been shown to cause overexpression of the mucin-type protein known as Muc5ac, they hypothesized that IL-6 antibodies (IL-6Ab) might block this protein elevation.

The researchers recruited 30 adults with COPD and 30 controls from a single center. Bronchial epithelial cells were isolated from the participants and measured the levels of Muc5ac protein and mRNA in the lung tissue. Compared with controls, COPD patients had elevated Muc5ac positively correlated with IL-6.

The researchers then created an organoid model of a trachea for COPD patients and controls. In the model, Muc5ac was similarly elevated in COPD patients, compared with controls. “Furthermore, IL-6 significantly induced excessive secretion of mucus in the organoid model of trachea in COPD patients as observed under electron microscope, and IL-6Ab attenuated these effects,” they noted.

IL-6 significantly increased both Muc5ac mRNA and protein expression in the organoid model of trachea (P < .0001 and P < .005, respectively), but both of these significantly decreased when treated with IL-6Ab (P < .0001 and P < .05, respectively).

The researchers also examined human and mouse cells to explore the mechanism of action of IL-6Ab. Using high-throughput sequencing, they found that the IL-6Ab induced nuclear translocation of the Nrt2 gene in COPD patients, and that this action promoted the effect of IL-6Ab on excessive mucus secretion.

The study findings were limited by the relatively small study population from a single center, the researchers noted.

However, the results support the potential of IL-6Ab as “a novel therapeutic strategy in the treatment of IL-6–induced hypersecretion of airway mucus so as to improve airflow limitations in COPD,” they concluded.

The study was supported by supported by the National Natural Science Foundation of China and the Scientific Research Project of Education Department of Anhui Province. The researchers had no financial conflicts to disclose.

Treatment with an interleukin-6 neutralizing antibody significantly reduced airway mucus hypersecretion (AMH) in chronic obstructive pulmonary disease (COPD), based on data from human and mouse cells in a human organoid model.

AMH plays a large part in aggravating airway obstruction in patients with COPD, Yuan-Yuan Wei, MD, of First Affiliated Hospital of Anhui Medical University, Hefei, China, and colleagues wrote.

Current pharmacotherapies relieve COPD symptoms and improve exercise tolerance, but have not proven effective for relieving the airflow limitations caused by mucus accumulation that “leads to irreversible structural damage and an unfavorable prognosis,” the researchers said. Although reducing AMH could help manage COPD, the molecular mechanisms of action have not been fully explored.

In a study published in Biomedicine & Pharmacotherapy , the researchers examined the relationship between IL-6 and AMH. Since IL-6 has been shown to cause overexpression of the mucin-type protein known as Muc5ac, they hypothesized that IL-6 antibodies (IL-6Ab) might block this protein elevation.

The researchers recruited 30 adults with COPD and 30 controls from a single center. Bronchial epithelial cells were isolated from the participants and measured the levels of Muc5ac protein and mRNA in the lung tissue. Compared with controls, COPD patients had elevated Muc5ac positively correlated with IL-6.

The researchers then created an organoid model of a trachea for COPD patients and controls. In the model, Muc5ac was similarly elevated in COPD patients, compared with controls. “Furthermore, IL-6 significantly induced excessive secretion of mucus in the organoid model of trachea in COPD patients as observed under electron microscope, and IL-6Ab attenuated these effects,” they noted.

IL-6 significantly increased both Muc5ac mRNA and protein expression in the organoid model of trachea (P < .0001 and P < .005, respectively), but both of these significantly decreased when treated with IL-6Ab (P < .0001 and P < .05, respectively).

The researchers also examined human and mouse cells to explore the mechanism of action of IL-6Ab. Using high-throughput sequencing, they found that the IL-6Ab induced nuclear translocation of the Nrt2 gene in COPD patients, and that this action promoted the effect of IL-6Ab on excessive mucus secretion.

The study findings were limited by the relatively small study population from a single center, the researchers noted.

However, the results support the potential of IL-6Ab as “a novel therapeutic strategy in the treatment of IL-6–induced hypersecretion of airway mucus so as to improve airflow limitations in COPD,” they concluded.

The study was supported by supported by the National Natural Science Foundation of China and the Scientific Research Project of Education Department of Anhui Province. The researchers had no financial conflicts to disclose.

High levels of eosinophils had a protective effect for individuals who experienced acute exacerbations of chronic obstructive pulmonary disease, based on data from nearly 1,000 patients.

Several blood biomarkers are under investigation for links to acute exacerbation of chronic obstructive pulmonary disease (AECOPD), which remains one of the top three causes of death worldwide, wrote Riuying Wang, MD, of Third Hospital of Shanxi Medical University, Taiyuan, China, and colleagues.

“Numerous studies have shown the relationship between eosinophilia and clinical outcomes of patients with AECOPD. However, the evidence lacks consensus, and the research thresholds are controversial,” they said.

In a study published in Heart & Lung, the researchers reviewed data from 984 adults with AECOPD over a 3-year follow-up period. The mean age of the patients was 71 years, and 78% were men. The patients’ blood eosinophil levels were grouped into three categories: EOS < 2%, EOS from 2% to < 3%, and 3% or higher. The researchers examined the association between eosinophilia and various comorbidities, treatment, and mortality.

Eosinophilia occurred in 477 cases. The prevalence of eosinophilia in the three groups was 36.48%, 22.87%, and 48.48% respectively, with eosinophilia defined as eosinophil counts of at least 100 cells per microliter, according to the report in Heart & Lung.

An EOS of 2% or higher was associated with significantly fewer cases of complicated pulmonary heart disease and atrial fibrillation than the lower EOS group. Similarly, patients in the EOS group of 2% or higher were less likely to use ventilators and systemic glucocorticoids and those in the EOS less than 2% group had significantly heavier airflow limitation, higher D-dimer, higher burden of infectious inflammation, and higher prevalence of respiratory failure than the other groups.

In addition, significantly fewer deaths occurred during the study period among patients with EOS of 2% or higher, compared with the lower EOS group (P < .01). The findings suggest that “Eosinophils can be used as a prognostic indicator of mortality in AECOPD,” the researchers said.

The researchers also used the area under the curve to examine the predictive value of EOS. The ROC curve showed that the indicators of AUC 0.5 included chest CT imaging, osteoporosis, mental illness, dust exposure, and being a former smoker; however, “the predictive value of EOS by the ROC curve was unstable. Further validation in large samples is needed,” the researchers wrote in their discussion.

The study findings were limited by several factors including the retrospective design and use of data from a single center, the researchers noted. Other limitations included the relatively small sample size and a lack of data on some clinical features and performance metrics, as well as lack of evaluation of chest CT subtypes.

However, the results are consistent with previous studies on infection and antibiotics and reviewed the optimal threshold of AECOPD, the researchers wrote. Based on their findings, “Eosinophils can not only guide clinical treatment but also be used as an index to predict the clinical outcome and prognosis of AECOPD patients,” they concluded.

The study received no outside funding. The researchers had no financial conflicts to disclose.

High levels of eosinophils had a protective effect for individuals who experienced acute exacerbations of chronic obstructive pulmonary disease, based on data from nearly 1,000 patients.

Several blood biomarkers are under investigation for links to acute exacerbation of chronic obstructive pulmonary disease (AECOPD), which remains one of the top three causes of death worldwide, wrote Riuying Wang, MD, of Third Hospital of Shanxi Medical University, Taiyuan, China, and colleagues.

“Numerous studies have shown the relationship between eosinophilia and clinical outcomes of patients with AECOPD. However, the evidence lacks consensus, and the research thresholds are controversial,” they said.

In a study published in Heart & Lung, the researchers reviewed data from 984 adults with AECOPD over a 3-year follow-up period. The mean age of the patients was 71 years, and 78% were men. The patients’ blood eosinophil levels were grouped into three categories: EOS < 2%, EOS from 2% to < 3%, and 3% or higher. The researchers examined the association between eosinophilia and various comorbidities, treatment, and mortality.

Eosinophilia occurred in 477 cases. The prevalence of eosinophilia in the three groups was 36.48%, 22.87%, and 48.48% respectively, with eosinophilia defined as eosinophil counts of at least 100 cells per microliter, according to the report in Heart & Lung.

An EOS of 2% or higher was associated with significantly fewer cases of complicated pulmonary heart disease and atrial fibrillation than the lower EOS group. Similarly, patients in the EOS group of 2% or higher were less likely to use ventilators and systemic glucocorticoids and those in the EOS less than 2% group had significantly heavier airflow limitation, higher D-dimer, higher burden of infectious inflammation, and higher prevalence of respiratory failure than the other groups.

In addition, significantly fewer deaths occurred during the study period among patients with EOS of 2% or higher, compared with the lower EOS group (P < .01). The findings suggest that “Eosinophils can be used as a prognostic indicator of mortality in AECOPD,” the researchers said.

The researchers also used the area under the curve to examine the predictive value of EOS. The ROC curve showed that the indicators of AUC 0.5 included chest CT imaging, osteoporosis, mental illness, dust exposure, and being a former smoker; however, “the predictive value of EOS by the ROC curve was unstable. Further validation in large samples is needed,” the researchers wrote in their discussion.

The study findings were limited by several factors including the retrospective design and use of data from a single center, the researchers noted. Other limitations included the relatively small sample size and a lack of data on some clinical features and performance metrics, as well as lack of evaluation of chest CT subtypes.

However, the results are consistent with previous studies on infection and antibiotics and reviewed the optimal threshold of AECOPD, the researchers wrote. Based on their findings, “Eosinophils can not only guide clinical treatment but also be used as an index to predict the clinical outcome and prognosis of AECOPD patients,” they concluded.

The study received no outside funding. The researchers had no financial conflicts to disclose.

High levels of eosinophils had a protective effect for individuals who experienced acute exacerbations of chronic obstructive pulmonary disease, based on data from nearly 1,000 patients.

Several blood biomarkers are under investigation for links to acute exacerbation of chronic obstructive pulmonary disease (AECOPD), which remains one of the top three causes of death worldwide, wrote Riuying Wang, MD, of Third Hospital of Shanxi Medical University, Taiyuan, China, and colleagues.

“Numerous studies have shown the relationship between eosinophilia and clinical outcomes of patients with AECOPD. However, the evidence lacks consensus, and the research thresholds are controversial,” they said.

In a study published in Heart & Lung, the researchers reviewed data from 984 adults with AECOPD over a 3-year follow-up period. The mean age of the patients was 71 years, and 78% were men. The patients’ blood eosinophil levels were grouped into three categories: EOS < 2%, EOS from 2% to < 3%, and 3% or higher. The researchers examined the association between eosinophilia and various comorbidities, treatment, and mortality.

Eosinophilia occurred in 477 cases. The prevalence of eosinophilia in the three groups was 36.48%, 22.87%, and 48.48% respectively, with eosinophilia defined as eosinophil counts of at least 100 cells per microliter, according to the report in Heart & Lung.

An EOS of 2% or higher was associated with significantly fewer cases of complicated pulmonary heart disease and atrial fibrillation than the lower EOS group. Similarly, patients in the EOS group of 2% or higher were less likely to use ventilators and systemic glucocorticoids and those in the EOS less than 2% group had significantly heavier airflow limitation, higher D-dimer, higher burden of infectious inflammation, and higher prevalence of respiratory failure than the other groups.

In addition, significantly fewer deaths occurred during the study period among patients with EOS of 2% or higher, compared with the lower EOS group (P < .01). The findings suggest that “Eosinophils can be used as a prognostic indicator of mortality in AECOPD,” the researchers said.

The researchers also used the area under the curve to examine the predictive value of EOS. The ROC curve showed that the indicators of AUC 0.5 included chest CT imaging, osteoporosis, mental illness, dust exposure, and being a former smoker; however, “the predictive value of EOS by the ROC curve was unstable. Further validation in large samples is needed,” the researchers wrote in their discussion.

The study findings were limited by several factors including the retrospective design and use of data from a single center, the researchers noted. Other limitations included the relatively small sample size and a lack of data on some clinical features and performance metrics, as well as lack of evaluation of chest CT subtypes.

However, the results are consistent with previous studies on infection and antibiotics and reviewed the optimal threshold of AECOPD, the researchers wrote. Based on their findings, “Eosinophils can not only guide clinical treatment but also be used as an index to predict the clinical outcome and prognosis of AECOPD patients,” they concluded.

The study received no outside funding. The researchers had no financial conflicts to disclose.

Poor sleep quality was linked to an increased risk of life-threatening exacerbations in people with chronic obstructive pulmonary disease (COPD), according to a study reported online in the journal Sleep.

Researchers followed 1,647 patients with confirmed COPD who were enrolled in the Subpopulations and Intermediate Outcome Measures in COPD Study (SPIROMICS). SPIROMICS is a multicenter study funded by the National Heart, Lung, and Blood Institute and the COPD Foundation and is designed to evaluate COPD subpopulations, outcomes, and biomarkers. All participants in the study were current or former smokers with confirmed COPD.

COPD exacerbations over a 3-year follow-up period were compared against reported sleep quality. The researchers used the Pittsburgh Sleep Quality Index (PSQI), a combination of seven sleep measures, including sleep duration, timing of sleep, and frequency of disturbances. The higher the score, the worse the quality of sleep.

Individuals who self-reported having poor-quality sleep had a 25%-95% higher risk of COPD exacerbations, compared with those who reported good-quality sleep, according to the results.

There was a significant association between PSQI score and total and mean exacerbations in the unadjusted analysis (incidence rate ratios, 1.09; 95% confidence interval, 1.05-1.13) and the analysis adjusted for demographics, medical comorbidities, disease severity, medication usage, and socioeconomic environmental exposure (IRR, 1.08; 95% CI, 1.03-1.13).

In addition, the PSQI score was independently associated with an increased risk of hospitalization, with a 7% increase in risk of hospitalization with each 1-point increase in PSQI, according to the researchers.
 

Surprising findings

These findings suggest that sleep quality may be a better predictor of flare-ups than the patient’s history of smoking, according to the researchers.

“Among those who already have COPD, knowing how they sleep at night will tell me much more about their risk of a flare-up than knowing whether they smoked for 40 versus 60 years. … That is very surprising and is not necessarily what I expected going into this study. Smoking is such a central process to COPD that I would have predicted it would be the more important predictor in the case of exacerbations,” said lead study author Aaron Baugh, MD, a practicing pulmonologist, and a clinical fellow at the University of California, San Francisco, in a National Institutes of Health press release on the study.

The study findings were applicable to all races and ethnicities studied, however the results may be particularly relevant to Black Americans, Dr. Baugh indicated, because past studies have shown that Black Americans tend to have poorer sleep quality than other races and ethnicities. With poorer sleep linked to worse COPD outcomes, the current study may help explain why Black Americans as a group tend to do worse when they have COPD, compared with other racial and ethnic groups, the researchers suggested.

The study was supported by the National Institutes of Health and the COPD Foundation. SPIROMICS was supported by NIH and the COPD Foundation as well as numerous pharmaceutical and biotechnology companies. The authors reported no other financial disclosures.

Poor sleep quality was linked to an increased risk of life-threatening exacerbations in people with chronic obstructive pulmonary disease (COPD), according to a study reported online in the journal Sleep.

Researchers followed 1,647 patients with confirmed COPD who were enrolled in the Subpopulations and Intermediate Outcome Measures in COPD Study (SPIROMICS). SPIROMICS is a multicenter study funded by the National Heart, Lung, and Blood Institute and the COPD Foundation and is designed to evaluate COPD subpopulations, outcomes, and biomarkers. All participants in the study were current or former smokers with confirmed COPD.

COPD exacerbations over a 3-year follow-up period were compared against reported sleep quality. The researchers used the Pittsburgh Sleep Quality Index (PSQI), a combination of seven sleep measures, including sleep duration, timing of sleep, and frequency of disturbances. The higher the score, the worse the quality of sleep.

Individuals who self-reported having poor-quality sleep had a 25%-95% higher risk of COPD exacerbations, compared with those who reported good-quality sleep, according to the results.

There was a significant association between PSQI score and total and mean exacerbations in the unadjusted analysis (incidence rate ratios, 1.09; 95% confidence interval, 1.05-1.13) and the analysis adjusted for demographics, medical comorbidities, disease severity, medication usage, and socioeconomic environmental exposure (IRR, 1.08; 95% CI, 1.03-1.13).

In addition, the PSQI score was independently associated with an increased risk of hospitalization, with a 7% increase in risk of hospitalization with each 1-point increase in PSQI, according to the researchers.
 

Surprising findings

These findings suggest that sleep quality may be a better predictor of flare-ups than the patient’s history of smoking, according to the researchers.

“Among those who already have COPD, knowing how they sleep at night will tell me much more about their risk of a flare-up than knowing whether they smoked for 40 versus 60 years. … That is very surprising and is not necessarily what I expected going into this study. Smoking is such a central process to COPD that I would have predicted it would be the more important predictor in the case of exacerbations,” said lead study author Aaron Baugh, MD, a practicing pulmonologist, and a clinical fellow at the University of California, San Francisco, in a National Institutes of Health press release on the study.

The study findings were applicable to all races and ethnicities studied, however the results may be particularly relevant to Black Americans, Dr. Baugh indicated, because past studies have shown that Black Americans tend to have poorer sleep quality than other races and ethnicities. With poorer sleep linked to worse COPD outcomes, the current study may help explain why Black Americans as a group tend to do worse when they have COPD, compared with other racial and ethnic groups, the researchers suggested.

The study was supported by the National Institutes of Health and the COPD Foundation. SPIROMICS was supported by NIH and the COPD Foundation as well as numerous pharmaceutical and biotechnology companies. The authors reported no other financial disclosures.

Poor sleep quality was linked to an increased risk of life-threatening exacerbations in people with chronic obstructive pulmonary disease (COPD), according to a study reported online in the journal Sleep.

Researchers followed 1,647 patients with confirmed COPD who were enrolled in the Subpopulations and Intermediate Outcome Measures in COPD Study (SPIROMICS). SPIROMICS is a multicenter study funded by the National Heart, Lung, and Blood Institute and the COPD Foundation and is designed to evaluate COPD subpopulations, outcomes, and biomarkers. All participants in the study were current or former smokers with confirmed COPD.

COPD exacerbations over a 3-year follow-up period were compared against reported sleep quality. The researchers used the Pittsburgh Sleep Quality Index (PSQI), a combination of seven sleep measures, including sleep duration, timing of sleep, and frequency of disturbances. The higher the score, the worse the quality of sleep.

Individuals who self-reported having poor-quality sleep had a 25%-95% higher risk of COPD exacerbations, compared with those who reported good-quality sleep, according to the results.

There was a significant association between PSQI score and total and mean exacerbations in the unadjusted analysis (incidence rate ratios, 1.09; 95% confidence interval, 1.05-1.13) and the analysis adjusted for demographics, medical comorbidities, disease severity, medication usage, and socioeconomic environmental exposure (IRR, 1.08; 95% CI, 1.03-1.13).

In addition, the PSQI score was independently associated with an increased risk of hospitalization, with a 7% increase in risk of hospitalization with each 1-point increase in PSQI, according to the researchers.
 

Surprising findings

These findings suggest that sleep quality may be a better predictor of flare-ups than the patient’s history of smoking, according to the researchers.

“Among those who already have COPD, knowing how they sleep at night will tell me much more about their risk of a flare-up than knowing whether they smoked for 40 versus 60 years. … That is very surprising and is not necessarily what I expected going into this study. Smoking is such a central process to COPD that I would have predicted it would be the more important predictor in the case of exacerbations,” said lead study author Aaron Baugh, MD, a practicing pulmonologist, and a clinical fellow at the University of California, San Francisco, in a National Institutes of Health press release on the study.

The study findings were applicable to all races and ethnicities studied, however the results may be particularly relevant to Black Americans, Dr. Baugh indicated, because past studies have shown that Black Americans tend to have poorer sleep quality than other races and ethnicities. With poorer sleep linked to worse COPD outcomes, the current study may help explain why Black Americans as a group tend to do worse when they have COPD, compared with other racial and ethnic groups, the researchers suggested.

The study was supported by the National Institutes of Health and the COPD Foundation. SPIROMICS was supported by NIH and the COPD Foundation as well as numerous pharmaceutical and biotechnology companies. The authors reported no other financial disclosures.

For many years, COPD has remained one of the top four leading causes of death in the United States according to CDC data. Around the world, it is responsible for about 3 million deaths annually. It is estimated that 16 million Americans are now diagnosed with COPD. However, it is commonly agreed by experts that it is widely underdiagnosed and there may be millions more suffering from this disease.

The direct costs of COPD are around $49 billion a year in direct costs, with billions more in indirect costs. Around the globe, COPD is one of the top three causes of death, with 90% of deaths happening in low- and middle-income countries. The burden of COPD is expected to grow over time because of the aging population and continued exposure to COPD risk factors.

The Global Initiative for Chronic Obstructive Lung Disease report (or GOLD) is revised every year, translated into many languages, and used by health care workers globally. It was started in 1998, and its aim was to produce guidelines based on the best scientific evidence available that was nonbiased to be used for assessment, diagnosis, and treatment of patients with COPD. The first report was issued in 2001. The method of producing the GOLD report was to do a search of PubMed for evidence-based, peer-reviewed studies. Those not captured by this method could be submitted for review. The science committee then meets twice a year and reviews each publication, eventually agreeing on a set of guidelines/updates.
 

2022 GOLD Report

For the 2022 GOLD report, 160 new references were added. Overall, the GOLD report is five chapters (more than 150 pages) giving in-depth guidance for the diagnosis, prevention, management, and treatment of patients with stable COPD, COPD exacerbations, and hospitalized patients.

The report suggests that COPD is being underdiagnosed. It’s important for primary care doctors to understand the new guidelines, because they are the clinicians who are most likely to be diagnosing and treating patients with COPD.

Family physicians and internists will be seeing more and more cases as the population ages, and we need to do a better job of recognizing patients who have COPD. If possible, we should try to have spirometry available in our practices. Like any other disease, we know prevention works best so primary care physicians also need to be looking for risk factors, such as smoking history, and help patients try to reduce them if possible. Below is more explanation of the latest guidelines.

For most of us, when we learned about COPD as a disease, the terms “chronic bronchitis” and “emphysema” were emphasized. These words are no longer used as synonymous for COPD.

The disease is now described as involving chronic limitation in airflow that results from a combination of small airway disease and parenchymal destruction (emphysema). The rates of each vary from person to person and progress at different rates. Key factors that contribute to COPD disease burden include chronic inflammation, narrowing of small airways, loss of alveolar attachments, loss of elastic recoil, and mucociliary dysfunction, according to the 2022 GOLD report.

Respiratory symptoms may precede the onset of airflow limitation. COPD should be considered in any patient with dyspnea, chronic cough or sputum production, a history of recurrent lower respiratory tract infections, and risk factors for the disease.

The biggest risk factor for COPD is smoking. Other risk factors include occupational exposure, e-cigarette use, pollution, genetic factors, and comorbid conditions. Symptoms of the disease can include chest tightness, wheezing, and fatigue.

To make a diagnosis of COPD, spirometry is required, the latest GOLD report says. A postbronchodilator FEV₁/FVC less than 0.70 confirms persistent airflow limitation and hence COPD. This value is used in clinical trials and forms the basis of what most treatment guidelines are derived from. It would be beneficial for any physician treating COPD patients to have easy access to spirometry. It provides the most reproducible and objective measurement of airflow limitation. Also, it was found that assessing the degree of reversibility of airflow limitation to decide therapeutic decisions is no longer recommended and thus, asking the patient to stop inhaled medications beforehand is unnecessary. To access the impact COPD has on a patient’s life beyond dyspnea, the guidelines recommend doing a disease-specific health questionnaire, such as the COPD Assessment Test (CAT).

Along with patient symptoms and history of exacerbations, spirometry is crucial for the diagnosis, prognosis, and therapeutic decisions in COPD patients, according to the GOLD guidance. The best predictor of frequent exacerbations, however, is a history of previous exacerbations. In cases where there is a discrepancy between airflow limitation and symptoms, additional testing should be considered. Alpha-1 antitrypsin deficiency (AATD) screening should be considered in younger patients (under 45 years) with perilobular emphysema, and those in areas of high AATD prevalence. Chest x-rays are not recommended in diagnosing COPD but can be helpful if other comorbidities are present. CT scan is not routinely recommended but should be used only for the detection of bronchiectasis, if the patient meets the criteria for lung cancer screening, if surgery is necessary, or if other diseases may need to be evaluated.

Pulse oximetry can be helpful in accessing degree of severity, respiratory failure, and right heart failure. Walking tests can be helpful for evaluating disability and mortality risk. Other tests that have been used but are not routinely recommended include plethysmography and diffusing capacity of the lungs for carbon monoxide.

Composite scores can identify patients who are at increased risk of mortality. One such score is the BODE (Body mass, Obstruction, Dyspnea, and Exercise) method. Biomarkers are being investigated, but data are still not available to recommend their routine use.
 

Dr. Girgis practices family medicine in South River, N.J., and is a clinical assistant professor of family medicine at Robert Wood Johnson Medical School, New Brunswick, N.J. You can contact her at fpnews@mdedge.com.

For many years, COPD has remained one of the top four leading causes of death in the United States according to CDC data. Around the world, it is responsible for about 3 million deaths annually. It is estimated that 16 million Americans are now diagnosed with COPD. However, it is commonly agreed by experts that it is widely underdiagnosed and there may be millions more suffering from this disease.

The direct costs of COPD are around $49 billion a year in direct costs, with billions more in indirect costs. Around the globe, COPD is one of the top three causes of death, with 90% of deaths happening in low- and middle-income countries. The burden of COPD is expected to grow over time because of the aging population and continued exposure to COPD risk factors.

The Global Initiative for Chronic Obstructive Lung Disease report (or GOLD) is revised every year, translated into many languages, and used by health care workers globally. It was started in 1998, and its aim was to produce guidelines based on the best scientific evidence available that was nonbiased to be used for assessment, diagnosis, and treatment of patients with COPD. The first report was issued in 2001. The method of producing the GOLD report was to do a search of PubMed for evidence-based, peer-reviewed studies. Those not captured by this method could be submitted for review. The science committee then meets twice a year and reviews each publication, eventually agreeing on a set of guidelines/updates.
 

2022 GOLD Report

For the 2022 GOLD report, 160 new references were added. Overall, the GOLD report is five chapters (more than 150 pages) giving in-depth guidance for the diagnosis, prevention, management, and treatment of patients with stable COPD, COPD exacerbations, and hospitalized patients.

The report suggests that COPD is being underdiagnosed. It’s important for primary care doctors to understand the new guidelines, because they are the clinicians who are most likely to be diagnosing and treating patients with COPD.

Family physicians and internists will be seeing more and more cases as the population ages, and we need to do a better job of recognizing patients who have COPD. If possible, we should try to have spirometry available in our practices. Like any other disease, we know prevention works best so primary care physicians also need to be looking for risk factors, such as smoking history, and help patients try to reduce them if possible. Below is more explanation of the latest guidelines.

For most of us, when we learned about COPD as a disease, the terms “chronic bronchitis” and “emphysema” were emphasized. These words are no longer used as synonymous for COPD.

The disease is now described as involving chronic limitation in airflow that results from a combination of small airway disease and parenchymal destruction (emphysema). The rates of each vary from person to person and progress at different rates. Key factors that contribute to COPD disease burden include chronic inflammation, narrowing of small airways, loss of alveolar attachments, loss of elastic recoil, and mucociliary dysfunction, according to the 2022 GOLD report.

Respiratory symptoms may precede the onset of airflow limitation. COPD should be considered in any patient with dyspnea, chronic cough or sputum production, a history of recurrent lower respiratory tract infections, and risk factors for the disease.

The biggest risk factor for COPD is smoking. Other risk factors include occupational exposure, e-cigarette use, pollution, genetic factors, and comorbid conditions. Symptoms of the disease can include chest tightness, wheezing, and fatigue.

To make a diagnosis of COPD, spirometry is required, the latest GOLD report says. A postbronchodilator FEV₁/FVC less than 0.70 confirms persistent airflow limitation and hence COPD. This value is used in clinical trials and forms the basis of what most treatment guidelines are derived from. It would be beneficial for any physician treating COPD patients to have easy access to spirometry. It provides the most reproducible and objective measurement of airflow limitation. Also, it was found that assessing the degree of reversibility of airflow limitation to decide therapeutic decisions is no longer recommended and thus, asking the patient to stop inhaled medications beforehand is unnecessary. To access the impact COPD has on a patient’s life beyond dyspnea, the guidelines recommend doing a disease-specific health questionnaire, such as the COPD Assessment Test (CAT).

Along with patient symptoms and history of exacerbations, spirometry is crucial for the diagnosis, prognosis, and therapeutic decisions in COPD patients, according to the GOLD guidance. The best predictor of frequent exacerbations, however, is a history of previous exacerbations. In cases where there is a discrepancy between airflow limitation and symptoms, additional testing should be considered. Alpha-1 antitrypsin deficiency (AATD) screening should be considered in younger patients (under 45 years) with perilobular emphysema, and those in areas of high AATD prevalence. Chest x-rays are not recommended in diagnosing COPD but can be helpful if other comorbidities are present. CT scan is not routinely recommended but should be used only for the detection of bronchiectasis, if the patient meets the criteria for lung cancer screening, if surgery is necessary, or if other diseases may need to be evaluated.

Pulse oximetry can be helpful in accessing degree of severity, respiratory failure, and right heart failure. Walking tests can be helpful for evaluating disability and mortality risk. Other tests that have been used but are not routinely recommended include plethysmography and diffusing capacity of the lungs for carbon monoxide.

Composite scores can identify patients who are at increased risk of mortality. One such score is the BODE (Body mass, Obstruction, Dyspnea, and Exercise) method. Biomarkers are being investigated, but data are still not available to recommend their routine use.
 

Dr. Girgis practices family medicine in South River, N.J., and is a clinical assistant professor of family medicine at Robert Wood Johnson Medical School, New Brunswick, N.J. You can contact her at fpnews@mdedge.com.

For many years, COPD has remained one of the top four leading causes of death in the United States according to CDC data. Around the world, it is responsible for about 3 million deaths annually. It is estimated that 16 million Americans are now diagnosed with COPD. However, it is commonly agreed by experts that it is widely underdiagnosed and there may be millions more suffering from this disease.

The direct costs of COPD are around $49 billion a year in direct costs, with billions more in indirect costs. Around the globe, COPD is one of the top three causes of death, with 90% of deaths happening in low- and middle-income countries. The burden of COPD is expected to grow over time because of the aging population and continued exposure to COPD risk factors.

The Global Initiative for Chronic Obstructive Lung Disease report (or GOLD) is revised every year, translated into many languages, and used by health care workers globally. It was started in 1998, and its aim was to produce guidelines based on the best scientific evidence available that was nonbiased to be used for assessment, diagnosis, and treatment of patients with COPD. The first report was issued in 2001. The method of producing the GOLD report was to do a search of PubMed for evidence-based, peer-reviewed studies. Those not captured by this method could be submitted for review. The science committee then meets twice a year and reviews each publication, eventually agreeing on a set of guidelines/updates.
 

2022 GOLD Report

For the 2022 GOLD report, 160 new references were added. Overall, the GOLD report is five chapters (more than 150 pages) giving in-depth guidance for the diagnosis, prevention, management, and treatment of patients with stable COPD, COPD exacerbations, and hospitalized patients.

The report suggests that COPD is being underdiagnosed. It’s important for primary care doctors to understand the new guidelines, because they are the clinicians who are most likely to be diagnosing and treating patients with COPD.

Family physicians and internists will be seeing more and more cases as the population ages, and we need to do a better job of recognizing patients who have COPD. If possible, we should try to have spirometry available in our practices. Like any other disease, we know prevention works best so primary care physicians also need to be looking for risk factors, such as smoking history, and help patients try to reduce them if possible. Below is more explanation of the latest guidelines.

For most of us, when we learned about COPD as a disease, the terms “chronic bronchitis” and “emphysema” were emphasized. These words are no longer used as synonymous for COPD.

The disease is now described as involving chronic limitation in airflow that results from a combination of small airway disease and parenchymal destruction (emphysema). The rates of each vary from person to person and progress at different rates. Key factors that contribute to COPD disease burden include chronic inflammation, narrowing of small airways, loss of alveolar attachments, loss of elastic recoil, and mucociliary dysfunction, according to the 2022 GOLD report.

Respiratory symptoms may precede the onset of airflow limitation. COPD should be considered in any patient with dyspnea, chronic cough or sputum production, a history of recurrent lower respiratory tract infections, and risk factors for the disease.

The biggest risk factor for COPD is smoking. Other risk factors include occupational exposure, e-cigarette use, pollution, genetic factors, and comorbid conditions. Symptoms of the disease can include chest tightness, wheezing, and fatigue.

To make a diagnosis of COPD, spirometry is required, the latest GOLD report says. A postbronchodilator FEV₁/FVC less than 0.70 confirms persistent airflow limitation and hence COPD. This value is used in clinical trials and forms the basis of what most treatment guidelines are derived from. It would be beneficial for any physician treating COPD patients to have easy access to spirometry. It provides the most reproducible and objective measurement of airflow limitation. Also, it was found that assessing the degree of reversibility of airflow limitation to decide therapeutic decisions is no longer recommended and thus, asking the patient to stop inhaled medications beforehand is unnecessary. To access the impact COPD has on a patient’s life beyond dyspnea, the guidelines recommend doing a disease-specific health questionnaire, such as the COPD Assessment Test (CAT).

Along with patient symptoms and history of exacerbations, spirometry is crucial for the diagnosis, prognosis, and therapeutic decisions in COPD patients, according to the GOLD guidance. The best predictor of frequent exacerbations, however, is a history of previous exacerbations. In cases where there is a discrepancy between airflow limitation and symptoms, additional testing should be considered. Alpha-1 antitrypsin deficiency (AATD) screening should be considered in younger patients (under 45 years) with perilobular emphysema, and those in areas of high AATD prevalence. Chest x-rays are not recommended in diagnosing COPD but can be helpful if other comorbidities are present. CT scan is not routinely recommended but should be used only for the detection of bronchiectasis, if the patient meets the criteria for lung cancer screening, if surgery is necessary, or if other diseases may need to be evaluated.

Pulse oximetry can be helpful in accessing degree of severity, respiratory failure, and right heart failure. Walking tests can be helpful for evaluating disability and mortality risk. Other tests that have been used but are not routinely recommended include plethysmography and diffusing capacity of the lungs for carbon monoxide.

Composite scores can identify patients who are at increased risk of mortality. One such score is the BODE (Body mass, Obstruction, Dyspnea, and Exercise) method. Biomarkers are being investigated, but data are still not available to recommend their routine use.
 

Dr. Girgis practices family medicine in South River, N.J., and is a clinical assistant professor of family medicine at Robert Wood Johnson Medical School, New Brunswick, N.J. You can contact her at fpnews@mdedge.com.

Not all patients with chronic obstructive pulmonary disease (COPD) respond equally well to pulmonary rehabilitation (PR).

Now, physicians can better categorize which patients will do well with PR and which ones less well or not well at all based on a new system of clustering of COPD patients according to their response to exercise therapy.

“We identified four clusters of COPD patients and their response to PR in the aim to better understand PR outcome and [adapt] it to patients’ profiles and needs,” lead author Yara Al Chikhanie, MD, of the cardiopulmonary rehabilitation center Dieulefit Sante (France), and colleagues observed.

“Identification of patients likely to show smaller responses to PR may help to target patients benefiting the most and to adapt PR settings for nonresponders to standard PR,” they suggested.

The study was published online in Respiratory Medicine.

Single-center cohort

The cohort consisted of 835 patients from a single center who had been admitted to a cardiopulmonary rehabilitation center over a 6-year period from 2021 to 2017. “The PR program used in the center was the same over the 6-year period,” the authors note – consisting of a 3- to 4-week, inpatient program with activities 5 days a week.

Each day, patients attended a 25-minute aerobic training session on a cycling ergometer or a treadmill; a 30-minute low-intensity gym session; a 30-minute group walk outdoors, and 30 minutes of strength training. “We aimed to cluster patients with COPD admitted to PR based on patients’ clinical characteristics and 6-meter walk test results (6MWT), pulse oxygen saturation (SPO₂), heart rate (HR), and dyspnea,” the authors explained.

They then evaluated patient response to PR in each of these clusters based on the amount of improvement in the 6-meter walk distance (6MWD), lung function, and quality of life observed, they added.

The population consisted of seniors, equally men and women, mostly GOLD II and III patients (a measure of lung function) with a limited walking capacity, some 84% of the cohort having a 6MWD <80% predicted. The characteristics of the four identified clusters were as follows:

• Cluster 1: Consisted of younger men, GOLD I to II, average walkers, obese. The average 6MWD was 430 meters and patients had a large exercise HR response to PR. This cluster had a 76 meter improvement in their 6MWD, although 16% of the same cluster still did not respond to PR.
• Cluster 2: Consisted of older women, GOLD II-III, who were slow walkers. This cluster had a reduced 6MWD of 362 meters, but they also had a significant 97-meter improvement in their 6MWD following PR. Some 18% were still nonresponders to PR.
• Cluster 3: Consisted of older men, GOLD II to III, dyspneic, slow walkers, some 32% of whom responded to PR. This cluster also had a reduced 6MWD at 388 meters, but again, they also had a significant improvement of 79 meters in their 6MWD following the introduction of PR. Some 11% were nonresponders to PR.
• Cluster 4: Consisted of older men, GOLD III to IV, very slow walkers, oxygen-dependent, very dyspneic. This cluster had a severely reduced 6MWD of only 290 meters with severe exercise desaturation and dyspnea, and almost all of them were on long-term oxygen therapy. Nevertheless, this cluster also had a significant, 66-meter improvement in their 6MWD. Twenty-eight percent of them were nonresponders to PR.

Clinical practice

“The highly heterogeneous nature of the enrolled patient population reflects clinical practice,” the authors point out. For example, cluster 1 included patients with the best lung function, compared with those in clusters 2, 3, and 4 – which may be due, at least in part, to the aggravation in disease severity with age given that patients in cluster 1 were the youngest overall.

The fact that those in cluster 4 had the worst performance may also have been because of age and disease severity, the authors note, as those in cluster 4 had the highest proportion of patients on long-term oxygen therapy, again suggestive of disease severity. “Of note, these patients show the most impaired 6MWT responses despite the use of oxygen supplementation during walking,” the researchers added.

The authors also suggest that patients such as those in cluster 4 may require specific PR modalities in order to optimize their functional benefits. In contrast, those in cluster 1 had a significantly higher body mass index, compared with those in the other 3 clusters, which, interestingly enough, was not associated with more severe functional exercise impairment. The fact that older age participants, such as those in cluster 3 as well as those with high BMI in cluster 1, were both able to improve their 6MWD post-PR to the same extent as younger patients without obesity suggests that most older or overweight/obese patients can still show clinically significant improvement in 6MWD post PR, as the authors suggest.

Notably, the 6MWT was the only test available both pre-and post PR, making this an important limitation of the study, because only one aspect of the effect of PR was evaluated, omitting other physical and psychosocial benefits of PR, investigators suggest.

Adds to the literature

Asked to comment on the findings, Sachin Gupta, MD, attending physician, pulmonary & critical care medicine, Alameda Health System, Highland Hospital, Oakland, Calif., felt that these data add to the literature in defining COPD patient profiles, helping to categorize those in whom to expect greater walk distance improvements with PR versus those who will respond less well.

“Because 6MWD is a surrogate marker for quality of life (QOL) and mortality, further analysis in the form of a randomized controlled trial to determine long-term outcomes among the four clusters with adjustment for baseline characteristics would help determine the extent to which certain patient clusters may respond to PR,” Dr. Gupta told this news organization in an email.

At the same time, he suggested that while patients may not experience much net benefit in their 6MWD, their QOL or mortality risk may still improve with PR. “I cannot recall a patient ever describing their experience with PR as anything other than positive,” Dr. Gupta stressed.

“And as the authors [themselves] note, because PR serves to benefit patients beyond the 6MWD, I would not recommend limiting PR referrals based on the patient clusters identified,” he said.

The authors had no conflicts of interest to declare. Dr. Gupta declared that he is an employee and shareholder at Genentech.

Not all patients with chronic obstructive pulmonary disease (COPD) respond equally well to pulmonary rehabilitation (PR).

Now, physicians can better categorize which patients will do well with PR and which ones less well or not well at all based on a new system of clustering of COPD patients according to their response to exercise therapy.

“We identified four clusters of COPD patients and their response to PR in the aim to better understand PR outcome and [adapt] it to patients’ profiles and needs,” lead author Yara Al Chikhanie, MD, of the cardiopulmonary rehabilitation center Dieulefit Sante (France), and colleagues observed.

“Identification of patients likely to show smaller responses to PR may help to target patients benefiting the most and to adapt PR settings for nonresponders to standard PR,” they suggested.

The study was published online in Respiratory Medicine.

Single-center cohort

The cohort consisted of 835 patients from a single center who had been admitted to a cardiopulmonary rehabilitation center over a 6-year period from 2021 to 2017. “The PR program used in the center was the same over the 6-year period,” the authors note – consisting of a 3- to 4-week, inpatient program with activities 5 days a week.

Each day, patients attended a 25-minute aerobic training session on a cycling ergometer or a treadmill; a 30-minute low-intensity gym session; a 30-minute group walk outdoors, and 30 minutes of strength training. “We aimed to cluster patients with COPD admitted to PR based on patients’ clinical characteristics and 6-meter walk test results (6MWT), pulse oxygen saturation (SPO₂), heart rate (HR), and dyspnea,” the authors explained.

They then evaluated patient response to PR in each of these clusters based on the amount of improvement in the 6-meter walk distance (6MWD), lung function, and quality of life observed, they added.

The population consisted of seniors, equally men and women, mostly GOLD II and III patients (a measure of lung function) with a limited walking capacity, some 84% of the cohort having a 6MWD <80% predicted. The characteristics of the four identified clusters were as follows:

• Cluster 1: Consisted of younger men, GOLD I to II, average walkers, obese. The average 6MWD was 430 meters and patients had a large exercise HR response to PR. This cluster had a 76 meter improvement in their 6MWD, although 16% of the same cluster still did not respond to PR.
• Cluster 2: Consisted of older women, GOLD II-III, who were slow walkers. This cluster had a reduced 6MWD of 362 meters, but they also had a significant 97-meter improvement in their 6MWD following PR. Some 18% were still nonresponders to PR.
• Cluster 3: Consisted of older men, GOLD II to III, dyspneic, slow walkers, some 32% of whom responded to PR. This cluster also had a reduced 6MWD at 388 meters, but again, they also had a significant improvement of 79 meters in their 6MWD following the introduction of PR. Some 11% were nonresponders to PR.
• Cluster 4: Consisted of older men, GOLD III to IV, very slow walkers, oxygen-dependent, very dyspneic. This cluster had a severely reduced 6MWD of only 290 meters with severe exercise desaturation and dyspnea, and almost all of them were on long-term oxygen therapy. Nevertheless, this cluster also had a significant, 66-meter improvement in their 6MWD. Twenty-eight percent of them were nonresponders to PR.

Clinical practice

“The highly heterogeneous nature of the enrolled patient population reflects clinical practice,” the authors point out. For example, cluster 1 included patients with the best lung function, compared with those in clusters 2, 3, and 4 – which may be due, at least in part, to the aggravation in disease severity with age given that patients in cluster 1 were the youngest overall.

The fact that those in cluster 4 had the worst performance may also have been because of age and disease severity, the authors note, as those in cluster 4 had the highest proportion of patients on long-term oxygen therapy, again suggestive of disease severity. “Of note, these patients show the most impaired 6MWT responses despite the use of oxygen supplementation during walking,” the researchers added.

The authors also suggest that patients such as those in cluster 4 may require specific PR modalities in order to optimize their functional benefits. In contrast, those in cluster 1 had a significantly higher body mass index, compared with those in the other 3 clusters, which, interestingly enough, was not associated with more severe functional exercise impairment. The fact that older age participants, such as those in cluster 3 as well as those with high BMI in cluster 1, were both able to improve their 6MWD post-PR to the same extent as younger patients without obesity suggests that most older or overweight/obese patients can still show clinically significant improvement in 6MWD post PR, as the authors suggest.

Notably, the 6MWT was the only test available both pre-and post PR, making this an important limitation of the study, because only one aspect of the effect of PR was evaluated, omitting other physical and psychosocial benefits of PR, investigators suggest.

Adds to the literature

Asked to comment on the findings, Sachin Gupta, MD, attending physician, pulmonary & critical care medicine, Alameda Health System, Highland Hospital, Oakland, Calif., felt that these data add to the literature in defining COPD patient profiles, helping to categorize those in whom to expect greater walk distance improvements with PR versus those who will respond less well.

“Because 6MWD is a surrogate marker for quality of life (QOL) and mortality, further analysis in the form of a randomized controlled trial to determine long-term outcomes among the four clusters with adjustment for baseline characteristics would help determine the extent to which certain patient clusters may respond to PR,” Dr. Gupta told this news organization in an email.

At the same time, he suggested that while patients may not experience much net benefit in their 6MWD, their QOL or mortality risk may still improve with PR. “I cannot recall a patient ever describing their experience with PR as anything other than positive,” Dr. Gupta stressed.

“And as the authors [themselves] note, because PR serves to benefit patients beyond the 6MWD, I would not recommend limiting PR referrals based on the patient clusters identified,” he said.

The authors had no conflicts of interest to declare. Dr. Gupta declared that he is an employee and shareholder at Genentech.

Not all patients with chronic obstructive pulmonary disease (COPD) respond equally well to pulmonary rehabilitation (PR).

Now, physicians can better categorize which patients will do well with PR and which ones less well or not well at all based on a new system of clustering of COPD patients according to their response to exercise therapy.

“We identified four clusters of COPD patients and their response to PR in the aim to better understand PR outcome and [adapt] it to patients’ profiles and needs,” lead author Yara Al Chikhanie, MD, of the cardiopulmonary rehabilitation center Dieulefit Sante (France), and colleagues observed.

“Identification of patients likely to show smaller responses to PR may help to target patients benefiting the most and to adapt PR settings for nonresponders to standard PR,” they suggested.

The study was published online in Respiratory Medicine.

Single-center cohort

The cohort consisted of 835 patients from a single center who had been admitted to a cardiopulmonary rehabilitation center over a 6-year period from 2021 to 2017. “The PR program used in the center was the same over the 6-year period,” the authors note – consisting of a 3- to 4-week, inpatient program with activities 5 days a week.

Each day, patients attended a 25-minute aerobic training session on a cycling ergometer or a treadmill; a 30-minute low-intensity gym session; a 30-minute group walk outdoors, and 30 minutes of strength training. “We aimed to cluster patients with COPD admitted to PR based on patients’ clinical characteristics and 6-meter walk test results (6MWT), pulse oxygen saturation (SPO₂), heart rate (HR), and dyspnea,” the authors explained.

They then evaluated patient response to PR in each of these clusters based on the amount of improvement in the 6-meter walk distance (6MWD), lung function, and quality of life observed, they added.

The population consisted of seniors, equally men and women, mostly GOLD II and III patients (a measure of lung function) with a limited walking capacity, some 84% of the cohort having a 6MWD <80% predicted. The characteristics of the four identified clusters were as follows:

• Cluster 1: Consisted of younger men, GOLD I to II, average walkers, obese. The average 6MWD was 430 meters and patients had a large exercise HR response to PR. This cluster had a 76 meter improvement in their 6MWD, although 16% of the same cluster still did not respond to PR.
• Cluster 2: Consisted of older women, GOLD II-III, who were slow walkers. This cluster had a reduced 6MWD of 362 meters, but they also had a significant 97-meter improvement in their 6MWD following PR. Some 18% were still nonresponders to PR.
• Cluster 3: Consisted of older men, GOLD II to III, dyspneic, slow walkers, some 32% of whom responded to PR. This cluster also had a reduced 6MWD at 388 meters, but again, they also had a significant improvement of 79 meters in their 6MWD following the introduction of PR. Some 11% were nonresponders to PR.
• Cluster 4: Consisted of older men, GOLD III to IV, very slow walkers, oxygen-dependent, very dyspneic. This cluster had a severely reduced 6MWD of only 290 meters with severe exercise desaturation and dyspnea, and almost all of them were on long-term oxygen therapy. Nevertheless, this cluster also had a significant, 66-meter improvement in their 6MWD. Twenty-eight percent of them were nonresponders to PR.

Clinical practice

“The highly heterogeneous nature of the enrolled patient population reflects clinical practice,” the authors point out. For example, cluster 1 included patients with the best lung function, compared with those in clusters 2, 3, and 4 – which may be due, at least in part, to the aggravation in disease severity with age given that patients in cluster 1 were the youngest overall.

The fact that those in cluster 4 had the worst performance may also have been because of age and disease severity, the authors note, as those in cluster 4 had the highest proportion of patients on long-term oxygen therapy, again suggestive of disease severity. “Of note, these patients show the most impaired 6MWT responses despite the use of oxygen supplementation during walking,” the researchers added.

The authors also suggest that patients such as those in cluster 4 may require specific PR modalities in order to optimize their functional benefits. In contrast, those in cluster 1 had a significantly higher body mass index, compared with those in the other 3 clusters, which, interestingly enough, was not associated with more severe functional exercise impairment. The fact that older age participants, such as those in cluster 3 as well as those with high BMI in cluster 1, were both able to improve their 6MWD post-PR to the same extent as younger patients without obesity suggests that most older or overweight/obese patients can still show clinically significant improvement in 6MWD post PR, as the authors suggest.

Notably, the 6MWT was the only test available both pre-and post PR, making this an important limitation of the study, because only one aspect of the effect of PR was evaluated, omitting other physical and psychosocial benefits of PR, investigators suggest.

Adds to the literature

Asked to comment on the findings, Sachin Gupta, MD, attending physician, pulmonary & critical care medicine, Alameda Health System, Highland Hospital, Oakland, Calif., felt that these data add to the literature in defining COPD patient profiles, helping to categorize those in whom to expect greater walk distance improvements with PR versus those who will respond less well.

“Because 6MWD is a surrogate marker for quality of life (QOL) and mortality, further analysis in the form of a randomized controlled trial to determine long-term outcomes among the four clusters with adjustment for baseline characteristics would help determine the extent to which certain patient clusters may respond to PR,” Dr. Gupta told this news organization in an email.

At the same time, he suggested that while patients may not experience much net benefit in their 6MWD, their QOL or mortality risk may still improve with PR. “I cannot recall a patient ever describing their experience with PR as anything other than positive,” Dr. Gupta stressed.

“And as the authors [themselves] note, because PR serves to benefit patients beyond the 6MWD, I would not recommend limiting PR referrals based on the patient clusters identified,” he said.

The authors had no conflicts of interest to declare. Dr. Gupta declared that he is an employee and shareholder at Genentech.