COPD

SAN FRANCISCO – It may be time to move beyond relying largely on spirometry to distinguish between healthy and abnormal lung function in diverse populations.

That conclusion comes from investigators who looked at patients with ostensibly normal spirometry values in a large population-based study and found that using standard equations to adjust for racial differences in lung-function measures appeared to miss emphysema in a significant proportion of Black patients.

“Our traditional measures of lung health based on spirometry may be under-recognizing impaired respiratory health in Black adults and particularly Black men,” said lead author Gabrielle Liu, MD, a fellow in the division of pulmonary and critical care medicine at the Northwestern University Feinberg School of Medicine, Chicago.

“CT imaging may be useful in the evaluation of those with suspected impaired respiratory health and normal spirometry,” she said in an oral abstract session at the American Thoracic Society International Conference 2022.

Dr. Liu and colleagues studied the association between self-identified race and visually identified emphysema among 2,674 participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study. The patients had CT scans at a mean age of 50 and spirometry at a mean age of 55.
 

Racial differences

The investigators found that among men with forced expiratory volume in 1 second (FEV1) ranging from 100% to 120% of predicted according to race-adjusted formulas, 14.6% of Black men had emphysema, compared with only 1.7% of White men (P < .001). Respective emphysema rates in Black women and White women were 3.8% and 1.9%; this difference was not statistically significant.

Among patients with FEV1 80% to 99% of predicted according to race-specific measures, 15.5% of Black men had emphysema, compared with 4% of White men (P < .001). Respective rates of emphysema were 6.9% for Black women versus 3.2% for White women (P = .025).

When the investigators applied race-neutral spirometry reference equations to the same population, they found that it attenuated but did not completely eliminate the racial disparity in emphysema prevalence among patients with FEV1, ranging from 80% to 120% of predicted.
 

Relic of the past

The results suggest that race-based adjustments of spirometry measures are a relic of less enlightened times, said Adam Gaffney, MD, MPH, assistant professor of medicine at Harvard Medical School, Boston, and a pulmonologist and critical care physician at Cambridge Health Alliance, Massachusetts.

“If the average lower lung function of Black people is being driven by adversity, structural racism, and deprivation, that means that race-specific equations are normalizing that adversity,” he said in an interview.

“In my opinion, it is time to move beyond race-based equations in clinical pulmonary medicine, particularly in the context of patients with established lung disease in whom use of race-based equations might actually lead to undertreatment,” said Dr. Gaffney, who was not involved in the study.

Dr. Liu agreed that it’s time to move to race-neutral measures and that the whole concept of race-based differences is flawed.

“The long-standing structural inequities in health likely made the reference populations have lower lung function than among Whites,” she told this news organization.

Dr. Liu said that evaluation of lung function should not rely on spirometry alone, but should also include – when appropriate – CT scans, as well as improved understanding of how symptoms may be predictive for poor outcomes.

The study was supported by grants from the National Institutes of Health. Dr. Liu and Dr. Gaffney have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

SAN FRANCISCO – It may be time to move beyond relying largely on spirometry to distinguish between healthy and abnormal lung function in diverse populations.

That conclusion comes from investigators who looked at patients with ostensibly normal spirometry values in a large population-based study and found that using standard equations to adjust for racial differences in lung-function measures appeared to miss emphysema in a significant proportion of Black patients.

“Our traditional measures of lung health based on spirometry may be under-recognizing impaired respiratory health in Black adults and particularly Black men,” said lead author Gabrielle Liu, MD, a fellow in the division of pulmonary and critical care medicine at the Northwestern University Feinberg School of Medicine, Chicago.

“CT imaging may be useful in the evaluation of those with suspected impaired respiratory health and normal spirometry,” she said in an oral abstract session at the American Thoracic Society International Conference 2022.

Dr. Liu and colleagues studied the association between self-identified race and visually identified emphysema among 2,674 participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study. The patients had CT scans at a mean age of 50 and spirometry at a mean age of 55.
 

Racial differences

The investigators found that among men with forced expiratory volume in 1 second (FEV1) ranging from 100% to 120% of predicted according to race-adjusted formulas, 14.6% of Black men had emphysema, compared with only 1.7% of White men (P < .001). Respective emphysema rates in Black women and White women were 3.8% and 1.9%; this difference was not statistically significant.

Among patients with FEV1 80% to 99% of predicted according to race-specific measures, 15.5% of Black men had emphysema, compared with 4% of White men (P < .001). Respective rates of emphysema were 6.9% for Black women versus 3.2% for White women (P = .025).

When the investigators applied race-neutral spirometry reference equations to the same population, they found that it attenuated but did not completely eliminate the racial disparity in emphysema prevalence among patients with FEV1, ranging from 80% to 120% of predicted.
 

Relic of the past

The results suggest that race-based adjustments of spirometry measures are a relic of less enlightened times, said Adam Gaffney, MD, MPH, assistant professor of medicine at Harvard Medical School, Boston, and a pulmonologist and critical care physician at Cambridge Health Alliance, Massachusetts.

“If the average lower lung function of Black people is being driven by adversity, structural racism, and deprivation, that means that race-specific equations are normalizing that adversity,” he said in an interview.

“In my opinion, it is time to move beyond race-based equations in clinical pulmonary medicine, particularly in the context of patients with established lung disease in whom use of race-based equations might actually lead to undertreatment,” said Dr. Gaffney, who was not involved in the study.

Dr. Liu agreed that it’s time to move to race-neutral measures and that the whole concept of race-based differences is flawed.

“The long-standing structural inequities in health likely made the reference populations have lower lung function than among Whites,” she told this news organization.

Dr. Liu said that evaluation of lung function should not rely on spirometry alone, but should also include – when appropriate – CT scans, as well as improved understanding of how symptoms may be predictive for poor outcomes.

The study was supported by grants from the National Institutes of Health. Dr. Liu and Dr. Gaffney have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

SAN FRANCISCO – It may be time to move beyond relying largely on spirometry to distinguish between healthy and abnormal lung function in diverse populations.

That conclusion comes from investigators who looked at patients with ostensibly normal spirometry values in a large population-based study and found that using standard equations to adjust for racial differences in lung-function measures appeared to miss emphysema in a significant proportion of Black patients.

“Our traditional measures of lung health based on spirometry may be under-recognizing impaired respiratory health in Black adults and particularly Black men,” said lead author Gabrielle Liu, MD, a fellow in the division of pulmonary and critical care medicine at the Northwestern University Feinberg School of Medicine, Chicago.

“CT imaging may be useful in the evaluation of those with suspected impaired respiratory health and normal spirometry,” she said in an oral abstract session at the American Thoracic Society International Conference 2022.

Dr. Liu and colleagues studied the association between self-identified race and visually identified emphysema among 2,674 participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study. The patients had CT scans at a mean age of 50 and spirometry at a mean age of 55.
 

Racial differences

The investigators found that among men with forced expiratory volume in 1 second (FEV1) ranging from 100% to 120% of predicted according to race-adjusted formulas, 14.6% of Black men had emphysema, compared with only 1.7% of White men (P < .001). Respective emphysema rates in Black women and White women were 3.8% and 1.9%; this difference was not statistically significant.

Among patients with FEV1 80% to 99% of predicted according to race-specific measures, 15.5% of Black men had emphysema, compared with 4% of White men (P < .001). Respective rates of emphysema were 6.9% for Black women versus 3.2% for White women (P = .025).

When the investigators applied race-neutral spirometry reference equations to the same population, they found that it attenuated but did not completely eliminate the racial disparity in emphysema prevalence among patients with FEV1, ranging from 80% to 120% of predicted.
 

Relic of the past

The results suggest that race-based adjustments of spirometry measures are a relic of less enlightened times, said Adam Gaffney, MD, MPH, assistant professor of medicine at Harvard Medical School, Boston, and a pulmonologist and critical care physician at Cambridge Health Alliance, Massachusetts.

“If the average lower lung function of Black people is being driven by adversity, structural racism, and deprivation, that means that race-specific equations are normalizing that adversity,” he said in an interview.

“In my opinion, it is time to move beyond race-based equations in clinical pulmonary medicine, particularly in the context of patients with established lung disease in whom use of race-based equations might actually lead to undertreatment,” said Dr. Gaffney, who was not involved in the study.

Dr. Liu agreed that it’s time to move to race-neutral measures and that the whole concept of race-based differences is flawed.

“The long-standing structural inequities in health likely made the reference populations have lower lung function than among Whites,” she told this news organization.

Dr. Liu said that evaluation of lung function should not rely on spirometry alone, but should also include – when appropriate – CT scans, as well as improved understanding of how symptoms may be predictive for poor outcomes.

The study was supported by grants from the National Institutes of Health. Dr. Liu and Dr. Gaffney have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Reduced exercise capacity and peak ventilation were significant predictors of early mortality in adults with chronic obstructive pulmonary disease, based on data from 126 individuals.

Cardiopulmonary exercise testing (CPET) is a common assessment for cardiorespiratory disease patients, but its role as a predictor of clinically relevant outcomes in chronic obstructive pulmonary disease (COPD) has not been investigated, and data on changes in exercise capacity over time in COPD patients are limited, wrote Cassia da Luz Goulart, MD, of the Federal University of São Carlos, Brazil, and colleagues.

The researchers hypothesized that CPET threshold values could be used as predictors of mortality in COPD.

In a prospective study published in Respiratory Medicine, the researchers identified 126 adults with COPD who were followed for 42 months. At study entry, each patient completed a clinical evaluation, followed by a pulmonary function test and CPET. The average age of the patients was 65 years, and 73% were men. All patients were on optimal medical management for COPD.

The researchers recorded data on peak oxygen consumption (VO₂, mL/min), VCO₂ (mL/min), minute ventilation (VE, L/min), the oxygen uptake efficiency slope (OUES), and ventilatory efficiency (the VE/VCO₂ slope).

The participants performed CPET on a cycle ergometer, with breath-by-breath analysis measured throughout the test using a computer-based system.

A total of 48 patients (38%) died during the 42-month follow-up period. Overall, the significant predictors of mortality were VE/VCO₂ slope of 30 or higher, peak VE of 25.7 L/min, and peak VO₂ ≤ 13.8 mLO₂ kg^–1 min^–1 were strong predictors of mortality in COPD patients in a Cox regression analysis.

When comparing the 78 survivors to the 48 nonsurvivors, the researchers found that the nonsurvivors were significantly more likely to be women, with worse lung function, inspiratory muscle weakness, and poorer CPET responses (P < .050 for all).

“The VE peak response is directly related to the FEV₁ in COPD patients, factors such as dyspnea and increased leg discomfort negatively impact the VE response during exercise,” the researchers wrote in their discussion of the findings. In this context, our results may hold clinical utility in refining the prognostic accuracy when a patient with COPD has a VE peak ≤ 25.7 L/min,” they explained.

The study findings were limited by the inability to assess complete pulmonary function in the COPD patients, and the assessment only of three CPET measures, the researchers noted.

However, the results support the use of CPET as a clinical assessment tool for COPD patients, they said. “Moreover, therapeutic approaches, such as cardiopulmonary rehabilitation, may consider focusing on improving these metabolic and ventilatory markers as an indicator of clinical improvement and prognosis in patients with COPD,” they added.

The study was supported by the Fundação de Amparo a Pesquisa do Estado de São Paulo, Brazil, and by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior-Brasil. The researchers had no financial conflicts to disclose.

Reduced exercise capacity and peak ventilation were significant predictors of early mortality in adults with chronic obstructive pulmonary disease, based on data from 126 individuals.

Cardiopulmonary exercise testing (CPET) is a common assessment for cardiorespiratory disease patients, but its role as a predictor of clinically relevant outcomes in chronic obstructive pulmonary disease (COPD) has not been investigated, and data on changes in exercise capacity over time in COPD patients are limited, wrote Cassia da Luz Goulart, MD, of the Federal University of São Carlos, Brazil, and colleagues.

The researchers hypothesized that CPET threshold values could be used as predictors of mortality in COPD.

In a prospective study published in Respiratory Medicine, the researchers identified 126 adults with COPD who were followed for 42 months. At study entry, each patient completed a clinical evaluation, followed by a pulmonary function test and CPET. The average age of the patients was 65 years, and 73% were men. All patients were on optimal medical management for COPD.

The researchers recorded data on peak oxygen consumption (VO₂, mL/min), VCO₂ (mL/min), minute ventilation (VE, L/min), the oxygen uptake efficiency slope (OUES), and ventilatory efficiency (the VE/VCO₂ slope).

The participants performed CPET on a cycle ergometer, with breath-by-breath analysis measured throughout the test using a computer-based system.

A total of 48 patients (38%) died during the 42-month follow-up period. Overall, the significant predictors of mortality were VE/VCO₂ slope of 30 or higher, peak VE of 25.7 L/min, and peak VO₂ ≤ 13.8 mLO₂ kg^–1 min^–1 were strong predictors of mortality in COPD patients in a Cox regression analysis.

When comparing the 78 survivors to the 48 nonsurvivors, the researchers found that the nonsurvivors were significantly more likely to be women, with worse lung function, inspiratory muscle weakness, and poorer CPET responses (P < .050 for all).

“The VE peak response is directly related to the FEV₁ in COPD patients, factors such as dyspnea and increased leg discomfort negatively impact the VE response during exercise,” the researchers wrote in their discussion of the findings. In this context, our results may hold clinical utility in refining the prognostic accuracy when a patient with COPD has a VE peak ≤ 25.7 L/min,” they explained.

The study findings were limited by the inability to assess complete pulmonary function in the COPD patients, and the assessment only of three CPET measures, the researchers noted.

However, the results support the use of CPET as a clinical assessment tool for COPD patients, they said. “Moreover, therapeutic approaches, such as cardiopulmonary rehabilitation, may consider focusing on improving these metabolic and ventilatory markers as an indicator of clinical improvement and prognosis in patients with COPD,” they added.

The study was supported by the Fundação de Amparo a Pesquisa do Estado de São Paulo, Brazil, and by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior-Brasil. The researchers had no financial conflicts to disclose.

Reduced exercise capacity and peak ventilation were significant predictors of early mortality in adults with chronic obstructive pulmonary disease, based on data from 126 individuals.

Cardiopulmonary exercise testing (CPET) is a common assessment for cardiorespiratory disease patients, but its role as a predictor of clinically relevant outcomes in chronic obstructive pulmonary disease (COPD) has not been investigated, and data on changes in exercise capacity over time in COPD patients are limited, wrote Cassia da Luz Goulart, MD, of the Federal University of São Carlos, Brazil, and colleagues.

The researchers hypothesized that CPET threshold values could be used as predictors of mortality in COPD.

In a prospective study published in Respiratory Medicine, the researchers identified 126 adults with COPD who were followed for 42 months. At study entry, each patient completed a clinical evaluation, followed by a pulmonary function test and CPET. The average age of the patients was 65 years, and 73% were men. All patients were on optimal medical management for COPD.

The researchers recorded data on peak oxygen consumption (VO₂, mL/min), VCO₂ (mL/min), minute ventilation (VE, L/min), the oxygen uptake efficiency slope (OUES), and ventilatory efficiency (the VE/VCO₂ slope).

The participants performed CPET on a cycle ergometer, with breath-by-breath analysis measured throughout the test using a computer-based system.

A total of 48 patients (38%) died during the 42-month follow-up period. Overall, the significant predictors of mortality were VE/VCO₂ slope of 30 or higher, peak VE of 25.7 L/min, and peak VO₂ ≤ 13.8 mLO₂ kg^–1 min^–1 were strong predictors of mortality in COPD patients in a Cox regression analysis.

When comparing the 78 survivors to the 48 nonsurvivors, the researchers found that the nonsurvivors were significantly more likely to be women, with worse lung function, inspiratory muscle weakness, and poorer CPET responses (P < .050 for all).

“The VE peak response is directly related to the FEV₁ in COPD patients, factors such as dyspnea and increased leg discomfort negatively impact the VE response during exercise,” the researchers wrote in their discussion of the findings. In this context, our results may hold clinical utility in refining the prognostic accuracy when a patient with COPD has a VE peak ≤ 25.7 L/min,” they explained.

The study findings were limited by the inability to assess complete pulmonary function in the COPD patients, and the assessment only of three CPET measures, the researchers noted.

However, the results support the use of CPET as a clinical assessment tool for COPD patients, they said. “Moreover, therapeutic approaches, such as cardiopulmonary rehabilitation, may consider focusing on improving these metabolic and ventilatory markers as an indicator of clinical improvement and prognosis in patients with COPD,” they added.

The study was supported by the Fundação de Amparo a Pesquisa do Estado de São Paulo, Brazil, and by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior-Brasil. The researchers had no financial conflicts to disclose.

Bronchoscopic lung volume reduction significantly increased survival in patients with severe chronic obstructive pulmonary disease, based on data from more than 1,400 individuals.

Previous studies have shown that patients with severe chronic obstructive pulmonary disease (COPD) can benefit from treatment with bronchoscopic lung volume reduction (BLVR) involving lung volume reduction coils or endobronchial valves (EBVs) in terms of improved pulmonary function, lung volume, exercise capacity, and quality of life.

However, data on the impact of the procedure on patient survival are limited, and most previous studies have been small, wrote Jorine E. Hartman, MD, of the University of Groningen, the Netherlands, and colleagues.

In a study published in Respiratory Medicine, the researchers reviewed data from 1,471 patients with severe COPD who had consultations for BLVR at a single center between June 2006 and July 2019. Of these, 483 (33%) underwent a BLVR treatment.

The follow-up period ranged from 633 days to 5,401 days. During this time, 531 patients died (35%); 165 of these (34%) were in the BLVR group.

Overall, the median survival of BLVR patients was significantly longer, compared with those who did not have the procedure, for a difference of approximately 1.7 years (3,133 days vs. 2,503 days, P < .001). No significant differences in survival were noted in BLVR patients treated with coils or EBVs.

The average age of the study population at baseline was 61 years, and 63% were women. Overall, patients treated with BLVR were more likely to be younger and female, with fewer COPD exacerbations but worse pulmonary function, as well as lower body mass index and more evidence of emphysema than the untreated patients, the researchers noted. Patients treated with BLVR also were more likely than untreated patients to have a history of myocardial infarction, percutaneous coronary intervention, or stroke.

However, BLVR was a significant independent predictor of survival after controlling for multiple variables, including age, sex, and disease severity, the researchers noted.

The current study supports existing literature on the value of BLVR for severe COPD but stands out from previous studies by comparing patients who underwent BLVR with those who did not, the researchers noted in their discussion of the findings.

The study findings were limited by several factors, including the fact that the non-treated patients were not eligible for treatment for various reasons that might have impacted survival, the researchers noted. Another limitation was the lack of data on cause of death and other medical events and treatments during the follow-up period, they said.

However, the results were strengthened by the large sample size and long-term follow-up and suggest that “reducing lung volume in patients with COPD and severe hyperinflation and reduced life expectancy may lead to a survival benefit,” they concluded.

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

Bronchoscopic lung volume reduction significantly increased survival in patients with severe chronic obstructive pulmonary disease, based on data from more than 1,400 individuals.

Previous studies have shown that patients with severe chronic obstructive pulmonary disease (COPD) can benefit from treatment with bronchoscopic lung volume reduction (BLVR) involving lung volume reduction coils or endobronchial valves (EBVs) in terms of improved pulmonary function, lung volume, exercise capacity, and quality of life.

However, data on the impact of the procedure on patient survival are limited, and most previous studies have been small, wrote Jorine E. Hartman, MD, of the University of Groningen, the Netherlands, and colleagues.

In a study published in Respiratory Medicine, the researchers reviewed data from 1,471 patients with severe COPD who had consultations for BLVR at a single center between June 2006 and July 2019. Of these, 483 (33%) underwent a BLVR treatment.

The follow-up period ranged from 633 days to 5,401 days. During this time, 531 patients died (35%); 165 of these (34%) were in the BLVR group.

Overall, the median survival of BLVR patients was significantly longer, compared with those who did not have the procedure, for a difference of approximately 1.7 years (3,133 days vs. 2,503 days, P < .001). No significant differences in survival were noted in BLVR patients treated with coils or EBVs.

The average age of the study population at baseline was 61 years, and 63% were women. Overall, patients treated with BLVR were more likely to be younger and female, with fewer COPD exacerbations but worse pulmonary function, as well as lower body mass index and more evidence of emphysema than the untreated patients, the researchers noted. Patients treated with BLVR also were more likely than untreated patients to have a history of myocardial infarction, percutaneous coronary intervention, or stroke.

However, BLVR was a significant independent predictor of survival after controlling for multiple variables, including age, sex, and disease severity, the researchers noted.

The current study supports existing literature on the value of BLVR for severe COPD but stands out from previous studies by comparing patients who underwent BLVR with those who did not, the researchers noted in their discussion of the findings.

The study findings were limited by several factors, including the fact that the non-treated patients were not eligible for treatment for various reasons that might have impacted survival, the researchers noted. Another limitation was the lack of data on cause of death and other medical events and treatments during the follow-up period, they said.

However, the results were strengthened by the large sample size and long-term follow-up and suggest that “reducing lung volume in patients with COPD and severe hyperinflation and reduced life expectancy may lead to a survival benefit,” they concluded.

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

Bronchoscopic lung volume reduction significantly increased survival in patients with severe chronic obstructive pulmonary disease, based on data from more than 1,400 individuals.

Previous studies have shown that patients with severe chronic obstructive pulmonary disease (COPD) can benefit from treatment with bronchoscopic lung volume reduction (BLVR) involving lung volume reduction coils or endobronchial valves (EBVs) in terms of improved pulmonary function, lung volume, exercise capacity, and quality of life.

However, data on the impact of the procedure on patient survival are limited, and most previous studies have been small, wrote Jorine E. Hartman, MD, of the University of Groningen, the Netherlands, and colleagues.

In a study published in Respiratory Medicine, the researchers reviewed data from 1,471 patients with severe COPD who had consultations for BLVR at a single center between June 2006 and July 2019. Of these, 483 (33%) underwent a BLVR treatment.

The follow-up period ranged from 633 days to 5,401 days. During this time, 531 patients died (35%); 165 of these (34%) were in the BLVR group.

Overall, the median survival of BLVR patients was significantly longer, compared with those who did not have the procedure, for a difference of approximately 1.7 years (3,133 days vs. 2,503 days, P < .001). No significant differences in survival were noted in BLVR patients treated with coils or EBVs.

The average age of the study population at baseline was 61 years, and 63% were women. Overall, patients treated with BLVR were more likely to be younger and female, with fewer COPD exacerbations but worse pulmonary function, as well as lower body mass index and more evidence of emphysema than the untreated patients, the researchers noted. Patients treated with BLVR also were more likely than untreated patients to have a history of myocardial infarction, percutaneous coronary intervention, or stroke.

However, BLVR was a significant independent predictor of survival after controlling for multiple variables, including age, sex, and disease severity, the researchers noted.

The current study supports existing literature on the value of BLVR for severe COPD but stands out from previous studies by comparing patients who underwent BLVR with those who did not, the researchers noted in their discussion of the findings.

The study findings were limited by several factors, including the fact that the non-treated patients were not eligible for treatment for various reasons that might have impacted survival, the researchers noted. Another limitation was the lack of data on cause of death and other medical events and treatments during the follow-up period, they said.

However, the results were strengthened by the large sample size and long-term follow-up and suggest that “reducing lung volume in patients with COPD and severe hyperinflation and reduced life expectancy may lead to a survival benefit,” they concluded.

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

Screening for chronic obstructive pulmonary disease (COPD) in asymptomatic adults has no net benefit, according to a U.S. Preventive Services Task Force (USPSTF) reassessment of its 2016 screening recommendations. The new recommendation is in line with the previous one and is made with moderate certainty (grade D evidence).

The USPSTF recommendation applies to adults who do not recognize or report respiratory symptoms. It does not apply to people with symptoms such as chronic cough, sputum production, difficulty breathing, or wheezing, or those known to be at very high risk for COPD. These latter include people with alpha-1 antitrypsin deficiency or workers exposed to certain toxins at their jobs, according to the report published in JAMA.

“Considering that the outcomes of several other chronic conditions, including cardiovascular disease and cancer, have been improved over the years with early detection and intervention, it is logical to ask whether screening to achieve early detection of COPD might also lead to better outcomes,” Surya P. Bhatt, MD, of the University of Alabama at Birmingham, and George T. O’Connor, MD, of the Boston University, explained in an editorial.
 

Task force assessment

The task force examined relevant publications after the 2016 deliberations and found no new studies that directly assessed the effects of screening for COPD in asymptomatic adults on morbidity, mortality, or health-related quality of life.

Although, as in their previous review, serious harms from treatment trials were not consistently reported, more recent large observational studies in screen-relevant populations suggested possible harms from the initiation of long-acting beta-agonists (LABAs), long-acting muscarinic antagonists (LAMAs), and the use of inhaled corticosteroids.

“In addition to potential treatment harms, there are opportunity costs to screening that may include time spent on counseling and providing services and patient referrals for diagnostic testing,” the task force stated.

Because cigarette smoking is the leading cause of COPD, the USPSTF has reiterated its recommendations for physicians to address tobacco smoking cessation in adults, including pregnant persons, as well as tobacco use in children and adolescents.
 

Not the whole story?

“Truly asymptomatic individuals with airflow obstruction do not meet criteria for COPD therapy, but sensitive questionnaires may detect symptoms not previously reported by the patient. It may be more effective to redirect the focus from screening for asymptomatic COPD to case finding using sensitive and cost-effective tools,” Dr. Bhatt and Dr. O’Connor suggested in their editorial.

“Even though available data may not support screening asymptomatic adults for COPD, there is substantial rationale for further investigation of strategies to enhance earlier detection of this condition,” they concluded.
 

More research needed

Despite the recommendation, the USPSTF indicated that further studies are needed to fill in research gaps, including:

• The effectiveness of screening asymptomatic adults for COPD to reduce morbidity or mortality or improve health-related quality of life, with long-term follow-up.
• The effectiveness of early treatment for asymptomatic, minimally symptomatic, or screen-detected populations to slow disease progression and improve health outcomes, with long-term follow-up.
• The harms of screening in and treatment of persons with asymptomatic or minimally symptomatic COPD.

The USPSTF is an independent, voluntary body, and potential conflicts of interest of the members are on file with the organization. Dr. Bhatt reported serving on an advisory board for Boehringer Ingelheim and receiving consulting fees from Sanofi/Regeneron; and Dr. O’Connor reported receiving consulting fees from Grupo Menarini and Dicerna Pharmaceuticals.

Screening for chronic obstructive pulmonary disease (COPD) in asymptomatic adults has no net benefit, according to a U.S. Preventive Services Task Force (USPSTF) reassessment of its 2016 screening recommendations. The new recommendation is in line with the previous one and is made with moderate certainty (grade D evidence).

The USPSTF recommendation applies to adults who do not recognize or report respiratory symptoms. It does not apply to people with symptoms such as chronic cough, sputum production, difficulty breathing, or wheezing, or those known to be at very high risk for COPD. These latter include people with alpha-1 antitrypsin deficiency or workers exposed to certain toxins at their jobs, according to the report published in JAMA.

“Considering that the outcomes of several other chronic conditions, including cardiovascular disease and cancer, have been improved over the years with early detection and intervention, it is logical to ask whether screening to achieve early detection of COPD might also lead to better outcomes,” Surya P. Bhatt, MD, of the University of Alabama at Birmingham, and George T. O’Connor, MD, of the Boston University, explained in an editorial.
 

Task force assessment

The task force examined relevant publications after the 2016 deliberations and found no new studies that directly assessed the effects of screening for COPD in asymptomatic adults on morbidity, mortality, or health-related quality of life.

Although, as in their previous review, serious harms from treatment trials were not consistently reported, more recent large observational studies in screen-relevant populations suggested possible harms from the initiation of long-acting beta-agonists (LABAs), long-acting muscarinic antagonists (LAMAs), and the use of inhaled corticosteroids.

“In addition to potential treatment harms, there are opportunity costs to screening that may include time spent on counseling and providing services and patient referrals for diagnostic testing,” the task force stated.

Because cigarette smoking is the leading cause of COPD, the USPSTF has reiterated its recommendations for physicians to address tobacco smoking cessation in adults, including pregnant persons, as well as tobacco use in children and adolescents.
 

Not the whole story?

“Truly asymptomatic individuals with airflow obstruction do not meet criteria for COPD therapy, but sensitive questionnaires may detect symptoms not previously reported by the patient. It may be more effective to redirect the focus from screening for asymptomatic COPD to case finding using sensitive and cost-effective tools,” Dr. Bhatt and Dr. O’Connor suggested in their editorial.

“Even though available data may not support screening asymptomatic adults for COPD, there is substantial rationale for further investigation of strategies to enhance earlier detection of this condition,” they concluded.
 

More research needed

Despite the recommendation, the USPSTF indicated that further studies are needed to fill in research gaps, including:

• The effectiveness of screening asymptomatic adults for COPD to reduce morbidity or mortality or improve health-related quality of life, with long-term follow-up.
• The effectiveness of early treatment for asymptomatic, minimally symptomatic, or screen-detected populations to slow disease progression and improve health outcomes, with long-term follow-up.
• The harms of screening in and treatment of persons with asymptomatic or minimally symptomatic COPD.

The USPSTF is an independent, voluntary body, and potential conflicts of interest of the members are on file with the organization. Dr. Bhatt reported serving on an advisory board for Boehringer Ingelheim and receiving consulting fees from Sanofi/Regeneron; and Dr. O’Connor reported receiving consulting fees from Grupo Menarini and Dicerna Pharmaceuticals.

Screening for chronic obstructive pulmonary disease (COPD) in asymptomatic adults has no net benefit, according to a U.S. Preventive Services Task Force (USPSTF) reassessment of its 2016 screening recommendations. The new recommendation is in line with the previous one and is made with moderate certainty (grade D evidence).

The USPSTF recommendation applies to adults who do not recognize or report respiratory symptoms. It does not apply to people with symptoms such as chronic cough, sputum production, difficulty breathing, or wheezing, or those known to be at very high risk for COPD. These latter include people with alpha-1 antitrypsin deficiency or workers exposed to certain toxins at their jobs, according to the report published in JAMA.

“Considering that the outcomes of several other chronic conditions, including cardiovascular disease and cancer, have been improved over the years with early detection and intervention, it is logical to ask whether screening to achieve early detection of COPD might also lead to better outcomes,” Surya P. Bhatt, MD, of the University of Alabama at Birmingham, and George T. O’Connor, MD, of the Boston University, explained in an editorial.
 

Task force assessment

The task force examined relevant publications after the 2016 deliberations and found no new studies that directly assessed the effects of screening for COPD in asymptomatic adults on morbidity, mortality, or health-related quality of life.

Although, as in their previous review, serious harms from treatment trials were not consistently reported, more recent large observational studies in screen-relevant populations suggested possible harms from the initiation of long-acting beta-agonists (LABAs), long-acting muscarinic antagonists (LAMAs), and the use of inhaled corticosteroids.

“In addition to potential treatment harms, there are opportunity costs to screening that may include time spent on counseling and providing services and patient referrals for diagnostic testing,” the task force stated.

Because cigarette smoking is the leading cause of COPD, the USPSTF has reiterated its recommendations for physicians to address tobacco smoking cessation in adults, including pregnant persons, as well as tobacco use in children and adolescents.
 

Not the whole story?

“Truly asymptomatic individuals with airflow obstruction do not meet criteria for COPD therapy, but sensitive questionnaires may detect symptoms not previously reported by the patient. It may be more effective to redirect the focus from screening for asymptomatic COPD to case finding using sensitive and cost-effective tools,” Dr. Bhatt and Dr. O’Connor suggested in their editorial.

“Even though available data may not support screening asymptomatic adults for COPD, there is substantial rationale for further investigation of strategies to enhance earlier detection of this condition,” they concluded.
 

More research needed

Despite the recommendation, the USPSTF indicated that further studies are needed to fill in research gaps, including:

• The effectiveness of screening asymptomatic adults for COPD to reduce morbidity or mortality or improve health-related quality of life, with long-term follow-up.
• The effectiveness of early treatment for asymptomatic, minimally symptomatic, or screen-detected populations to slow disease progression and improve health outcomes, with long-term follow-up.
• The harms of screening in and treatment of persons with asymptomatic or minimally symptomatic COPD.

The USPSTF is an independent, voluntary body, and potential conflicts of interest of the members are on file with the organization. Dr. Bhatt reported serving on an advisory board for Boehringer Ingelheim and receiving consulting fees from Sanofi/Regeneron; and Dr. O’Connor reported receiving consulting fees from Grupo Menarini and Dicerna Pharmaceuticals.

Researchers in Scotland have developed a risk calculator using a large electronic health records database that has shown a high reliability in predicting the risk of death for patients hospitalized for chronic occlusive pulmonary disease (COPD), providing another potential tool for improving postdischarge survival in these patients.

In a study published online in the journal Pharmacological Research, Pierpalo Pellicori, MD, and colleagues reported that a few variables, including prescriptions and laboratory data in routine EHRs, could help predict a patient’s risk of dying within 90 days after a hospital stay for COPD. Dr. Pellicori is a clinical cardiologist and research fellow at the Robertson Center for Biostatistics at the University of Glasgow.

“Identification of patients at high risk is valuable information for multidisciplinary teams,” Dr. Pellicori said in a written comment. “It allows the most vulnerable patients to be highlighted and prioritized for consideration of optimized value-based care, and for anticipatory care plan discussions.”

The retrospective cohort study analyzed EHR records of 17,973 patients who had an unplanned hospitalization for COPD in the Glasgow area from 2011 to 2017. The risk calculator model achieved a potential accuracy of 80%.

The study noted that, while a number of models have been developed to calculate the risk of exacerbations, inpatient death and prognosis in patients hospitalized for COPD, most of those models were based on cohorts of 1000 patients or less.

“Older age, male sex, and a longer hospital stay were important predictors of mortality in patients with COPD,” Dr. Pellicori said. “We also found that use of commonly prescribed medications such as digoxin identify patients with COPD more likely to die, perhaps because many have underlying heart failure, a highly prevalent but frequently missed diagnosis.”

He noted that heart failure and COPD share many risk factors, signs, and symptoms, such as smoking history, peripheral edema, and breathlessness. “Distinguishing between COPD and heart failure can be difficult, but is very important, as appropriate treatment for heart failure can improve a patient’s quality of life and survival substantially in many cases.”

The study also found that routinely collected and inexpensive blood markers – such as hemoglobin, neutrophil/lymphocyte ratio, serum chloride, urea, creatinine, and albumin – can also improve predictability of outcomes.

For example, the study found a linear increase in mortality of blood hemoglobin concentration less than 14 g/dL, but higher levels posed no greater risk. Higher white blood cell and neutrophil counts and lower lymphocyte and eosinophil counts were associated with a worse prognosis.

The study also found a linear increase in mortality with serum sodium less than 140 mmol/L or serum chloride less than 105 mmol/L –  but that higher concentrations of each were associated with a worse outcome.

“Interestingly,” Pellicori added, “social deprivation was not associated with mortality in this cohort.”

The final predictive model included age, sex, length of stay, and just nine other variables. “The model can be applied easily in clinical practice, even if electronic records are not available, because there are only 12 variables,” Dr. Pellicori said. “These could easily be entered manually into the risk calculator that we provide.”

“What is notable about this risk calculator is that it uses some of the techniques of machine learning, although it’s not specifically machine learning,” Angel Coz, MD, a pulmonologist at the Cleveland Clinic Respiratory Institute, said in an interview. “But it’s a retrospective data analysis, and actually by doing that it may catch some factors that we may not have necessarily paid attention to on a regular basis.”

While he called it a “well-done study,” Dr. Coz cautioned that “we have to be conservative in how to interpret and apply this because it is retrospective,” adding that future research should also use a prospective cohort.

For future consideration, Dr. Pellicori said that, while EHRs provide a “rich source” of data for such risk calculators, systems differ greatly across hospitals and health care systems and don’t link easily.

Future research would focus on validating the model in other large national datasets and seeing if machine learning can improve its predictability, Dr. Pellicori said. “Whether such models can provide a real-time, refined risk assessment for all patients in both primary or secondary care settings and improve the efficacy, efficiency, and quality of health care is our long-term goal.”

Dr. Pellicori and Dr. Coz disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Researchers in Scotland have developed a risk calculator using a large electronic health records database that has shown a high reliability in predicting the risk of death for patients hospitalized for chronic occlusive pulmonary disease (COPD), providing another potential tool for improving postdischarge survival in these patients.

In a study published online in the journal Pharmacological Research, Pierpalo Pellicori, MD, and colleagues reported that a few variables, including prescriptions and laboratory data in routine EHRs, could help predict a patient’s risk of dying within 90 days after a hospital stay for COPD. Dr. Pellicori is a clinical cardiologist and research fellow at the Robertson Center for Biostatistics at the University of Glasgow.

“Identification of patients at high risk is valuable information for multidisciplinary teams,” Dr. Pellicori said in a written comment. “It allows the most vulnerable patients to be highlighted and prioritized for consideration of optimized value-based care, and for anticipatory care plan discussions.”

The retrospective cohort study analyzed EHR records of 17,973 patients who had an unplanned hospitalization for COPD in the Glasgow area from 2011 to 2017. The risk calculator model achieved a potential accuracy of 80%.

The study noted that, while a number of models have been developed to calculate the risk of exacerbations, inpatient death and prognosis in patients hospitalized for COPD, most of those models were based on cohorts of 1000 patients or less.

“Older age, male sex, and a longer hospital stay were important predictors of mortality in patients with COPD,” Dr. Pellicori said. “We also found that use of commonly prescribed medications such as digoxin identify patients with COPD more likely to die, perhaps because many have underlying heart failure, a highly prevalent but frequently missed diagnosis.”

He noted that heart failure and COPD share many risk factors, signs, and symptoms, such as smoking history, peripheral edema, and breathlessness. “Distinguishing between COPD and heart failure can be difficult, but is very important, as appropriate treatment for heart failure can improve a patient’s quality of life and survival substantially in many cases.”

The study also found that routinely collected and inexpensive blood markers – such as hemoglobin, neutrophil/lymphocyte ratio, serum chloride, urea, creatinine, and albumin – can also improve predictability of outcomes.

For example, the study found a linear increase in mortality of blood hemoglobin concentration less than 14 g/dL, but higher levels posed no greater risk. Higher white blood cell and neutrophil counts and lower lymphocyte and eosinophil counts were associated with a worse prognosis.

The study also found a linear increase in mortality with serum sodium less than 140 mmol/L or serum chloride less than 105 mmol/L –  but that higher concentrations of each were associated with a worse outcome.

“Interestingly,” Pellicori added, “social deprivation was not associated with mortality in this cohort.”

The final predictive model included age, sex, length of stay, and just nine other variables. “The model can be applied easily in clinical practice, even if electronic records are not available, because there are only 12 variables,” Dr. Pellicori said. “These could easily be entered manually into the risk calculator that we provide.”

“What is notable about this risk calculator is that it uses some of the techniques of machine learning, although it’s not specifically machine learning,” Angel Coz, MD, a pulmonologist at the Cleveland Clinic Respiratory Institute, said in an interview. “But it’s a retrospective data analysis, and actually by doing that it may catch some factors that we may not have necessarily paid attention to on a regular basis.”

While he called it a “well-done study,” Dr. Coz cautioned that “we have to be conservative in how to interpret and apply this because it is retrospective,” adding that future research should also use a prospective cohort.

For future consideration, Dr. Pellicori said that, while EHRs provide a “rich source” of data for such risk calculators, systems differ greatly across hospitals and health care systems and don’t link easily.

Future research would focus on validating the model in other large national datasets and seeing if machine learning can improve its predictability, Dr. Pellicori said. “Whether such models can provide a real-time, refined risk assessment for all patients in both primary or secondary care settings and improve the efficacy, efficiency, and quality of health care is our long-term goal.”

Dr. Pellicori and Dr. Coz disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Researchers in Scotland have developed a risk calculator using a large electronic health records database that has shown a high reliability in predicting the risk of death for patients hospitalized for chronic occlusive pulmonary disease (COPD), providing another potential tool for improving postdischarge survival in these patients.

In a study published online in the journal Pharmacological Research, Pierpalo Pellicori, MD, and colleagues reported that a few variables, including prescriptions and laboratory data in routine EHRs, could help predict a patient’s risk of dying within 90 days after a hospital stay for COPD. Dr. Pellicori is a clinical cardiologist and research fellow at the Robertson Center for Biostatistics at the University of Glasgow.

“Identification of patients at high risk is valuable information for multidisciplinary teams,” Dr. Pellicori said in a written comment. “It allows the most vulnerable patients to be highlighted and prioritized for consideration of optimized value-based care, and for anticipatory care plan discussions.”

The retrospective cohort study analyzed EHR records of 17,973 patients who had an unplanned hospitalization for COPD in the Glasgow area from 2011 to 2017. The risk calculator model achieved a potential accuracy of 80%.

The study noted that, while a number of models have been developed to calculate the risk of exacerbations, inpatient death and prognosis in patients hospitalized for COPD, most of those models were based on cohorts of 1000 patients or less.

“Older age, male sex, and a longer hospital stay were important predictors of mortality in patients with COPD,” Dr. Pellicori said. “We also found that use of commonly prescribed medications such as digoxin identify patients with COPD more likely to die, perhaps because many have underlying heart failure, a highly prevalent but frequently missed diagnosis.”

He noted that heart failure and COPD share many risk factors, signs, and symptoms, such as smoking history, peripheral edema, and breathlessness. “Distinguishing between COPD and heart failure can be difficult, but is very important, as appropriate treatment for heart failure can improve a patient’s quality of life and survival substantially in many cases.”

The study also found that routinely collected and inexpensive blood markers – such as hemoglobin, neutrophil/lymphocyte ratio, serum chloride, urea, creatinine, and albumin – can also improve predictability of outcomes.

For example, the study found a linear increase in mortality of blood hemoglobin concentration less than 14 g/dL, but higher levels posed no greater risk. Higher white blood cell and neutrophil counts and lower lymphocyte and eosinophil counts were associated with a worse prognosis.

The study also found a linear increase in mortality with serum sodium less than 140 mmol/L or serum chloride less than 105 mmol/L –  but that higher concentrations of each were associated with a worse outcome.

“Interestingly,” Pellicori added, “social deprivation was not associated with mortality in this cohort.”

The final predictive model included age, sex, length of stay, and just nine other variables. “The model can be applied easily in clinical practice, even if electronic records are not available, because there are only 12 variables,” Dr. Pellicori said. “These could easily be entered manually into the risk calculator that we provide.”

“What is notable about this risk calculator is that it uses some of the techniques of machine learning, although it’s not specifically machine learning,” Angel Coz, MD, a pulmonologist at the Cleveland Clinic Respiratory Institute, said in an interview. “But it’s a retrospective data analysis, and actually by doing that it may catch some factors that we may not have necessarily paid attention to on a regular basis.”

While he called it a “well-done study,” Dr. Coz cautioned that “we have to be conservative in how to interpret and apply this because it is retrospective,” adding that future research should also use a prospective cohort.

For future consideration, Dr. Pellicori said that, while EHRs provide a “rich source” of data for such risk calculators, systems differ greatly across hospitals and health care systems and don’t link easily.

Future research would focus on validating the model in other large national datasets and seeing if machine learning can improve its predictability, Dr. Pellicori said. “Whether such models can provide a real-time, refined risk assessment for all patients in both primary or secondary care settings and improve the efficacy, efficiency, and quality of health care is our long-term goal.”

Dr. Pellicori and Dr. Coz disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

When Sigmund Freud claimed that “anatomy is destiny” he was referring to anatomical sex as a determinant of personality traits. Expert consensus statements have previously offered some recommendations for managing these syndromes, but clinical data are scarce, so the present review “is intended to establish a starting point for future research,”

That notion has been widely discredited, but Freud appears to be inadvertently right in one respect: When it comes to chronic obstructive pulmonary disease (COPD), anatomy really is destiny, and sex may be as well, pulmonary researchers say.

There is a growing body of evidence to indicate that COPD affects men and women differently, and that men and women patients with COPD require different clinical management. Yet women are often underdiagnosed or misdiagnosed, partly because of poorly understood sex differences, but also because of cultural biases.

But plunging any farther into the weeds, it’s important to define terms. Although various investigators have used the terms “sex” and “gender” interchangeably, sex is the preferred term when referring to biological attributes of individual patients, while gender refers to personal identity.

These distinctions are important, contended Amik Sodhi, MBBS, MPH, from the division of allergy, pulmonology, and critical care medicine at the University of Wisconsin–Madison.

“Sex is essentially a biologic construct, so it’s got to do with the sex chromosomes, the genetics of that person, and it refers to the anatomic variations that can change susceptibility to different diseases,” she said in an interview.

An example of sex differences or “sexual dimorphism” can be found in a recent meta-analysis of sex-based genetic associations by Megan Hardin, MD, MPH from Brigham & Women’s Hospital in Boston and colleagues.

They reported that CELSR1, a gene involved in fetal lung development, was expressed more among women than among men and that a single nucleotide polymorphism in the gene was associated with COPD among women smokers, but not among men smokers.

The finding points to a potential risk locus for COPD in women, and could help shed light on sexual dimorphism in COPD, Dr. Hardin and colleagues said.

In contrast to sex, “gender is more of a psychosocial construct which can impact how diseases manifest themselves, how they are potentially managed, and what outcomes might occur for that particular disease,” Dr. Sodhi said.

She and her colleagues recently published a review of sex and gender in common lung disorders and sleep in the journal CHEST, where they wrote that the “influence of sex and gender is portrayed in epidemiological data, disease pathogenesis and pathophysiology, clinical manifestations, response to treatment, access to care, and health outcomes. Hence, sex and gender should be considered in all types of research, clinical practice and educational curricula.”

For example, as previously reported at the 2021 annual meeting of the American Thoracic Society, sex-specific differences in the severity of symptoms and prevalence of comorbidities in patients with COPD may point to different criteria for diagnosing cardiac comorbidities in women and men.

Those conclusions came from a retrospective analysis of data on 795 women and 1,251 men with GOLD (Global Initiative for Chronic Obstructive Lung Disease) class 1-3 disease.

The investigators looked at the patients’ clinical history, comorbidities, lung function, COPD Assessment Test scores, and modified Medical Research Council (mMRC) dyspnea score, and found significant differences between men and women for most functional parameters and comorbidities, and for CAT items of cough, phlegm, and energy.

In logistic regression analysis, predictors for cardiac disease in men were energy, mMRC score, smoking status, body mass index, age, and spirometric lung function, but in women only age was significantly predictive for cardiac disease.

An example of gender effects on COPD differences in men and women is the increase in cigarette advertising aimed at women in the 1960s and the advent of women-targeted brands such as Virginia Slims, which in turn lead to increased smoking rates among women. In addition, in the developing world, where the sex/gender gap in COPD is narrowing, women tend to have greater exposure to wood smoke and cooking fuels in unventilated or poorly ventilated spaces, compared with men.
 

Increasing incidence among women

According to the Centers for Disease Control and Prevention, chronic lower respiratory diseases, primarily COPD, were the fourth-leading cause of death in women in the United States in 2018, following only heart disease, cancer, and accidents/injuries.

And as a CDC analysis of data from the 2013 Behavioral Risk Factor Surveillance System showed, women were more likely to report being told by a physician that they had COPD than did men (6.6%, compared with 5.4%).

Dr. Sodhi and colleagues noted that, at all time points examined from 2005 to 2014, women had a higher proportion than men of COPD hospitalizations and in-hospital deaths. They also noted that female sex is associated with a threefold risk for severe early-onset COPD, and that women with COPD have lower diffusion capacity of lungs for carbon monoxide, despite having higher predicted forced expiratory volume in 1 second, compared with men.

“Historically, COPD wasn’t a disease that was so prevalent in women. It’s been in the past 20 years that the trends have changed,” said Patricia Silveyra, MSc, PhD, ATSF, associate professor of environmental and occupational health at Indiana University, Bloomington.

The increasing prevalence of COPD among women cannot be explained by smoking alone, she said in an interview.

“It used to be thought that it was because more women smoked, but actually a lot of women who don’t smoke can develop COPD, so it appears to be probably something environmental, but because it used to be a disease of older men, in the clinic there was also a bias to diagnose men with COPD, and women with asthma, so a lot of women went underdiagnosed,” Dr. Silveyra said.

In their review, Dr. Sodhi and colleagues noted that women with COPD “may be underdiagnosed as a result of having different symptoms from those classically recognized. Reasons for underdiagnosis or a delay in diagnosis may also be due to lack of a formal evaluation with spirometry, women seeking care later in the course of disease, physician bias, or associated fatigue or depression misdirecting diagnostic strategies. Underdiagnosis may be associated with psychological distress and worse health-related quality of life.”

Although the evidence is mixed, women tend to present more frequently with the chronic bronchitis phenotype of COPD, compared with the emphysema phenotype, and women tend to have greater degrees of pulmonary function impairment when exposed to tobacco smoke, even after controlling for differences in height and weight.

“For the same amount of exposure to tobacco smoke, females are likely to develop more severe airflow limitation at an earlier age than males, and have more exacerbation,” Dr. Sodhi and colleagues wrote.

Both Dr. Silveyra and Dr. Sodhi said that reason why men and women differ in their physiological reactions to smoke are still unknown.
 

Sex differences in drug responses

There is only limited evidence to indicate that women and men respond differently to various therapeutic agents, but what is clear is that more research into this area is needed, Dr. Sodhi and Dr. Silveyra said.

For example, among the few studies that have documented sex differences, one showed no sex differences in the efficacy of salmeterol/fluticasone combination therapy for reducing exacerbations or improving quality of life, whereas another showed that women were more likely than men to experience COPD symptoms or exacerbations after stopping inhaled corticosteroids, Dr. Sodhi and colleagues noted.

Both Dr. Sodhi and Dr. Silveyra emphasized the need for clinical trials that study the effects of sex on treatment outcomes in COPD, which could lead to better, more personalized therapeutic regimens that take sex and gender into account.

Dr. Sodhi and colleagues offered the following advice to clinicians: “Interaction with female patients should take into account that their symptoms may not conform to traditionally accepted presentations. Challenges exist for female patients at all levels of health care interaction and as clinicians we need to acknowledge the bias and willfully work toward recognition and elimination of unconscious and conscious bias. Empowering our patients to have frank discussions with their health care team when they perceive bias is another step to help promote equity.”

The review by Dr. Sodhi and colleagues was supported by grants from the National Institutes of Health. Dr. Sodhi and Dr. Silveyra reported having no conflicts of interest to disclose.

When Sigmund Freud claimed that “anatomy is destiny” he was referring to anatomical sex as a determinant of personality traits. Expert consensus statements have previously offered some recommendations for managing these syndromes, but clinical data are scarce, so the present review “is intended to establish a starting point for future research,”

That notion has been widely discredited, but Freud appears to be inadvertently right in one respect: When it comes to chronic obstructive pulmonary disease (COPD), anatomy really is destiny, and sex may be as well, pulmonary researchers say.

There is a growing body of evidence to indicate that COPD affects men and women differently, and that men and women patients with COPD require different clinical management. Yet women are often underdiagnosed or misdiagnosed, partly because of poorly understood sex differences, but also because of cultural biases.

But plunging any farther into the weeds, it’s important to define terms. Although various investigators have used the terms “sex” and “gender” interchangeably, sex is the preferred term when referring to biological attributes of individual patients, while gender refers to personal identity.

These distinctions are important, contended Amik Sodhi, MBBS, MPH, from the division of allergy, pulmonology, and critical care medicine at the University of Wisconsin–Madison.

“Sex is essentially a biologic construct, so it’s got to do with the sex chromosomes, the genetics of that person, and it refers to the anatomic variations that can change susceptibility to different diseases,” she said in an interview.

An example of sex differences or “sexual dimorphism” can be found in a recent meta-analysis of sex-based genetic associations by Megan Hardin, MD, MPH from Brigham & Women’s Hospital in Boston and colleagues.

They reported that CELSR1, a gene involved in fetal lung development, was expressed more among women than among men and that a single nucleotide polymorphism in the gene was associated with COPD among women smokers, but not among men smokers.

The finding points to a potential risk locus for COPD in women, and could help shed light on sexual dimorphism in COPD, Dr. Hardin and colleagues said.

In contrast to sex, “gender is more of a psychosocial construct which can impact how diseases manifest themselves, how they are potentially managed, and what outcomes might occur for that particular disease,” Dr. Sodhi said.

She and her colleagues recently published a review of sex and gender in common lung disorders and sleep in the journal CHEST, where they wrote that the “influence of sex and gender is portrayed in epidemiological data, disease pathogenesis and pathophysiology, clinical manifestations, response to treatment, access to care, and health outcomes. Hence, sex and gender should be considered in all types of research, clinical practice and educational curricula.”

For example, as previously reported at the 2021 annual meeting of the American Thoracic Society, sex-specific differences in the severity of symptoms and prevalence of comorbidities in patients with COPD may point to different criteria for diagnosing cardiac comorbidities in women and men.

Those conclusions came from a retrospective analysis of data on 795 women and 1,251 men with GOLD (Global Initiative for Chronic Obstructive Lung Disease) class 1-3 disease.

The investigators looked at the patients’ clinical history, comorbidities, lung function, COPD Assessment Test scores, and modified Medical Research Council (mMRC) dyspnea score, and found significant differences between men and women for most functional parameters and comorbidities, and for CAT items of cough, phlegm, and energy.

In logistic regression analysis, predictors for cardiac disease in men were energy, mMRC score, smoking status, body mass index, age, and spirometric lung function, but in women only age was significantly predictive for cardiac disease.

An example of gender effects on COPD differences in men and women is the increase in cigarette advertising aimed at women in the 1960s and the advent of women-targeted brands such as Virginia Slims, which in turn lead to increased smoking rates among women. In addition, in the developing world, where the sex/gender gap in COPD is narrowing, women tend to have greater exposure to wood smoke and cooking fuels in unventilated or poorly ventilated spaces, compared with men.
 

Increasing incidence among women

According to the Centers for Disease Control and Prevention, chronic lower respiratory diseases, primarily COPD, were the fourth-leading cause of death in women in the United States in 2018, following only heart disease, cancer, and accidents/injuries.

And as a CDC analysis of data from the 2013 Behavioral Risk Factor Surveillance System showed, women were more likely to report being told by a physician that they had COPD than did men (6.6%, compared with 5.4%).

Dr. Sodhi and colleagues noted that, at all time points examined from 2005 to 2014, women had a higher proportion than men of COPD hospitalizations and in-hospital deaths. They also noted that female sex is associated with a threefold risk for severe early-onset COPD, and that women with COPD have lower diffusion capacity of lungs for carbon monoxide, despite having higher predicted forced expiratory volume in 1 second, compared with men.

“Historically, COPD wasn’t a disease that was so prevalent in women. It’s been in the past 20 years that the trends have changed,” said Patricia Silveyra, MSc, PhD, ATSF, associate professor of environmental and occupational health at Indiana University, Bloomington.

The increasing prevalence of COPD among women cannot be explained by smoking alone, she said in an interview.

“It used to be thought that it was because more women smoked, but actually a lot of women who don’t smoke can develop COPD, so it appears to be probably something environmental, but because it used to be a disease of older men, in the clinic there was also a bias to diagnose men with COPD, and women with asthma, so a lot of women went underdiagnosed,” Dr. Silveyra said.

In their review, Dr. Sodhi and colleagues noted that women with COPD “may be underdiagnosed as a result of having different symptoms from those classically recognized. Reasons for underdiagnosis or a delay in diagnosis may also be due to lack of a formal evaluation with spirometry, women seeking care later in the course of disease, physician bias, or associated fatigue or depression misdirecting diagnostic strategies. Underdiagnosis may be associated with psychological distress and worse health-related quality of life.”

Although the evidence is mixed, women tend to present more frequently with the chronic bronchitis phenotype of COPD, compared with the emphysema phenotype, and women tend to have greater degrees of pulmonary function impairment when exposed to tobacco smoke, even after controlling for differences in height and weight.

“For the same amount of exposure to tobacco smoke, females are likely to develop more severe airflow limitation at an earlier age than males, and have more exacerbation,” Dr. Sodhi and colleagues wrote.

Both Dr. Silveyra and Dr. Sodhi said that reason why men and women differ in their physiological reactions to smoke are still unknown.
 

Sex differences in drug responses

There is only limited evidence to indicate that women and men respond differently to various therapeutic agents, but what is clear is that more research into this area is needed, Dr. Sodhi and Dr. Silveyra said.

For example, among the few studies that have documented sex differences, one showed no sex differences in the efficacy of salmeterol/fluticasone combination therapy for reducing exacerbations or improving quality of life, whereas another showed that women were more likely than men to experience COPD symptoms or exacerbations after stopping inhaled corticosteroids, Dr. Sodhi and colleagues noted.

Both Dr. Sodhi and Dr. Silveyra emphasized the need for clinical trials that study the effects of sex on treatment outcomes in COPD, which could lead to better, more personalized therapeutic regimens that take sex and gender into account.

Dr. Sodhi and colleagues offered the following advice to clinicians: “Interaction with female patients should take into account that their symptoms may not conform to traditionally accepted presentations. Challenges exist for female patients at all levels of health care interaction and as clinicians we need to acknowledge the bias and willfully work toward recognition and elimination of unconscious and conscious bias. Empowering our patients to have frank discussions with their health care team when they perceive bias is another step to help promote equity.”

The review by Dr. Sodhi and colleagues was supported by grants from the National Institutes of Health. Dr. Sodhi and Dr. Silveyra reported having no conflicts of interest to disclose.

When Sigmund Freud claimed that “anatomy is destiny” he was referring to anatomical sex as a determinant of personality traits. Expert consensus statements have previously offered some recommendations for managing these syndromes, but clinical data are scarce, so the present review “is intended to establish a starting point for future research,”

That notion has been widely discredited, but Freud appears to be inadvertently right in one respect: When it comes to chronic obstructive pulmonary disease (COPD), anatomy really is destiny, and sex may be as well, pulmonary researchers say.

There is a growing body of evidence to indicate that COPD affects men and women differently, and that men and women patients with COPD require different clinical management. Yet women are often underdiagnosed or misdiagnosed, partly because of poorly understood sex differences, but also because of cultural biases.

But plunging any farther into the weeds, it’s important to define terms. Although various investigators have used the terms “sex” and “gender” interchangeably, sex is the preferred term when referring to biological attributes of individual patients, while gender refers to personal identity.

These distinctions are important, contended Amik Sodhi, MBBS, MPH, from the division of allergy, pulmonology, and critical care medicine at the University of Wisconsin–Madison.

“Sex is essentially a biologic construct, so it’s got to do with the sex chromosomes, the genetics of that person, and it refers to the anatomic variations that can change susceptibility to different diseases,” she said in an interview.

An example of sex differences or “sexual dimorphism” can be found in a recent meta-analysis of sex-based genetic associations by Megan Hardin, MD, MPH from Brigham & Women’s Hospital in Boston and colleagues.

They reported that CELSR1, a gene involved in fetal lung development, was expressed more among women than among men and that a single nucleotide polymorphism in the gene was associated with COPD among women smokers, but not among men smokers.

The finding points to a potential risk locus for COPD in women, and could help shed light on sexual dimorphism in COPD, Dr. Hardin and colleagues said.

In contrast to sex, “gender is more of a psychosocial construct which can impact how diseases manifest themselves, how they are potentially managed, and what outcomes might occur for that particular disease,” Dr. Sodhi said.

She and her colleagues recently published a review of sex and gender in common lung disorders and sleep in the journal CHEST, where they wrote that the “influence of sex and gender is portrayed in epidemiological data, disease pathogenesis and pathophysiology, clinical manifestations, response to treatment, access to care, and health outcomes. Hence, sex and gender should be considered in all types of research, clinical practice and educational curricula.”

For example, as previously reported at the 2021 annual meeting of the American Thoracic Society, sex-specific differences in the severity of symptoms and prevalence of comorbidities in patients with COPD may point to different criteria for diagnosing cardiac comorbidities in women and men.

Those conclusions came from a retrospective analysis of data on 795 women and 1,251 men with GOLD (Global Initiative for Chronic Obstructive Lung Disease) class 1-3 disease.

The investigators looked at the patients’ clinical history, comorbidities, lung function, COPD Assessment Test scores, and modified Medical Research Council (mMRC) dyspnea score, and found significant differences between men and women for most functional parameters and comorbidities, and for CAT items of cough, phlegm, and energy.

In logistic regression analysis, predictors for cardiac disease in men were energy, mMRC score, smoking status, body mass index, age, and spirometric lung function, but in women only age was significantly predictive for cardiac disease.

An example of gender effects on COPD differences in men and women is the increase in cigarette advertising aimed at women in the 1960s and the advent of women-targeted brands such as Virginia Slims, which in turn lead to increased smoking rates among women. In addition, in the developing world, where the sex/gender gap in COPD is narrowing, women tend to have greater exposure to wood smoke and cooking fuels in unventilated or poorly ventilated spaces, compared with men.
 

Increasing incidence among women

According to the Centers for Disease Control and Prevention, chronic lower respiratory diseases, primarily COPD, were the fourth-leading cause of death in women in the United States in 2018, following only heart disease, cancer, and accidents/injuries.

And as a CDC analysis of data from the 2013 Behavioral Risk Factor Surveillance System showed, women were more likely to report being told by a physician that they had COPD than did men (6.6%, compared with 5.4%).

Dr. Sodhi and colleagues noted that, at all time points examined from 2005 to 2014, women had a higher proportion than men of COPD hospitalizations and in-hospital deaths. They also noted that female sex is associated with a threefold risk for severe early-onset COPD, and that women with COPD have lower diffusion capacity of lungs for carbon monoxide, despite having higher predicted forced expiratory volume in 1 second, compared with men.

“Historically, COPD wasn’t a disease that was so prevalent in women. It’s been in the past 20 years that the trends have changed,” said Patricia Silveyra, MSc, PhD, ATSF, associate professor of environmental and occupational health at Indiana University, Bloomington.

The increasing prevalence of COPD among women cannot be explained by smoking alone, she said in an interview.

“It used to be thought that it was because more women smoked, but actually a lot of women who don’t smoke can develop COPD, so it appears to be probably something environmental, but because it used to be a disease of older men, in the clinic there was also a bias to diagnose men with COPD, and women with asthma, so a lot of women went underdiagnosed,” Dr. Silveyra said.

In their review, Dr. Sodhi and colleagues noted that women with COPD “may be underdiagnosed as a result of having different symptoms from those classically recognized. Reasons for underdiagnosis or a delay in diagnosis may also be due to lack of a formal evaluation with spirometry, women seeking care later in the course of disease, physician bias, or associated fatigue or depression misdirecting diagnostic strategies. Underdiagnosis may be associated with psychological distress and worse health-related quality of life.”

Although the evidence is mixed, women tend to present more frequently with the chronic bronchitis phenotype of COPD, compared with the emphysema phenotype, and women tend to have greater degrees of pulmonary function impairment when exposed to tobacco smoke, even after controlling for differences in height and weight.

“For the same amount of exposure to tobacco smoke, females are likely to develop more severe airflow limitation at an earlier age than males, and have more exacerbation,” Dr. Sodhi and colleagues wrote.

Both Dr. Silveyra and Dr. Sodhi said that reason why men and women differ in their physiological reactions to smoke are still unknown.
 

Sex differences in drug responses

There is only limited evidence to indicate that women and men respond differently to various therapeutic agents, but what is clear is that more research into this area is needed, Dr. Sodhi and Dr. Silveyra said.

For example, among the few studies that have documented sex differences, one showed no sex differences in the efficacy of salmeterol/fluticasone combination therapy for reducing exacerbations or improving quality of life, whereas another showed that women were more likely than men to experience COPD symptoms or exacerbations after stopping inhaled corticosteroids, Dr. Sodhi and colleagues noted.

Both Dr. Sodhi and Dr. Silveyra emphasized the need for clinical trials that study the effects of sex on treatment outcomes in COPD, which could lead to better, more personalized therapeutic regimens that take sex and gender into account.

Dr. Sodhi and colleagues offered the following advice to clinicians: “Interaction with female patients should take into account that their symptoms may not conform to traditionally accepted presentations. Challenges exist for female patients at all levels of health care interaction and as clinicians we need to acknowledge the bias and willfully work toward recognition and elimination of unconscious and conscious bias. Empowering our patients to have frank discussions with their health care team when they perceive bias is another step to help promote equity.”

The review by Dr. Sodhi and colleagues was supported by grants from the National Institutes of Health. Dr. Sodhi and Dr. Silveyra reported having no conflicts of interest to disclose.

The U.S. Food and Drug Administration approved the first generic of Symbicort (budesonide and formoterol fumarate dihydrate) inhalation aerosol for the treatment of asthma in patients 6 years of age and older and for the maintenance treatment of patients with chronic obstructive pulmonary disease (COPD), including chronic bronchitis and/or emphysema.

The approval was given for a complex generic drug-device combination product – a metered-dose inhaler that contains both budesonide (a corticosteroid that reduces inflammation) and formoterol (a long-acting bronchodilator that relaxes muscles in the airways to improve breathing). It is intended to be used as two inhalations, two times a day (usually morning and night, about 12 hours apart), to treat both diseases by preventing symptoms, such as wheezing for those with asthma and for improved breathing for patients with COPD.

The inhaler is approved at two strengths (160/4.5 mcg/actuation and 80/4.5 mcg/actuation), according to the March 15 FDA announcement. The device is not intended for the treatment of acute asthma.

“Today’s approval of the first generic for one of the most commonly prescribed complex drug-device combination products to treat asthma and COPD is another step forward in our commitment to bring generic copies of complex drugs to the market, which can improve quality of life and help reduce the cost of treatment,” said Sally Choe, PhD, director of the Office of Generic Drugs in the FDA’s Center for Drug Evaluation and Research.

The most common side effects associated with budesonide and formoterol fumarate dihydrate oral inhalation aerosol for those with asthma are nasopharyngitis pain, sinusitis, influenza, back pain, nasal congestion, stomach discomfort, vomiting, and oral candidiasis (thrush). For those with COPD, the most common side effects are nasopharyngitis, oral candidiasis, bronchitis, sinusitis, and upper respiratory tract infection, the FDA reported.

The approval of this generic drug-device combination was granted to Mylan Pharmaceuticals.

A version of this article first appeared on Medscape.com.

The U.S. Food and Drug Administration approved the first generic of Symbicort (budesonide and formoterol fumarate dihydrate) inhalation aerosol for the treatment of asthma in patients 6 years of age and older and for the maintenance treatment of patients with chronic obstructive pulmonary disease (COPD), including chronic bronchitis and/or emphysema.

The approval was given for a complex generic drug-device combination product – a metered-dose inhaler that contains both budesonide (a corticosteroid that reduces inflammation) and formoterol (a long-acting bronchodilator that relaxes muscles in the airways to improve breathing). It is intended to be used as two inhalations, two times a day (usually morning and night, about 12 hours apart), to treat both diseases by preventing symptoms, such as wheezing for those with asthma and for improved breathing for patients with COPD.

The inhaler is approved at two strengths (160/4.5 mcg/actuation and 80/4.5 mcg/actuation), according to the March 15 FDA announcement. The device is not intended for the treatment of acute asthma.

“Today’s approval of the first generic for one of the most commonly prescribed complex drug-device combination products to treat asthma and COPD is another step forward in our commitment to bring generic copies of complex drugs to the market, which can improve quality of life and help reduce the cost of treatment,” said Sally Choe, PhD, director of the Office of Generic Drugs in the FDA’s Center for Drug Evaluation and Research.

The most common side effects associated with budesonide and formoterol fumarate dihydrate oral inhalation aerosol for those with asthma are nasopharyngitis pain, sinusitis, influenza, back pain, nasal congestion, stomach discomfort, vomiting, and oral candidiasis (thrush). For those with COPD, the most common side effects are nasopharyngitis, oral candidiasis, bronchitis, sinusitis, and upper respiratory tract infection, the FDA reported.

The approval of this generic drug-device combination was granted to Mylan Pharmaceuticals.

A version of this article first appeared on Medscape.com.

The U.S. Food and Drug Administration approved the first generic of Symbicort (budesonide and formoterol fumarate dihydrate) inhalation aerosol for the treatment of asthma in patients 6 years of age and older and for the maintenance treatment of patients with chronic obstructive pulmonary disease (COPD), including chronic bronchitis and/or emphysema.

The approval was given for a complex generic drug-device combination product – a metered-dose inhaler that contains both budesonide (a corticosteroid that reduces inflammation) and formoterol (a long-acting bronchodilator that relaxes muscles in the airways to improve breathing). It is intended to be used as two inhalations, two times a day (usually morning and night, about 12 hours apart), to treat both diseases by preventing symptoms, such as wheezing for those with asthma and for improved breathing for patients with COPD.

The inhaler is approved at two strengths (160/4.5 mcg/actuation and 80/4.5 mcg/actuation), according to the March 15 FDA announcement. The device is not intended for the treatment of acute asthma.

“Today’s approval of the first generic for one of the most commonly prescribed complex drug-device combination products to treat asthma and COPD is another step forward in our commitment to bring generic copies of complex drugs to the market, which can improve quality of life and help reduce the cost of treatment,” said Sally Choe, PhD, director of the Office of Generic Drugs in the FDA’s Center for Drug Evaluation and Research.

The most common side effects associated with budesonide and formoterol fumarate dihydrate oral inhalation aerosol for those with asthma are nasopharyngitis pain, sinusitis, influenza, back pain, nasal congestion, stomach discomfort, vomiting, and oral candidiasis (thrush). For those with COPD, the most common side effects are nasopharyngitis, oral candidiasis, bronchitis, sinusitis, and upper respiratory tract infection, the FDA reported.

The approval of this generic drug-device combination was granted to Mylan Pharmaceuticals.

A version of this article first appeared on Medscape.com.

Pseudomonas aeruginosa persisted in the airways of patients with chronic obstructive pulmonary disease (COPD), based on data from 23 patients over a 1-year period.

P. aeruginosa is cultured in as many as 20% of bacterial exacerbations and has been linked to increased morbidity and mortality in patients with COPD, wrote Josefin Eklöf, MD, of the University of Copenhagen and colleagues. However, its patterns and characteristics have not been well studied, and researchers proposed that P. aerunginosa persists in COPD patients in part because of genetic adaptations in the genes related to antibiotic resistance.

In a study published in Clinical Microbiology and Infection, the researchers identified 23 consecutive patients enrolled in an ongoing randomized clinical trial at four sites in Denmark between Jan. 2018 and Jan. 2020. Participants were randomized 1:1 to targeted antipseudomonal antibiotic treatment for 14 days (between visit day 1 and visit day 14) or no antipseudomonal treatment. Sputum samples were collected at baseline on day 1 and on days 14, 30, 60, 90, and 365.

The researchers sequenced isolates from 23 adult patients over 365 days of follow-up. The recurrence of P. aeruginosa occurred in 19 patients (83%) during this period. Ultimately, a total of 153 isolates were analyzed. The researchers found that each patient carried their own unique lineage, with the except of one patient in whom two distinct lineages were identified.

“Independent mutation of the same gene across multiple lineages may be the result of positive selection of adaptive mutations,” Dr. Eklöf and colleagues wrote. They found 38 genes for P. aeruginosa that were mutated in at least two lineages, which suggested adaptive mutations. Some of the more frequently mutated genes were those important to antibiotic resistance and chronic infections, the researchers said. Specifically, mutations occurred in 40 of 140 pathoadaptive genes, compared with 265 of 5,572 other genes (P < .001). In addition, the 24 total lineages carried 4-6 antibiotic resistance genes, and no evidence suggested that lineages acquired or lost these genes during carriage.

Overall, the results indicate that the recurrence of P. aeruginosa was caused by persistence of the same clonal lineage in each patient. “This pattern of persistence was associated with genetic adaptation related to phenotypes considered important for P. aeruginosa infections,” the researchers said.

The study findings were limited by the relatively small number of samples and isolates per sample, the follow-up of only 1 year, and the inability to account for mutations in the early stage because few patients were naive to P. aeruginosa at the start of the study, the researchers noted. However, the results were strengthened by the relatively large and well-defined study population and high rate of sampling compliance, they said.

Overall, “the findings warrant research to improve therapy, including trial data on possible clinical benefits of attempting antibiotic eradication of P. aeruginosa in this vulnerable group of patients,” they concluded.

The study was supported by the Independent Research Fund Denmark and the Research committee at Copenhagen University Hospital-Herlev and Gentofte Hospital. The researchers had no financial conflicts to disclose.

Pseudomonas aeruginosa persisted in the airways of patients with chronic obstructive pulmonary disease (COPD), based on data from 23 patients over a 1-year period.

P. aeruginosa is cultured in as many as 20% of bacterial exacerbations and has been linked to increased morbidity and mortality in patients with COPD, wrote Josefin Eklöf, MD, of the University of Copenhagen and colleagues. However, its patterns and characteristics have not been well studied, and researchers proposed that P. aerunginosa persists in COPD patients in part because of genetic adaptations in the genes related to antibiotic resistance.

In a study published in Clinical Microbiology and Infection, the researchers identified 23 consecutive patients enrolled in an ongoing randomized clinical trial at four sites in Denmark between Jan. 2018 and Jan. 2020. Participants were randomized 1:1 to targeted antipseudomonal antibiotic treatment for 14 days (between visit day 1 and visit day 14) or no antipseudomonal treatment. Sputum samples were collected at baseline on day 1 and on days 14, 30, 60, 90, and 365.

The researchers sequenced isolates from 23 adult patients over 365 days of follow-up. The recurrence of P. aeruginosa occurred in 19 patients (83%) during this period. Ultimately, a total of 153 isolates were analyzed. The researchers found that each patient carried their own unique lineage, with the except of one patient in whom two distinct lineages were identified.

“Independent mutation of the same gene across multiple lineages may be the result of positive selection of adaptive mutations,” Dr. Eklöf and colleagues wrote. They found 38 genes for P. aeruginosa that were mutated in at least two lineages, which suggested adaptive mutations. Some of the more frequently mutated genes were those important to antibiotic resistance and chronic infections, the researchers said. Specifically, mutations occurred in 40 of 140 pathoadaptive genes, compared with 265 of 5,572 other genes (P < .001). In addition, the 24 total lineages carried 4-6 antibiotic resistance genes, and no evidence suggested that lineages acquired or lost these genes during carriage.

Overall, the results indicate that the recurrence of P. aeruginosa was caused by persistence of the same clonal lineage in each patient. “This pattern of persistence was associated with genetic adaptation related to phenotypes considered important for P. aeruginosa infections,” the researchers said.

The study findings were limited by the relatively small number of samples and isolates per sample, the follow-up of only 1 year, and the inability to account for mutations in the early stage because few patients were naive to P. aeruginosa at the start of the study, the researchers noted. However, the results were strengthened by the relatively large and well-defined study population and high rate of sampling compliance, they said.

Overall, “the findings warrant research to improve therapy, including trial data on possible clinical benefits of attempting antibiotic eradication of P. aeruginosa in this vulnerable group of patients,” they concluded.

The study was supported by the Independent Research Fund Denmark and the Research committee at Copenhagen University Hospital-Herlev and Gentofte Hospital. The researchers had no financial conflicts to disclose.

Pseudomonas aeruginosa persisted in the airways of patients with chronic obstructive pulmonary disease (COPD), based on data from 23 patients over a 1-year period.

P. aeruginosa is cultured in as many as 20% of bacterial exacerbations and has been linked to increased morbidity and mortality in patients with COPD, wrote Josefin Eklöf, MD, of the University of Copenhagen and colleagues. However, its patterns and characteristics have not been well studied, and researchers proposed that P. aerunginosa persists in COPD patients in part because of genetic adaptations in the genes related to antibiotic resistance.

In a study published in Clinical Microbiology and Infection, the researchers identified 23 consecutive patients enrolled in an ongoing randomized clinical trial at four sites in Denmark between Jan. 2018 and Jan. 2020. Participants were randomized 1:1 to targeted antipseudomonal antibiotic treatment for 14 days (between visit day 1 and visit day 14) or no antipseudomonal treatment. Sputum samples were collected at baseline on day 1 and on days 14, 30, 60, 90, and 365.

The researchers sequenced isolates from 23 adult patients over 365 days of follow-up. The recurrence of P. aeruginosa occurred in 19 patients (83%) during this period. Ultimately, a total of 153 isolates were analyzed. The researchers found that each patient carried their own unique lineage, with the except of one patient in whom two distinct lineages were identified.

“Independent mutation of the same gene across multiple lineages may be the result of positive selection of adaptive mutations,” Dr. Eklöf and colleagues wrote. They found 38 genes for P. aeruginosa that were mutated in at least two lineages, which suggested adaptive mutations. Some of the more frequently mutated genes were those important to antibiotic resistance and chronic infections, the researchers said. Specifically, mutations occurred in 40 of 140 pathoadaptive genes, compared with 265 of 5,572 other genes (P < .001). In addition, the 24 total lineages carried 4-6 antibiotic resistance genes, and no evidence suggested that lineages acquired or lost these genes during carriage.

Overall, the results indicate that the recurrence of P. aeruginosa was caused by persistence of the same clonal lineage in each patient. “This pattern of persistence was associated with genetic adaptation related to phenotypes considered important for P. aeruginosa infections,” the researchers said.

The study findings were limited by the relatively small number of samples and isolates per sample, the follow-up of only 1 year, and the inability to account for mutations in the early stage because few patients were naive to P. aeruginosa at the start of the study, the researchers noted. However, the results were strengthened by the relatively large and well-defined study population and high rate of sampling compliance, they said.

Overall, “the findings warrant research to improve therapy, including trial data on possible clinical benefits of attempting antibiotic eradication of P. aeruginosa in this vulnerable group of patients,” they concluded.

The study was supported by the Independent Research Fund Denmark and the Research committee at Copenhagen University Hospital-Herlev and Gentofte Hospital. The researchers had no financial conflicts to disclose.

Heavier smoking significantly increased mortality in adults with progressive fibrosing interstitial lung disease (PF-ILD), based on data from 377 individuals.

The negative impact of smoking on pulmonary diseases is well documented, but the specific impact on patients with PF-ILD has not been well studied, Mark Platenburg, MD, of St. Antonious Hospital, Nieuwegein, the Netherlands, and colleagues wrote in Respiratory Medicine .

GaryPhoto/ThinkStock

“Patients with PF-ILD or IPF [idiopathic pulmonary fibrosis] are prone to early mortality, indicating a need for prognostic [bio]marker studies for precision medicine,” they said.

The researchers identified adults older than 18 years with PF-ILD who were diagnosed at a single center. All study participants had at least 10% fibrosis, and showed either a decline of at least 10% in forced vital capacity, a 5.0%-9.9% relative FVC decline plus progressive respiratory symptoms and/or an increase in extent of fibrosis on subsequent high-resolution (HRCT progression), or progressive respiratory symptoms and HRCT progression over 24 months after ILD diagnosis.

Pack-years of smoking was a prognostic variable; the researchers also compared median transplant-free survival in heavy smokers and mild to moderate smokers. They also investigated the association between smoking quantity and emphysema in the study population.

Overall, the increased risk for mortality was 11%, 22%, and 44% in patients with 10, 20, and 40 pack-years of smoking, respectively.

Both the unadjusted and adjusted hazard ratio for pack-years were significant (1.014, P < .001 and 1.011, P = .022, respectively).

The median transplant-free survival of ever-smokers versus never-smokers with PF-ILD was 3.3 years versus 4.8 years; median transplant-free survival was 3.0 years for heavy smokers and 3.8 years for mild to moderate smokers. Similarly, median survival was 4.2 years in never-smokers versus 3.0 years in former smokers.

Emphysema was significantly more comment in heavy smokers, compared with never smokers and mild to moderate smokers (P < .001 for both).

“We observed a gradual decrease in survival starting from never to mild-moderate and subsequent heavy smokers supporting our finding that [pack-years] is an independent predictor for mortality in PF-ILD,” the researchers wrote. “This is an important message that clinicians could convey to their ILD patients, but also to patients at-risk for ILD.”

The study findings were limited by several factors, mainly the retrospective design, incomplete data for some patients, and lack of data on comorbidities, the researchers noted. However, the results strengthen the evidence for the detrimental effect of heavy smoking in PF-ILD, they said. Consequently, “efforts to reduce pack-years in those with, and at risk for, PF-ILD may translate into a survival benefit and should have high priority in clinical practice.”

The study was supported by grants from ZonMw TopZorg Care and TZO. The researchers had no financial conflicts to disclose.

Heavier smoking significantly increased mortality in adults with progressive fibrosing interstitial lung disease (PF-ILD), based on data from 377 individuals.

The negative impact of smoking on pulmonary diseases is well documented, but the specific impact on patients with PF-ILD has not been well studied, Mark Platenburg, MD, of St. Antonious Hospital, Nieuwegein, the Netherlands, and colleagues wrote in Respiratory Medicine .

GaryPhoto/ThinkStock

“Patients with PF-ILD or IPF [idiopathic pulmonary fibrosis] are prone to early mortality, indicating a need for prognostic [bio]marker studies for precision medicine,” they said.

The researchers identified adults older than 18 years with PF-ILD who were diagnosed at a single center. All study participants had at least 10% fibrosis, and showed either a decline of at least 10% in forced vital capacity, a 5.0%-9.9% relative FVC decline plus progressive respiratory symptoms and/or an increase in extent of fibrosis on subsequent high-resolution (HRCT progression), or progressive respiratory symptoms and HRCT progression over 24 months after ILD diagnosis.

Pack-years of smoking was a prognostic variable; the researchers also compared median transplant-free survival in heavy smokers and mild to moderate smokers. They also investigated the association between smoking quantity and emphysema in the study population.

Overall, the increased risk for mortality was 11%, 22%, and 44% in patients with 10, 20, and 40 pack-years of smoking, respectively.

Both the unadjusted and adjusted hazard ratio for pack-years were significant (1.014, P < .001 and 1.011, P = .022, respectively).

The median transplant-free survival of ever-smokers versus never-smokers with PF-ILD was 3.3 years versus 4.8 years; median transplant-free survival was 3.0 years for heavy smokers and 3.8 years for mild to moderate smokers. Similarly, median survival was 4.2 years in never-smokers versus 3.0 years in former smokers.

Emphysema was significantly more comment in heavy smokers, compared with never smokers and mild to moderate smokers (P < .001 for both).

“We observed a gradual decrease in survival starting from never to mild-moderate and subsequent heavy smokers supporting our finding that [pack-years] is an independent predictor for mortality in PF-ILD,” the researchers wrote. “This is an important message that clinicians could convey to their ILD patients, but also to patients at-risk for ILD.”

The study findings were limited by several factors, mainly the retrospective design, incomplete data for some patients, and lack of data on comorbidities, the researchers noted. However, the results strengthen the evidence for the detrimental effect of heavy smoking in PF-ILD, they said. Consequently, “efforts to reduce pack-years in those with, and at risk for, PF-ILD may translate into a survival benefit and should have high priority in clinical practice.”

The study was supported by grants from ZonMw TopZorg Care and TZO. The researchers had no financial conflicts to disclose.

Heavier smoking significantly increased mortality in adults with progressive fibrosing interstitial lung disease (PF-ILD), based on data from 377 individuals.

The negative impact of smoking on pulmonary diseases is well documented, but the specific impact on patients with PF-ILD has not been well studied, Mark Platenburg, MD, of St. Antonious Hospital, Nieuwegein, the Netherlands, and colleagues wrote in Respiratory Medicine .

GaryPhoto/ThinkStock

“Patients with PF-ILD or IPF [idiopathic pulmonary fibrosis] are prone to early mortality, indicating a need for prognostic [bio]marker studies for precision medicine,” they said.

The researchers identified adults older than 18 years with PF-ILD who were diagnosed at a single center. All study participants had at least 10% fibrosis, and showed either a decline of at least 10% in forced vital capacity, a 5.0%-9.9% relative FVC decline plus progressive respiratory symptoms and/or an increase in extent of fibrosis on subsequent high-resolution (HRCT progression), or progressive respiratory symptoms and HRCT progression over 24 months after ILD diagnosis.

Pack-years of smoking was a prognostic variable; the researchers also compared median transplant-free survival in heavy smokers and mild to moderate smokers. They also investigated the association between smoking quantity and emphysema in the study population.

Overall, the increased risk for mortality was 11%, 22%, and 44% in patients with 10, 20, and 40 pack-years of smoking, respectively.

Both the unadjusted and adjusted hazard ratio for pack-years were significant (1.014, P < .001 and 1.011, P = .022, respectively).

The median transplant-free survival of ever-smokers versus never-smokers with PF-ILD was 3.3 years versus 4.8 years; median transplant-free survival was 3.0 years for heavy smokers and 3.8 years for mild to moderate smokers. Similarly, median survival was 4.2 years in never-smokers versus 3.0 years in former smokers.

Emphysema was significantly more comment in heavy smokers, compared with never smokers and mild to moderate smokers (P < .001 for both).

“We observed a gradual decrease in survival starting from never to mild-moderate and subsequent heavy smokers supporting our finding that [pack-years] is an independent predictor for mortality in PF-ILD,” the researchers wrote. “This is an important message that clinicians could convey to their ILD patients, but also to patients at-risk for ILD.”

The study findings were limited by several factors, mainly the retrospective design, incomplete data for some patients, and lack of data on comorbidities, the researchers noted. However, the results strengthen the evidence for the detrimental effect of heavy smoking in PF-ILD, they said. Consequently, “efforts to reduce pack-years in those with, and at risk for, PF-ILD may translate into a survival benefit and should have high priority in clinical practice.”

The study was supported by grants from ZonMw TopZorg Care and TZO. The researchers had no financial conflicts to disclose.

Younger and older patients with severe chronic obstructive pulmonary disease have similar pulmonary and physical health limitations, based on data from 1,058 adults.

Although chronic obstructive pulmonary disease (COPD) generally appears in older patients, the prevalence among adults aged 45-55 years was 6.5% in 2014-2015, wrote Rosanne J.H.C.G. Beijers, PhD, of Maastricht (the Netherlands) University Medical Center, and colleagues. However, data on the early-onset COPD phenotype are limited. In particular, the extent to which younger patients with early-onset severe COPD experienced the same physical and mental health problems as older patients with similar degree of airflow limitation has not been examined, they said.

In a study published in Clinical Nutrition, the researchers analyzed data from adults with COPD who were referred for pulmonary rehabilitation at a single center between July 2013 and August 2018. Severe disease was defined as FEV1< 50%, and early onset was defined as younger than 55 years. The mean age difference between older and younger patient groups was 15.8 years.

The study population included 79 individuals with early-onset severe disease, 54 with early-onset mild to moderate disease, 158 older adults with severe disease, and 103 older adults with mild to moderate disease. The researchers compared disease markers including body composition, physical performance, and mental health between the groups. A significantly greater proportion of the early-onset group were women, compared to the older group (64% vs. 44%).

In comparing early-onset and older patients with severe COPD, the researchers found that clinical characteristics were similar for body composition, skeletal muscle index, fat percentage, and bone mineral content, and for physical performance factors including the percent predicted maximal work capacity (Wmax), 6-minute walk test, and isokinetic strength. However, a higher prevalence of depression appeared in the early-onset severe-disease patients, compared with the older severe-disease patients (51.9% vs. 32.7%; P = .029).

Although the prevalence of depression was not based on a clinical diagnosis, this finding should prompt health care professionals to pay more attention to psychosocial and emotional well-being in early-onset severe COPD patients, the researchers noted.

In comparing early-onset severe-disease patients and early-onset patients with mild to moderate disease, patients with early-onset severe COPD had significantly lower exercise performance, based on a 6-minute walk test and percent predicted Wmax. However, body composition and isokinetic muscle strength were not significantly different between both early-onset groups.

The findings were limited by several factors including the relatively small number of early-onset patients and the lack of data on whether older patients were diagnosed with severe COPD at a younger age, and more research using age and lung function at the time of diagnosis is needed, the researchers noted. However, the results highlight the importance of early identification of patients at risk for early-onset severe COPD, they said. “Within these individuals at risk, special attention should also be paid to the development of extrapulmonary disease manifestations such as exercise limitations, impaired body composition, and psychological and emotional problems,” the researchers said. “Subsequently, intervention strategies need to be applied that not only focus on the regular advice of quitting smoking but also include decreasing the exposure to air pollutants and promoting a healthy lifestyle including physical activity and a healthy diet,” they added.

The study received no outside funding. Lead author Dr. Beijers had no financial conflicts to disclose.

Younger and older patients with severe chronic obstructive pulmonary disease have similar pulmonary and physical health limitations, based on data from 1,058 adults.

Although chronic obstructive pulmonary disease (COPD) generally appears in older patients, the prevalence among adults aged 45-55 years was 6.5% in 2014-2015, wrote Rosanne J.H.C.G. Beijers, PhD, of Maastricht (the Netherlands) University Medical Center, and colleagues. However, data on the early-onset COPD phenotype are limited. In particular, the extent to which younger patients with early-onset severe COPD experienced the same physical and mental health problems as older patients with similar degree of airflow limitation has not been examined, they said.

In a study published in Clinical Nutrition, the researchers analyzed data from adults with COPD who were referred for pulmonary rehabilitation at a single center between July 2013 and August 2018. Severe disease was defined as FEV1< 50%, and early onset was defined as younger than 55 years. The mean age difference between older and younger patient groups was 15.8 years.

The study population included 79 individuals with early-onset severe disease, 54 with early-onset mild to moderate disease, 158 older adults with severe disease, and 103 older adults with mild to moderate disease. The researchers compared disease markers including body composition, physical performance, and mental health between the groups. A significantly greater proportion of the early-onset group were women, compared to the older group (64% vs. 44%).

In comparing early-onset and older patients with severe COPD, the researchers found that clinical characteristics were similar for body composition, skeletal muscle index, fat percentage, and bone mineral content, and for physical performance factors including the percent predicted maximal work capacity (Wmax), 6-minute walk test, and isokinetic strength. However, a higher prevalence of depression appeared in the early-onset severe-disease patients, compared with the older severe-disease patients (51.9% vs. 32.7%; P = .029).

Although the prevalence of depression was not based on a clinical diagnosis, this finding should prompt health care professionals to pay more attention to psychosocial and emotional well-being in early-onset severe COPD patients, the researchers noted.

In comparing early-onset severe-disease patients and early-onset patients with mild to moderate disease, patients with early-onset severe COPD had significantly lower exercise performance, based on a 6-minute walk test and percent predicted Wmax. However, body composition and isokinetic muscle strength were not significantly different between both early-onset groups.

The findings were limited by several factors including the relatively small number of early-onset patients and the lack of data on whether older patients were diagnosed with severe COPD at a younger age, and more research using age and lung function at the time of diagnosis is needed, the researchers noted. However, the results highlight the importance of early identification of patients at risk for early-onset severe COPD, they said. “Within these individuals at risk, special attention should also be paid to the development of extrapulmonary disease manifestations such as exercise limitations, impaired body composition, and psychological and emotional problems,” the researchers said. “Subsequently, intervention strategies need to be applied that not only focus on the regular advice of quitting smoking but also include decreasing the exposure to air pollutants and promoting a healthy lifestyle including physical activity and a healthy diet,” they added.

The study received no outside funding. Lead author Dr. Beijers had no financial conflicts to disclose.

Younger and older patients with severe chronic obstructive pulmonary disease have similar pulmonary and physical health limitations, based on data from 1,058 adults.

Although chronic obstructive pulmonary disease (COPD) generally appears in older patients, the prevalence among adults aged 45-55 years was 6.5% in 2014-2015, wrote Rosanne J.H.C.G. Beijers, PhD, of Maastricht (the Netherlands) University Medical Center, and colleagues. However, data on the early-onset COPD phenotype are limited. In particular, the extent to which younger patients with early-onset severe COPD experienced the same physical and mental health problems as older patients with similar degree of airflow limitation has not been examined, they said.

In a study published in Clinical Nutrition, the researchers analyzed data from adults with COPD who were referred for pulmonary rehabilitation at a single center between July 2013 and August 2018. Severe disease was defined as FEV1< 50%, and early onset was defined as younger than 55 years. The mean age difference between older and younger patient groups was 15.8 years.

The study population included 79 individuals with early-onset severe disease, 54 with early-onset mild to moderate disease, 158 older adults with severe disease, and 103 older adults with mild to moderate disease. The researchers compared disease markers including body composition, physical performance, and mental health between the groups. A significantly greater proportion of the early-onset group were women, compared to the older group (64% vs. 44%).

In comparing early-onset and older patients with severe COPD, the researchers found that clinical characteristics were similar for body composition, skeletal muscle index, fat percentage, and bone mineral content, and for physical performance factors including the percent predicted maximal work capacity (Wmax), 6-minute walk test, and isokinetic strength. However, a higher prevalence of depression appeared in the early-onset severe-disease patients, compared with the older severe-disease patients (51.9% vs. 32.7%; P = .029).

Although the prevalence of depression was not based on a clinical diagnosis, this finding should prompt health care professionals to pay more attention to psychosocial and emotional well-being in early-onset severe COPD patients, the researchers noted.

In comparing early-onset severe-disease patients and early-onset patients with mild to moderate disease, patients with early-onset severe COPD had significantly lower exercise performance, based on a 6-minute walk test and percent predicted Wmax. However, body composition and isokinetic muscle strength were not significantly different between both early-onset groups.

The findings were limited by several factors including the relatively small number of early-onset patients and the lack of data on whether older patients were diagnosed with severe COPD at a younger age, and more research using age and lung function at the time of diagnosis is needed, the researchers noted. However, the results highlight the importance of early identification of patients at risk for early-onset severe COPD, they said. “Within these individuals at risk, special attention should also be paid to the development of extrapulmonary disease manifestations such as exercise limitations, impaired body composition, and psychological and emotional problems,” the researchers said. “Subsequently, intervention strategies need to be applied that not only focus on the regular advice of quitting smoking but also include decreasing the exposure to air pollutants and promoting a healthy lifestyle including physical activity and a healthy diet,” they added.

The study received no outside funding. Lead author Dr. Beijers had no financial conflicts to disclose.