COPD

In patients with chronic obstructive pulmonary disease (COPD), comorbid chronic cough is associated with more respiratory symptoms and health care utilization, decreased lung function, and increased inflammatory markers in blood, according to research published in CHEST.

The results indicate “that chronic cough in individuals with COPD is associated with a more severe disease phenotype, which could be helpful for stratifying management of COPD in the future,” wrote Eskild Landt, PhD, a research assistant at Zealand University Hospital in Køge, Denmark, and colleagues.

A study by published in the Journal of Allergy and Clinical Immunology: In Practice (2019;7[6]:1783-92.e8) indicated that in patients with asthma, chronic cough was associated with worse respiratory symptoms, more health care utilization, decreased lung function, and increased inflammatory markers in blood. Dr. Landt and colleagues hypothesized that patients with COPD and chronic cough had a similar pattern of disease severity.

To test their hypothesis, they identified individuals with COPD and chronic cough among 43,271 participants in the Copenhagen General Population Study, a population-based cohort study. The researchers defined COPD as a ratio of forced expiratory volume in 1 second (FEV₁) to forced vital capacity (FVC) of less than 0.70 in individuals without asthma. Consecutive individuals answered questions about chronic cough, which was defined as a cough lasting more than 8 weeks, and responded to the Leicester Cough Questionnaire. They also underwent a physical health examination, including prebronchodilatory spirometry, and gave blood for biochemical analyses. The blood was analyzed for high-sensitive C-reactive protein, fibrinogen, leukocytes, eosinophils, neutrophils, and immunoglobulin E (i.e., inflammatory biomarkers).

Dr. Landt and colleagues identified 8,181 patients (19% of the population) with COPD, 796 (10%) of whom had chronic cough. Of the 33,364 participants without COPD, 1,585 (5%) had chronic cough. For patients with COPD and chronic cough, median total Leicester Cough Questionnaire score was 17.7, corresponding to 5.9 for the physical domain, 5.6 for the psychological domain, and 6.3 for the social domain.

Among participants with COPD, those with chronic cough had higher rates of sputum production (60% versus 8%), wheezing (46% versus 14%), dyspnea (66% versus 38%), chest pain or tightness (9% versus 4%), nighttime dyspnea (8% versus 3%), episodes of acute bronchitis or pneumonias in the past 10 years (45% versus 25%), and general practitioner visits in the past 12 months (53% versus 37%). In addition, these participants had lower FEV₁% of predicted (81% versus 89%), lower ratio of FEV₁ to FVC (0.64 versus 0.66), and higher levels of high-sensitive C-reactive protein, fibrinogen, leukocytes, neutrophils, eosinophils, and immunoglobulin E in blood.

“To our knowledge, this is the first study reporting Leicester Cough Questionnaire score for randomly selected individuals with COPD from a general population setting,” wrote Dr. Landt and colleagues. The study’s strengths include its randomly chosen population-based sample and investigator blinding to disease status and clinical outcome, they added. Some patients with the most severe types of COPD and chronic cough may not have attended the physical examination and participated in the study, however, and this factor could have biased the results. Furthermore, nearly the entire sample was white, so the results may not be generalizable to other ethnicities. “That said, we are not aware of results to suggest that our findings should not be relevant to individuals of all races,” wrote the investigators.

The study was funded by the private Lundbeck Foundation, as well as by the Danish Lung Association and the Danish Cancer Society. Several authors reported receiving grants and fees from AstraZeneca, GlaxoSmithKline, and Novartis that were unrelated to the study.

[email protected]

SOURCE: Landt E et al. CHEST. 2020 Jan 24. doi: 10.1016/j.chest.2019.12.038.

In patients with chronic obstructive pulmonary disease (COPD), comorbid chronic cough is associated with more respiratory symptoms and health care utilization, decreased lung function, and increased inflammatory markers in blood, according to research published in CHEST.

The results indicate “that chronic cough in individuals with COPD is associated with a more severe disease phenotype, which could be helpful for stratifying management of COPD in the future,” wrote Eskild Landt, PhD, a research assistant at Zealand University Hospital in Køge, Denmark, and colleagues.

A study by published in the Journal of Allergy and Clinical Immunology: In Practice (2019;7[6]:1783-92.e8) indicated that in patients with asthma, chronic cough was associated with worse respiratory symptoms, more health care utilization, decreased lung function, and increased inflammatory markers in blood. Dr. Landt and colleagues hypothesized that patients with COPD and chronic cough had a similar pattern of disease severity.

To test their hypothesis, they identified individuals with COPD and chronic cough among 43,271 participants in the Copenhagen General Population Study, a population-based cohort study. The researchers defined COPD as a ratio of forced expiratory volume in 1 second (FEV₁) to forced vital capacity (FVC) of less than 0.70 in individuals without asthma. Consecutive individuals answered questions about chronic cough, which was defined as a cough lasting more than 8 weeks, and responded to the Leicester Cough Questionnaire. They also underwent a physical health examination, including prebronchodilatory spirometry, and gave blood for biochemical analyses. The blood was analyzed for high-sensitive C-reactive protein, fibrinogen, leukocytes, eosinophils, neutrophils, and immunoglobulin E (i.e., inflammatory biomarkers).

Dr. Landt and colleagues identified 8,181 patients (19% of the population) with COPD, 796 (10%) of whom had chronic cough. Of the 33,364 participants without COPD, 1,585 (5%) had chronic cough. For patients with COPD and chronic cough, median total Leicester Cough Questionnaire score was 17.7, corresponding to 5.9 for the physical domain, 5.6 for the psychological domain, and 6.3 for the social domain.

Among participants with COPD, those with chronic cough had higher rates of sputum production (60% versus 8%), wheezing (46% versus 14%), dyspnea (66% versus 38%), chest pain or tightness (9% versus 4%), nighttime dyspnea (8% versus 3%), episodes of acute bronchitis or pneumonias in the past 10 years (45% versus 25%), and general practitioner visits in the past 12 months (53% versus 37%). In addition, these participants had lower FEV₁% of predicted (81% versus 89%), lower ratio of FEV₁ to FVC (0.64 versus 0.66), and higher levels of high-sensitive C-reactive protein, fibrinogen, leukocytes, neutrophils, eosinophils, and immunoglobulin E in blood.

“To our knowledge, this is the first study reporting Leicester Cough Questionnaire score for randomly selected individuals with COPD from a general population setting,” wrote Dr. Landt and colleagues. The study’s strengths include its randomly chosen population-based sample and investigator blinding to disease status and clinical outcome, they added. Some patients with the most severe types of COPD and chronic cough may not have attended the physical examination and participated in the study, however, and this factor could have biased the results. Furthermore, nearly the entire sample was white, so the results may not be generalizable to other ethnicities. “That said, we are not aware of results to suggest that our findings should not be relevant to individuals of all races,” wrote the investigators.

The study was funded by the private Lundbeck Foundation, as well as by the Danish Lung Association and the Danish Cancer Society. Several authors reported receiving grants and fees from AstraZeneca, GlaxoSmithKline, and Novartis that were unrelated to the study.

[email protected]

SOURCE: Landt E et al. CHEST. 2020 Jan 24. doi: 10.1016/j.chest.2019.12.038.

In patients with chronic obstructive pulmonary disease (COPD), comorbid chronic cough is associated with more respiratory symptoms and health care utilization, decreased lung function, and increased inflammatory markers in blood, according to research published in CHEST.

The results indicate “that chronic cough in individuals with COPD is associated with a more severe disease phenotype, which could be helpful for stratifying management of COPD in the future,” wrote Eskild Landt, PhD, a research assistant at Zealand University Hospital in Køge, Denmark, and colleagues.

A study by published in the Journal of Allergy and Clinical Immunology: In Practice (2019;7[6]:1783-92.e8) indicated that in patients with asthma, chronic cough was associated with worse respiratory symptoms, more health care utilization, decreased lung function, and increased inflammatory markers in blood. Dr. Landt and colleagues hypothesized that patients with COPD and chronic cough had a similar pattern of disease severity.

To test their hypothesis, they identified individuals with COPD and chronic cough among 43,271 participants in the Copenhagen General Population Study, a population-based cohort study. The researchers defined COPD as a ratio of forced expiratory volume in 1 second (FEV₁) to forced vital capacity (FVC) of less than 0.70 in individuals without asthma. Consecutive individuals answered questions about chronic cough, which was defined as a cough lasting more than 8 weeks, and responded to the Leicester Cough Questionnaire. They also underwent a physical health examination, including prebronchodilatory spirometry, and gave blood for biochemical analyses. The blood was analyzed for high-sensitive C-reactive protein, fibrinogen, leukocytes, eosinophils, neutrophils, and immunoglobulin E (i.e., inflammatory biomarkers).

Dr. Landt and colleagues identified 8,181 patients (19% of the population) with COPD, 796 (10%) of whom had chronic cough. Of the 33,364 participants without COPD, 1,585 (5%) had chronic cough. For patients with COPD and chronic cough, median total Leicester Cough Questionnaire score was 17.7, corresponding to 5.9 for the physical domain, 5.6 for the psychological domain, and 6.3 for the social domain.

Among participants with COPD, those with chronic cough had higher rates of sputum production (60% versus 8%), wheezing (46% versus 14%), dyspnea (66% versus 38%), chest pain or tightness (9% versus 4%), nighttime dyspnea (8% versus 3%), episodes of acute bronchitis or pneumonias in the past 10 years (45% versus 25%), and general practitioner visits in the past 12 months (53% versus 37%). In addition, these participants had lower FEV₁% of predicted (81% versus 89%), lower ratio of FEV₁ to FVC (0.64 versus 0.66), and higher levels of high-sensitive C-reactive protein, fibrinogen, leukocytes, neutrophils, eosinophils, and immunoglobulin E in blood.

“To our knowledge, this is the first study reporting Leicester Cough Questionnaire score for randomly selected individuals with COPD from a general population setting,” wrote Dr. Landt and colleagues. The study’s strengths include its randomly chosen population-based sample and investigator blinding to disease status and clinical outcome, they added. Some patients with the most severe types of COPD and chronic cough may not have attended the physical examination and participated in the study, however, and this factor could have biased the results. Furthermore, nearly the entire sample was white, so the results may not be generalizable to other ethnicities. “That said, we are not aware of results to suggest that our findings should not be relevant to individuals of all races,” wrote the investigators.

The study was funded by the private Lundbeck Foundation, as well as by the Danish Lung Association and the Danish Cancer Society. Several authors reported receiving grants and fees from AstraZeneca, GlaxoSmithKline, and Novartis that were unrelated to the study.

[email protected]

SOURCE: Landt E et al. CHEST. 2020 Jan 24. doi: 10.1016/j.chest.2019.12.038.

A study using a new definition of early chronic obstructive pulmonary disease (COPD) has found that about 15% of Danish smokers under the age of 50 years meet the criteria.

The population-based cohort looked at individuals who had been exposed to at least 10 pack-years, and defined early COPD as the ratio of forced expiratory volume to forced vital capacity being less than the lower limit of normal (FEV₁/FVC less than LLN). The definition of early COPD, published in 2018 (Am J Resp and Crit Care Med. 2018;197:1540-51), also included the presence of abnormalities on a CT scan or a decline in FEV₁ (greater than 60 mL/year) that is accelerated relative to FVC, but the new population study did not include the latter two criteria.

The researchers, under corresponding author Peter Lange, MD, of the University of Copenhagen found that those with early COPD were more likely to have chronic respiratory symptoms, severe impairment of lung function, acute respirator hospitalization, and early mortality at baseline and at follow-up. The work was published in the American Journal of Respiratory and Critical Care Medicine.

“To dig through the smokers and try to figure out which smokers are more at risk than other smokers is probably the best way to summarize what they’ve done here,” said Robert Reed, MD, from the University of Maryland, Baltimore, in an interview. However, he added that he would like to see the research extended to an even younger population, as well as nonsmokers. “We don’t need all of this information to tell us that smoking is bad. I think nonsmokers would be really interesting – creating a definition of COPD that excludes patients that meet the usual definition for COPD would be of potential interest,” added Dr. Reed, who was not involved in the study.

Using a cohort of 105,630 randomly selected individuals from Danish nationwide health registries, the study identified 8,064 individuals aged under 50 years with 10 or more pack-years of tobacco exposure. In this group, 1,175 (15%) had early COPD, of whom 58% were current smokers. The cohort of smokers was followed for up to 14.4 years. Multivariate analyses found that those with early COPD, compared with smokers without COPD, were at substantially greater risk of acute obstructive lung disease hospitalization (hazard ratio, 6.42; 95% confidence interval, 3.39-12.2), acute pneumonia hospitalization (HR, 2.03; 95% CI, 1.43-2.88), and all-cause mortality (HR, 1.79; 95% CI, 1.28-2.52).

There is value in gaining a better understanding of which smokers are at greatest risk of COPD down the line, but data on younger people, even 30-year-olds, could guide therapeutic decisions when and if new drugs that can alter the state of the disease become available. Focusing more on younger, high-risk patients could also be used to create greater incentives to quit smoking, though Dr. Reed has mixed feelings even about that. “What if we identified 15% of smokers that are at risk of COPD, and the other 85% say, ‘I’ll keep smoking,’ and they fall over dead from a heart attack?” said Dr. Reed, noting that smoking has a wide range of known risks. “They should all stop,” he added.

The study also captures a wide range of patients, from some with early disease that will likely progress to COPD later in life along with some who already developed full-blown COPD in, for example, their early 40s. “Those are very different patients and to lump them together is potentially problematic,” said Dr. Reed. More granulated data could potentially inform more personalized medicine, and the discovery and verification of genetic risk factors.

Nevertheless, Dr. Reed expects the data to move the field forward. “They created a nice, rich database that I think will generate a lot more analysis and discussion.”

The study was funded by the Lundbeck Foundation. One of the authors has received support from the National Institute for Health Research Manchester (England) Biomedical Research Centre. Dr. Reed has no relevant financial disclosures.

SOURCE: Colak Y et al. Am J Resp Crit Care Med. 2019 Nov 26. doi: 10.1164/rccm.201908-1644OC

A study using a new definition of early chronic obstructive pulmonary disease (COPD) has found that about 15% of Danish smokers under the age of 50 years meet the criteria.

The population-based cohort looked at individuals who had been exposed to at least 10 pack-years, and defined early COPD as the ratio of forced expiratory volume to forced vital capacity being less than the lower limit of normal (FEV₁/FVC less than LLN). The definition of early COPD, published in 2018 (Am J Resp and Crit Care Med. 2018;197:1540-51), also included the presence of abnormalities on a CT scan or a decline in FEV₁ (greater than 60 mL/year) that is accelerated relative to FVC, but the new population study did not include the latter two criteria.

The researchers, under corresponding author Peter Lange, MD, of the University of Copenhagen found that those with early COPD were more likely to have chronic respiratory symptoms, severe impairment of lung function, acute respirator hospitalization, and early mortality at baseline and at follow-up. The work was published in the American Journal of Respiratory and Critical Care Medicine.

“To dig through the smokers and try to figure out which smokers are more at risk than other smokers is probably the best way to summarize what they’ve done here,” said Robert Reed, MD, from the University of Maryland, Baltimore, in an interview. However, he added that he would like to see the research extended to an even younger population, as well as nonsmokers. “We don’t need all of this information to tell us that smoking is bad. I think nonsmokers would be really interesting – creating a definition of COPD that excludes patients that meet the usual definition for COPD would be of potential interest,” added Dr. Reed, who was not involved in the study.

Using a cohort of 105,630 randomly selected individuals from Danish nationwide health registries, the study identified 8,064 individuals aged under 50 years with 10 or more pack-years of tobacco exposure. In this group, 1,175 (15%) had early COPD, of whom 58% were current smokers. The cohort of smokers was followed for up to 14.4 years. Multivariate analyses found that those with early COPD, compared with smokers without COPD, were at substantially greater risk of acute obstructive lung disease hospitalization (hazard ratio, 6.42; 95% confidence interval, 3.39-12.2), acute pneumonia hospitalization (HR, 2.03; 95% CI, 1.43-2.88), and all-cause mortality (HR, 1.79; 95% CI, 1.28-2.52).

There is value in gaining a better understanding of which smokers are at greatest risk of COPD down the line, but data on younger people, even 30-year-olds, could guide therapeutic decisions when and if new drugs that can alter the state of the disease become available. Focusing more on younger, high-risk patients could also be used to create greater incentives to quit smoking, though Dr. Reed has mixed feelings even about that. “What if we identified 15% of smokers that are at risk of COPD, and the other 85% say, ‘I’ll keep smoking,’ and they fall over dead from a heart attack?” said Dr. Reed, noting that smoking has a wide range of known risks. “They should all stop,” he added.

The study also captures a wide range of patients, from some with early disease that will likely progress to COPD later in life along with some who already developed full-blown COPD in, for example, their early 40s. “Those are very different patients and to lump them together is potentially problematic,” said Dr. Reed. More granulated data could potentially inform more personalized medicine, and the discovery and verification of genetic risk factors.

Nevertheless, Dr. Reed expects the data to move the field forward. “They created a nice, rich database that I think will generate a lot more analysis and discussion.”

The study was funded by the Lundbeck Foundation. One of the authors has received support from the National Institute for Health Research Manchester (England) Biomedical Research Centre. Dr. Reed has no relevant financial disclosures.

SOURCE: Colak Y et al. Am J Resp Crit Care Med. 2019 Nov 26. doi: 10.1164/rccm.201908-1644OC

A study using a new definition of early chronic obstructive pulmonary disease (COPD) has found that about 15% of Danish smokers under the age of 50 years meet the criteria.

The population-based cohort looked at individuals who had been exposed to at least 10 pack-years, and defined early COPD as the ratio of forced expiratory volume to forced vital capacity being less than the lower limit of normal (FEV₁/FVC less than LLN). The definition of early COPD, published in 2018 (Am J Resp and Crit Care Med. 2018;197:1540-51), also included the presence of abnormalities on a CT scan or a decline in FEV₁ (greater than 60 mL/year) that is accelerated relative to FVC, but the new population study did not include the latter two criteria.

The researchers, under corresponding author Peter Lange, MD, of the University of Copenhagen found that those with early COPD were more likely to have chronic respiratory symptoms, severe impairment of lung function, acute respirator hospitalization, and early mortality at baseline and at follow-up. The work was published in the American Journal of Respiratory and Critical Care Medicine.

“To dig through the smokers and try to figure out which smokers are more at risk than other smokers is probably the best way to summarize what they’ve done here,” said Robert Reed, MD, from the University of Maryland, Baltimore, in an interview. However, he added that he would like to see the research extended to an even younger population, as well as nonsmokers. “We don’t need all of this information to tell us that smoking is bad. I think nonsmokers would be really interesting – creating a definition of COPD that excludes patients that meet the usual definition for COPD would be of potential interest,” added Dr. Reed, who was not involved in the study.

Using a cohort of 105,630 randomly selected individuals from Danish nationwide health registries, the study identified 8,064 individuals aged under 50 years with 10 or more pack-years of tobacco exposure. In this group, 1,175 (15%) had early COPD, of whom 58% were current smokers. The cohort of smokers was followed for up to 14.4 years. Multivariate analyses found that those with early COPD, compared with smokers without COPD, were at substantially greater risk of acute obstructive lung disease hospitalization (hazard ratio, 6.42; 95% confidence interval, 3.39-12.2), acute pneumonia hospitalization (HR, 2.03; 95% CI, 1.43-2.88), and all-cause mortality (HR, 1.79; 95% CI, 1.28-2.52).

There is value in gaining a better understanding of which smokers are at greatest risk of COPD down the line, but data on younger people, even 30-year-olds, could guide therapeutic decisions when and if new drugs that can alter the state of the disease become available. Focusing more on younger, high-risk patients could also be used to create greater incentives to quit smoking, though Dr. Reed has mixed feelings even about that. “What if we identified 15% of smokers that are at risk of COPD, and the other 85% say, ‘I’ll keep smoking,’ and they fall over dead from a heart attack?” said Dr. Reed, noting that smoking has a wide range of known risks. “They should all stop,” he added.

The study also captures a wide range of patients, from some with early disease that will likely progress to COPD later in life along with some who already developed full-blown COPD in, for example, their early 40s. “Those are very different patients and to lump them together is potentially problematic,” said Dr. Reed. More granulated data could potentially inform more personalized medicine, and the discovery and verification of genetic risk factors.

Nevertheless, Dr. Reed expects the data to move the field forward. “They created a nice, rich database that I think will generate a lot more analysis and discussion.”

The study was funded by the Lundbeck Foundation. One of the authors has received support from the National Institute for Health Research Manchester (England) Biomedical Research Centre. Dr. Reed has no relevant financial disclosures.

SOURCE: Colak Y et al. Am J Resp Crit Care Med. 2019 Nov 26. doi: 10.1164/rccm.201908-1644OC

A study has found that consistent occupational exposure to disinfectants is associated with an increased risk of chronic obstructive pulmonary disease (COPD).

“Clinicians should be aware of this new risk factor and systematically look for sources of exposure to cleaning products and disinfectants in addition to other occupational exposures in patients with COPD,” wrote Orianne Dumas, PhD, of the Université de Versailles St-Quentin-en-Yvelines (France) and coauthors. The study was published in JAMA Network Open.

To determine if regular use of disinfectants had a negative impact on respiratory health, the researchers analyzed data from 73,262 active female nurses who had no history of COPD and completed questionnaires every 2 years for the Nurses’ Health Study II. Their mean age at baseline was 54.7. Exposure to commonly used disinfectants was evaluated by a job-task-exposure matrix (JTEM) specific to nurses.

Between 2009 and 2015, 582 nurses reported incident physician-diagnosed COPD. Weekly use of disinfectants was associated with COPD incidence (adjusted hazard ratio 1.35; 95% confidence interval, 1.14-1.59). Additional associations were found in nurses who used disinfectants to clean surfaces (AHR, 1.38; 95% CI, 1.13-1.68) and to clean medical instruments (AHR, 1.31; 95% CI, 1.07-1.61). High-level exposure to certain disinfectants – including glutaraldehyde, bleach, hydrogen peroxide, alcohol, and quaternary ammonium compounds – were significantly associated with increased risk of COPD incidence.

The authors acknowledged their study’s limitations, including the JTEM only assessing exposure to seven of the major cleaning products commonly used in health care. In addition, detailed data on exposure to disinfectants was not available before 2009. However, they added that, because the study has been ongoing since 1989, it could be expected that women who had been nurses for decades had “already accumulated a long history of exposure.”

The study was supported in part by grants from the Centers for Disease Control and Prevention and the National Institutes of Health. Five of the authors reported receiving grants from the CDC’s National Institute for Occupational Safety and Health (NIOSH); one additional author reported being a consultant on a NIOSH grant and receiving personal fees from a health care system. No other conflicts of interest were reported.

SOURCE: Dumas O et al. JAMA Netw Open. 2019 Oct 18. doi: 10.1001/jamanetworkopen.2019.13563.

A study has found that consistent occupational exposure to disinfectants is associated with an increased risk of chronic obstructive pulmonary disease (COPD).

“Clinicians should be aware of this new risk factor and systematically look for sources of exposure to cleaning products and disinfectants in addition to other occupational exposures in patients with COPD,” wrote Orianne Dumas, PhD, of the Université de Versailles St-Quentin-en-Yvelines (France) and coauthors. The study was published in JAMA Network Open.

To determine if regular use of disinfectants had a negative impact on respiratory health, the researchers analyzed data from 73,262 active female nurses who had no history of COPD and completed questionnaires every 2 years for the Nurses’ Health Study II. Their mean age at baseline was 54.7. Exposure to commonly used disinfectants was evaluated by a job-task-exposure matrix (JTEM) specific to nurses.

Between 2009 and 2015, 582 nurses reported incident physician-diagnosed COPD. Weekly use of disinfectants was associated with COPD incidence (adjusted hazard ratio 1.35; 95% confidence interval, 1.14-1.59). Additional associations were found in nurses who used disinfectants to clean surfaces (AHR, 1.38; 95% CI, 1.13-1.68) and to clean medical instruments (AHR, 1.31; 95% CI, 1.07-1.61). High-level exposure to certain disinfectants – including glutaraldehyde, bleach, hydrogen peroxide, alcohol, and quaternary ammonium compounds – were significantly associated with increased risk of COPD incidence.

The authors acknowledged their study’s limitations, including the JTEM only assessing exposure to seven of the major cleaning products commonly used in health care. In addition, detailed data on exposure to disinfectants was not available before 2009. However, they added that, because the study has been ongoing since 1989, it could be expected that women who had been nurses for decades had “already accumulated a long history of exposure.”

The study was supported in part by grants from the Centers for Disease Control and Prevention and the National Institutes of Health. Five of the authors reported receiving grants from the CDC’s National Institute for Occupational Safety and Health (NIOSH); one additional author reported being a consultant on a NIOSH grant and receiving personal fees from a health care system. No other conflicts of interest were reported.

SOURCE: Dumas O et al. JAMA Netw Open. 2019 Oct 18. doi: 10.1001/jamanetworkopen.2019.13563.

A study has found that consistent occupational exposure to disinfectants is associated with an increased risk of chronic obstructive pulmonary disease (COPD).

“Clinicians should be aware of this new risk factor and systematically look for sources of exposure to cleaning products and disinfectants in addition to other occupational exposures in patients with COPD,” wrote Orianne Dumas, PhD, of the Université de Versailles St-Quentin-en-Yvelines (France) and coauthors. The study was published in JAMA Network Open.

To determine if regular use of disinfectants had a negative impact on respiratory health, the researchers analyzed data from 73,262 active female nurses who had no history of COPD and completed questionnaires every 2 years for the Nurses’ Health Study II. Their mean age at baseline was 54.7. Exposure to commonly used disinfectants was evaluated by a job-task-exposure matrix (JTEM) specific to nurses.

Between 2009 and 2015, 582 nurses reported incident physician-diagnosed COPD. Weekly use of disinfectants was associated with COPD incidence (adjusted hazard ratio 1.35; 95% confidence interval, 1.14-1.59). Additional associations were found in nurses who used disinfectants to clean surfaces (AHR, 1.38; 95% CI, 1.13-1.68) and to clean medical instruments (AHR, 1.31; 95% CI, 1.07-1.61). High-level exposure to certain disinfectants – including glutaraldehyde, bleach, hydrogen peroxide, alcohol, and quaternary ammonium compounds – were significantly associated with increased risk of COPD incidence.

The authors acknowledged their study’s limitations, including the JTEM only assessing exposure to seven of the major cleaning products commonly used in health care. In addition, detailed data on exposure to disinfectants was not available before 2009. However, they added that, because the study has been ongoing since 1989, it could be expected that women who had been nurses for decades had “already accumulated a long history of exposure.”

The study was supported in part by grants from the Centers for Disease Control and Prevention and the National Institutes of Health. Five of the authors reported receiving grants from the CDC’s National Institute for Occupational Safety and Health (NIOSH); one additional author reported being a consultant on a NIOSH grant and receiving personal fees from a health care system. No other conflicts of interest were reported.

SOURCE: Dumas O et al. JAMA Netw Open. 2019 Oct 18. doi: 10.1001/jamanetworkopen.2019.13563.

NEW ORLEANS – When looking specifically at the subgroup patients with no recent exacerbations, the triple fixed-dose combination budesonide/glycopyrrolate/formoterol fumarate metered-dose inhaler (BGF MDI) improved lung function and exacerbations, compared with dual therapy in patients with moderate to very severe chronic obstructive pulmonary disorder (COPD), an analysis of the phase 3 KRONOS study shows.

For that subgroup of patients with no moderate to severe exacerbations in the past year, BGF MDI was associated with a nominally significant reduction in the rate of subsequent COPD exacerbations, compared with glycopyrrolate/formoterol fumarate (GFF) MDI, according to investigator Fernando J. Martinez MD, of Weill Cornell Medical College, New York.

Results for the COPD patients with no recent history of exacerbation were consistent with the overall results of KRONOS, suggesting that the benefits of BGF MDI shown in that study were not driven by patients with a recent exacerbation history, Dr. Martinez said at the annual meeting of the American College of Chest Physicians.

“It was clear that the effect of this particular triple did not really appear to be dramatically different by the prior history or not in the comparison of the triple versus dual bronchodilator,” he said in a late-breaking clinical trial session.

About three-quarters of the patients in KRONOS (1,411 out of 1,896) lacked a recent exacerbation history. These patients had a mean age of 65.5 years, 72.8% were male, and 69.9% used inhaled corticosteroids at screening, which are demographics were similar to the overall KRONOS patient population, Dr. Martinez said.

In this subset of patients with no recent exacerbation history, treatment with BGF MDI significantly reduced the rate of moderate or severe exacerbations, compared with GFF MDI, with a treatment incidence rate ratio of 0.52 (95% confidence interval, 0.37-0.72; P = .0001).

“The results were remarkably similar,” Dr. Martinez said. “I was surprised, to be honest with you, when I saw these results. I did not anticipate that would be the case.”

By contrast, BGF MDI did not significantly reduce the rate of moderate or severe exacerbations, compared with budesonide/formoterol fumarate (BFF) MDI or open-label budesonide/formoterol fumarate dihydrate dry-powder inhaler (BUD/FORM DPI) as studied in KRONOS, Dr. Martinez said.

The change from baseline in morning predose trough forced expiratory volume in 1 second (FEV₁) at week 24 was significantly improved for BGF MDI, compared with BFF MDI and BUD/FORM DPI, but not compared with GFF MDI, according to the investigator. Similarly, the FEV₁ area under the curve from 0 to 4 hours was significantly improved for BGF MDI, compared with BFF MDI and BUD/FORM DPI, but not compared with GFF MDI.

Dr. Martinez reported disclosures related to AstraZeneca, GlaxoSmithKline, Boehringer Ingelheim, Chiesi, Sunovion, and Teva.

SOURCE: Martinez FJ et al. CHEST 2019, Abstract.

NEW ORLEANS – When looking specifically at the subgroup patients with no recent exacerbations, the triple fixed-dose combination budesonide/glycopyrrolate/formoterol fumarate metered-dose inhaler (BGF MDI) improved lung function and exacerbations, compared with dual therapy in patients with moderate to very severe chronic obstructive pulmonary disorder (COPD), an analysis of the phase 3 KRONOS study shows.

For that subgroup of patients with no moderate to severe exacerbations in the past year, BGF MDI was associated with a nominally significant reduction in the rate of subsequent COPD exacerbations, compared with glycopyrrolate/formoterol fumarate (GFF) MDI, according to investigator Fernando J. Martinez MD, of Weill Cornell Medical College, New York.

Results for the COPD patients with no recent history of exacerbation were consistent with the overall results of KRONOS, suggesting that the benefits of BGF MDI shown in that study were not driven by patients with a recent exacerbation history, Dr. Martinez said at the annual meeting of the American College of Chest Physicians.

“It was clear that the effect of this particular triple did not really appear to be dramatically different by the prior history or not in the comparison of the triple versus dual bronchodilator,” he said in a late-breaking clinical trial session.

About three-quarters of the patients in KRONOS (1,411 out of 1,896) lacked a recent exacerbation history. These patients had a mean age of 65.5 years, 72.8% were male, and 69.9% used inhaled corticosteroids at screening, which are demographics were similar to the overall KRONOS patient population, Dr. Martinez said.

In this subset of patients with no recent exacerbation history, treatment with BGF MDI significantly reduced the rate of moderate or severe exacerbations, compared with GFF MDI, with a treatment incidence rate ratio of 0.52 (95% confidence interval, 0.37-0.72; P = .0001).

“The results were remarkably similar,” Dr. Martinez said. “I was surprised, to be honest with you, when I saw these results. I did not anticipate that would be the case.”

By contrast, BGF MDI did not significantly reduce the rate of moderate or severe exacerbations, compared with budesonide/formoterol fumarate (BFF) MDI or open-label budesonide/formoterol fumarate dihydrate dry-powder inhaler (BUD/FORM DPI) as studied in KRONOS, Dr. Martinez said.

The change from baseline in morning predose trough forced expiratory volume in 1 second (FEV₁) at week 24 was significantly improved for BGF MDI, compared with BFF MDI and BUD/FORM DPI, but not compared with GFF MDI, according to the investigator. Similarly, the FEV₁ area under the curve from 0 to 4 hours was significantly improved for BGF MDI, compared with BFF MDI and BUD/FORM DPI, but not compared with GFF MDI.

Dr. Martinez reported disclosures related to AstraZeneca, GlaxoSmithKline, Boehringer Ingelheim, Chiesi, Sunovion, and Teva.

SOURCE: Martinez FJ et al. CHEST 2019, Abstract.

NEW ORLEANS – When looking specifically at the subgroup patients with no recent exacerbations, the triple fixed-dose combination budesonide/glycopyrrolate/formoterol fumarate metered-dose inhaler (BGF MDI) improved lung function and exacerbations, compared with dual therapy in patients with moderate to very severe chronic obstructive pulmonary disorder (COPD), an analysis of the phase 3 KRONOS study shows.

For that subgroup of patients with no moderate to severe exacerbations in the past year, BGF MDI was associated with a nominally significant reduction in the rate of subsequent COPD exacerbations, compared with glycopyrrolate/formoterol fumarate (GFF) MDI, according to investigator Fernando J. Martinez MD, of Weill Cornell Medical College, New York.

Results for the COPD patients with no recent history of exacerbation were consistent with the overall results of KRONOS, suggesting that the benefits of BGF MDI shown in that study were not driven by patients with a recent exacerbation history, Dr. Martinez said at the annual meeting of the American College of Chest Physicians.

“It was clear that the effect of this particular triple did not really appear to be dramatically different by the prior history or not in the comparison of the triple versus dual bronchodilator,” he said in a late-breaking clinical trial session.

About three-quarters of the patients in KRONOS (1,411 out of 1,896) lacked a recent exacerbation history. These patients had a mean age of 65.5 years, 72.8% were male, and 69.9% used inhaled corticosteroids at screening, which are demographics were similar to the overall KRONOS patient population, Dr. Martinez said.

In this subset of patients with no recent exacerbation history, treatment with BGF MDI significantly reduced the rate of moderate or severe exacerbations, compared with GFF MDI, with a treatment incidence rate ratio of 0.52 (95% confidence interval, 0.37-0.72; P = .0001).

“The results were remarkably similar,” Dr. Martinez said. “I was surprised, to be honest with you, when I saw these results. I did not anticipate that would be the case.”

By contrast, BGF MDI did not significantly reduce the rate of moderate or severe exacerbations, compared with budesonide/formoterol fumarate (BFF) MDI or open-label budesonide/formoterol fumarate dihydrate dry-powder inhaler (BUD/FORM DPI) as studied in KRONOS, Dr. Martinez said.

The change from baseline in morning predose trough forced expiratory volume in 1 second (FEV₁) at week 24 was significantly improved for BGF MDI, compared with BFF MDI and BUD/FORM DPI, but not compared with GFF MDI, according to the investigator. Similarly, the FEV₁ area under the curve from 0 to 4 hours was significantly improved for BGF MDI, compared with BFF MDI and BUD/FORM DPI, but not compared with GFF MDI.

Dr. Martinez reported disclosures related to AstraZeneca, GlaxoSmithKline, Boehringer Ingelheim, Chiesi, Sunovion, and Teva.

SOURCE: Martinez FJ et al. CHEST 2019, Abstract.

New Orleans – In patients with moderate to severe COPD who are not receiving inhaled corticosteroids (ICS), treatment with tiotropium/olodaterol combination therapy improved outcomes, compared with tiotropium alone, according to results of a pooled analysis of phase 3 trial data.

Lung function, symptoms, and quality of life were all improved irrespective of disease severity and baseline symptoms, and these benefits were apparent across multiple subgroups of non-ICS patients, investigator Peter M. Calverley, MBChB, of the University of Liverpool (England) reported at the annual meeting of the American College of Chest Physicians.

“Perhaps frustratingly, we can’t personalize [treatment] – everybody seemed to get benefit across the board, and the magnitude of that benefit was rather similar,” Dr. Calverley said in a podium presentation of the results.

The subgroup analysis was undertaken to fill a knowledge gap, according to Dr. Calverley, regarding the efficacy of combined long-acting muscarinic antagonist/long-acting beta2-agonist (LAMA/LABA) treatment in the sizable proportion of COPD patients who are not receiving ICS.

Patients in LAMA/LABA clinical trials are frequently taking multiple therapies, including ICS, he explained.

The post hoc analysis of pooled data from the TONADO 1 and 2 and OTEMTO 1 and 2 trials included a total of 1,596 patients with COPD who were not receiving ICS at trial enrollment.

The no-ICS patients receiving tiotropium/olodaterol had a significantly greater improvement in trough forced expiratory volume in 1 second (FEV₁) response by week 12 of treatment, compared with patients receiving tiotropium alone (0.054 L; P less than .0001), the researcher reported.

The trough FEV₁ improvement accruing to the tiotropium/olodaterol–treated patients was consistent across subgroups stratified according to GOLD stage and symptoms at baseline (such as Baseline Dyspnea Index), he added.

Transition Dyspnea Index (TDI) score at 12 weeks in these patients not receiving ICS was likewise superior in the tiotropium/olodaterol treated patients, compared with the tiotropium monotherapy group (.575; P less than .0001), while changes in St. George’s Respiratory Questionnaire (SGRQ) total scores also favored the combination treatment, according to the analyses presented.

Taken together, results of this post hoc analysis support the use of dual bronchodilator therapy to improve key COPD outcomes, compared with single bronchodilator therapy. In addition, this strategy should be considered as an earlier treatment option, according to Dr. Calverley.

“Clearly dual bronchodilator therapy improves the key outcomes, compared with an effective single bronchodilator, and this perhaps is why it’s being picked up as an earlier treatment option, and certainly in some guidelines like the current [National Institute for Health Care and Excellence] guidelines where I live in the U.K., it’s becoming standard of care for most people with COPD,” he said in his presentation.

Dr. Calverley reported grants and personal fees from GlaxoSmithKline; personal fees from AstraZeneca, Recipharm, and Zambon; and personal and other fees from Boehringer Ingelheim outside the submitted work.

SOURCE: Calverley PM et al. CHEST 2019. Abstract, doi: 10.1016/j.chest.2019.08.310.

New Orleans – In patients with moderate to severe COPD who are not receiving inhaled corticosteroids (ICS), treatment with tiotropium/olodaterol combination therapy improved outcomes, compared with tiotropium alone, according to results of a pooled analysis of phase 3 trial data.

Lung function, symptoms, and quality of life were all improved irrespective of disease severity and baseline symptoms, and these benefits were apparent across multiple subgroups of non-ICS patients, investigator Peter M. Calverley, MBChB, of the University of Liverpool (England) reported at the annual meeting of the American College of Chest Physicians.

“Perhaps frustratingly, we can’t personalize [treatment] – everybody seemed to get benefit across the board, and the magnitude of that benefit was rather similar,” Dr. Calverley said in a podium presentation of the results.

The subgroup analysis was undertaken to fill a knowledge gap, according to Dr. Calverley, regarding the efficacy of combined long-acting muscarinic antagonist/long-acting beta2-agonist (LAMA/LABA) treatment in the sizable proportion of COPD patients who are not receiving ICS.

Patients in LAMA/LABA clinical trials are frequently taking multiple therapies, including ICS, he explained.

The post hoc analysis of pooled data from the TONADO 1 and 2 and OTEMTO 1 and 2 trials included a total of 1,596 patients with COPD who were not receiving ICS at trial enrollment.

The no-ICS patients receiving tiotropium/olodaterol had a significantly greater improvement in trough forced expiratory volume in 1 second (FEV₁) response by week 12 of treatment, compared with patients receiving tiotropium alone (0.054 L; P less than .0001), the researcher reported.

The trough FEV₁ improvement accruing to the tiotropium/olodaterol–treated patients was consistent across subgroups stratified according to GOLD stage and symptoms at baseline (such as Baseline Dyspnea Index), he added.

Transition Dyspnea Index (TDI) score at 12 weeks in these patients not receiving ICS was likewise superior in the tiotropium/olodaterol treated patients, compared with the tiotropium monotherapy group (.575; P less than .0001), while changes in St. George’s Respiratory Questionnaire (SGRQ) total scores also favored the combination treatment, according to the analyses presented.

Taken together, results of this post hoc analysis support the use of dual bronchodilator therapy to improve key COPD outcomes, compared with single bronchodilator therapy. In addition, this strategy should be considered as an earlier treatment option, according to Dr. Calverley.

“Clearly dual bronchodilator therapy improves the key outcomes, compared with an effective single bronchodilator, and this perhaps is why it’s being picked up as an earlier treatment option, and certainly in some guidelines like the current [National Institute for Health Care and Excellence] guidelines where I live in the U.K., it’s becoming standard of care for most people with COPD,” he said in his presentation.

Dr. Calverley reported grants and personal fees from GlaxoSmithKline; personal fees from AstraZeneca, Recipharm, and Zambon; and personal and other fees from Boehringer Ingelheim outside the submitted work.

SOURCE: Calverley PM et al. CHEST 2019. Abstract, doi: 10.1016/j.chest.2019.08.310.

New Orleans – In patients with moderate to severe COPD who are not receiving inhaled corticosteroids (ICS), treatment with tiotropium/olodaterol combination therapy improved outcomes, compared with tiotropium alone, according to results of a pooled analysis of phase 3 trial data.

Lung function, symptoms, and quality of life were all improved irrespective of disease severity and baseline symptoms, and these benefits were apparent across multiple subgroups of non-ICS patients, investigator Peter M. Calverley, MBChB, of the University of Liverpool (England) reported at the annual meeting of the American College of Chest Physicians.

“Perhaps frustratingly, we can’t personalize [treatment] – everybody seemed to get benefit across the board, and the magnitude of that benefit was rather similar,” Dr. Calverley said in a podium presentation of the results.

The subgroup analysis was undertaken to fill a knowledge gap, according to Dr. Calverley, regarding the efficacy of combined long-acting muscarinic antagonist/long-acting beta2-agonist (LAMA/LABA) treatment in the sizable proportion of COPD patients who are not receiving ICS.

Patients in LAMA/LABA clinical trials are frequently taking multiple therapies, including ICS, he explained.

The post hoc analysis of pooled data from the TONADO 1 and 2 and OTEMTO 1 and 2 trials included a total of 1,596 patients with COPD who were not receiving ICS at trial enrollment.

The no-ICS patients receiving tiotropium/olodaterol had a significantly greater improvement in trough forced expiratory volume in 1 second (FEV₁) response by week 12 of treatment, compared with patients receiving tiotropium alone (0.054 L; P less than .0001), the researcher reported.

The trough FEV₁ improvement accruing to the tiotropium/olodaterol–treated patients was consistent across subgroups stratified according to GOLD stage and symptoms at baseline (such as Baseline Dyspnea Index), he added.

Transition Dyspnea Index (TDI) score at 12 weeks in these patients not receiving ICS was likewise superior in the tiotropium/olodaterol treated patients, compared with the tiotropium monotherapy group (.575; P less than .0001), while changes in St. George’s Respiratory Questionnaire (SGRQ) total scores also favored the combination treatment, according to the analyses presented.

Taken together, results of this post hoc analysis support the use of dual bronchodilator therapy to improve key COPD outcomes, compared with single bronchodilator therapy. In addition, this strategy should be considered as an earlier treatment option, according to Dr. Calverley.

“Clearly dual bronchodilator therapy improves the key outcomes, compared with an effective single bronchodilator, and this perhaps is why it’s being picked up as an earlier treatment option, and certainly in some guidelines like the current [National Institute for Health Care and Excellence] guidelines where I live in the U.K., it’s becoming standard of care for most people with COPD,” he said in his presentation.

Dr. Calverley reported grants and personal fees from GlaxoSmithKline; personal fees from AstraZeneca, Recipharm, and Zambon; and personal and other fees from Boehringer Ingelheim outside the submitted work.

SOURCE: Calverley PM et al. CHEST 2019. Abstract, doi: 10.1016/j.chest.2019.08.310.

NEW ORLEANS – Reduction of readmission rates among individuals hospitalized for an acute exacerbation of COPD could reduce mortality and health care expenditures, results of a large, retrospective study suggest.

“This is not a small problem,” Dr. Krishnan said in a podium presentation at the annual meeting of the American College of Chest Physicians. “The amount of money that can be saved can be put into primary care for curbing COPD and better patient outcomes, basically, if you’re able to put in checkpoints to stop this problem.”

Bundled care interventions by interdisciplinary teams have thus far proven effective at improving quality of care and improving process measures in this setting, said Dr. Krishnan.

The retrospective cohort study by Dr. Krishnan and colleagues included 530,229 adult patients in the 2016 National Readmission Database who had a principal diagnosis of acute COPD exacerbation. The mean age of the patients was 68 years, and 58% were female.

The rates of readmission at 30 days after discharge were 16.3% for any cause and 5.4% specifically for COPD, the researchers found. Of note, the in-hospital mortality rate increased from 1.1% to 3.8% during readmission (P less than .01), Dr. Krishnan said.

Readmissions were linked to a cumulative length of stay of 458,677 days, with corresponding hospital costs of $0.97 billion and charges of $4.0 billion; the COPD-specific readmissions were associated with cumulative length of stay of 132,026 days, costs of $253 million, and charges of $1 billion, Dr. Krishnan reported.

Dr. Krishnan and coauthors disclosed no relationships relevant to their study.

SOURCE: Krishnan AM et al. CHEST 2019. Abstract, doi: 10.1016/j.chest.2019.08.229.

NEW ORLEANS – Reduction of readmission rates among individuals hospitalized for an acute exacerbation of COPD could reduce mortality and health care expenditures, results of a large, retrospective study suggest.

“This is not a small problem,” Dr. Krishnan said in a podium presentation at the annual meeting of the American College of Chest Physicians. “The amount of money that can be saved can be put into primary care for curbing COPD and better patient outcomes, basically, if you’re able to put in checkpoints to stop this problem.”

Bundled care interventions by interdisciplinary teams have thus far proven effective at improving quality of care and improving process measures in this setting, said Dr. Krishnan.

The retrospective cohort study by Dr. Krishnan and colleagues included 530,229 adult patients in the 2016 National Readmission Database who had a principal diagnosis of acute COPD exacerbation. The mean age of the patients was 68 years, and 58% were female.

The rates of readmission at 30 days after discharge were 16.3% for any cause and 5.4% specifically for COPD, the researchers found. Of note, the in-hospital mortality rate increased from 1.1% to 3.8% during readmission (P less than .01), Dr. Krishnan said.

Readmissions were linked to a cumulative length of stay of 458,677 days, with corresponding hospital costs of $0.97 billion and charges of $4.0 billion; the COPD-specific readmissions were associated with cumulative length of stay of 132,026 days, costs of $253 million, and charges of $1 billion, Dr. Krishnan reported.

Dr. Krishnan and coauthors disclosed no relationships relevant to their study.

SOURCE: Krishnan AM et al. CHEST 2019. Abstract, doi: 10.1016/j.chest.2019.08.229.

NEW ORLEANS – Reduction of readmission rates among individuals hospitalized for an acute exacerbation of COPD could reduce mortality and health care expenditures, results of a large, retrospective study suggest.

“This is not a small problem,” Dr. Krishnan said in a podium presentation at the annual meeting of the American College of Chest Physicians. “The amount of money that can be saved can be put into primary care for curbing COPD and better patient outcomes, basically, if you’re able to put in checkpoints to stop this problem.”

Bundled care interventions by interdisciplinary teams have thus far proven effective at improving quality of care and improving process measures in this setting, said Dr. Krishnan.

The retrospective cohort study by Dr. Krishnan and colleagues included 530,229 adult patients in the 2016 National Readmission Database who had a principal diagnosis of acute COPD exacerbation. The mean age of the patients was 68 years, and 58% were female.

The rates of readmission at 30 days after discharge were 16.3% for any cause and 5.4% specifically for COPD, the researchers found. Of note, the in-hospital mortality rate increased from 1.1% to 3.8% during readmission (P less than .01), Dr. Krishnan said.

Readmissions were linked to a cumulative length of stay of 458,677 days, with corresponding hospital costs of $0.97 billion and charges of $4.0 billion; the COPD-specific readmissions were associated with cumulative length of stay of 132,026 days, costs of $253 million, and charges of $1 billion, Dr. Krishnan reported.

Dr. Krishnan and coauthors disclosed no relationships relevant to their study.

SOURCE: Krishnan AM et al. CHEST 2019. Abstract, doi: 10.1016/j.chest.2019.08.229.

Patients with chronic obstructive pulmonary disease who received opioids or benzodiazepines had a greater risk of hospitalization for respiratory-related adverse events, according to recent research from Annals of the American Thoracic Society.

sdominick/Getty Images

In addition, the risk of hospitalization because of respiratory events for patients with chronic obstructive pulmonary disease (COPD) was greater when opioid and benzodiazepine medications were combined, compared with patients who did not take either medication, Jacques G. Baillargeon, PhD, of the department of preventive medicine and community health at the University of Texas, Galveston, and colleagues wrote.

“Patients with COPD and their physicians should judiciously assess the risks and benefits of opioids and benzodiazepines, alone and in combination, and preferentially recommend nonopioid and nonbenzodiazepine approaches for pain, sleep, and anxiety management in patients with COPD,” the investigators wrote.

The researchers performed a case-control study of 3,232 Medicare beneficiary cases of COPD patients who were aged at least 66 years. Patients were included if they experienced a hospitalization related to a COPD-related adverse event with a respiratory diagnosis in 2014 and then matched to one or two control patients (total, 6,247 patients) based on age at hospitalization, gender, COPD medication, COPD complexity, obstructive sleep apnea, and socioeconomic status. COPD complexity was assigned to three levels (low, moderate, high) and calculated using the patient’s comorbid respiratory conditions and associated medical procedures in the 12 months prior to their hospitalization.

They found that, in the 30 days before COPD-related hospitalization, use of opioids was associated with greater likelihood of hospitalization (adjusted odds ratio, 1.73; 95% confidence interval, 1.52-1.97), as was use of benzodiazepines (aOR, 1.42; 95% CI, 1.21-1.66). When patients used both opioids and benzodiazepines, they had a significantly higher risk of hospitalization, compared with patients who did not use opioids or benzodiazepines (aOR, 2.32; 95% CI, 1.94-2.77).

In the 60 days prior to hospitalization, there was also a greater likelihood of hospitalization among COPD patients who used opioids (aOR, 1.66; 95% CI, 1.47-1.88), benzodiazepines (aOR, 1.44; 95% CI, 1.24-1.67), and both opioids and benzodiazepines (aOR, 2.27; 95% CI, 1.93-2.67); at 90 days, this higher risk of hospitalization persisted among COPD patients taking opioids (aOR, 1.58; 95% CI, 1.40-1.78), benzodiazepines (aOR, 1.40; 95% CI, 1.20-1.63), and both opioids and benzodiazepines (aOR, 2.21; 95% CI, 1.88-2.59).

The researchers acknowledged that one potential limitation in the study was how COPD diagnoses were obtained through coding performed by clinicians instead of from laboratory testing. Confounding by COPD indication and severity; use of over-the-counter medication or opioids and benzodiazepines received illegally; and lack of analyses of potential confounders such as diet, alcohol use, smoking status and herbal supplement use were other limitations.

This study was supported by an award from the National Center for Advancing Translational Sciences and National Institutes of Health. Dr. Baillargeon had no disclosures.

SOURCE: Baillargeon JG et al. Ann Am Thorac Soc. 2019 Oct 1. doi: 10.1513/AnnalsATS.201901-024OC.

Patients with chronic obstructive pulmonary disease who received opioids or benzodiazepines had a greater risk of hospitalization for respiratory-related adverse events, according to recent research from Annals of the American Thoracic Society.

sdominick/Getty Images

In addition, the risk of hospitalization because of respiratory events for patients with chronic obstructive pulmonary disease (COPD) was greater when opioid and benzodiazepine medications were combined, compared with patients who did not take either medication, Jacques G. Baillargeon, PhD, of the department of preventive medicine and community health at the University of Texas, Galveston, and colleagues wrote.

“Patients with COPD and their physicians should judiciously assess the risks and benefits of opioids and benzodiazepines, alone and in combination, and preferentially recommend nonopioid and nonbenzodiazepine approaches for pain, sleep, and anxiety management in patients with COPD,” the investigators wrote.

The researchers performed a case-control study of 3,232 Medicare beneficiary cases of COPD patients who were aged at least 66 years. Patients were included if they experienced a hospitalization related to a COPD-related adverse event with a respiratory diagnosis in 2014 and then matched to one or two control patients (total, 6,247 patients) based on age at hospitalization, gender, COPD medication, COPD complexity, obstructive sleep apnea, and socioeconomic status. COPD complexity was assigned to three levels (low, moderate, high) and calculated using the patient’s comorbid respiratory conditions and associated medical procedures in the 12 months prior to their hospitalization.

They found that, in the 30 days before COPD-related hospitalization, use of opioids was associated with greater likelihood of hospitalization (adjusted odds ratio, 1.73; 95% confidence interval, 1.52-1.97), as was use of benzodiazepines (aOR, 1.42; 95% CI, 1.21-1.66). When patients used both opioids and benzodiazepines, they had a significantly higher risk of hospitalization, compared with patients who did not use opioids or benzodiazepines (aOR, 2.32; 95% CI, 1.94-2.77).

In the 60 days prior to hospitalization, there was also a greater likelihood of hospitalization among COPD patients who used opioids (aOR, 1.66; 95% CI, 1.47-1.88), benzodiazepines (aOR, 1.44; 95% CI, 1.24-1.67), and both opioids and benzodiazepines (aOR, 2.27; 95% CI, 1.93-2.67); at 90 days, this higher risk of hospitalization persisted among COPD patients taking opioids (aOR, 1.58; 95% CI, 1.40-1.78), benzodiazepines (aOR, 1.40; 95% CI, 1.20-1.63), and both opioids and benzodiazepines (aOR, 2.21; 95% CI, 1.88-2.59).

The researchers acknowledged that one potential limitation in the study was how COPD diagnoses were obtained through coding performed by clinicians instead of from laboratory testing. Confounding by COPD indication and severity; use of over-the-counter medication or opioids and benzodiazepines received illegally; and lack of analyses of potential confounders such as diet, alcohol use, smoking status and herbal supplement use were other limitations.

This study was supported by an award from the National Center for Advancing Translational Sciences and National Institutes of Health. Dr. Baillargeon had no disclosures.

SOURCE: Baillargeon JG et al. Ann Am Thorac Soc. 2019 Oct 1. doi: 10.1513/AnnalsATS.201901-024OC.

Patients with chronic obstructive pulmonary disease who received opioids or benzodiazepines had a greater risk of hospitalization for respiratory-related adverse events, according to recent research from Annals of the American Thoracic Society.

sdominick/Getty Images

In addition, the risk of hospitalization because of respiratory events for patients with chronic obstructive pulmonary disease (COPD) was greater when opioid and benzodiazepine medications were combined, compared with patients who did not take either medication, Jacques G. Baillargeon, PhD, of the department of preventive medicine and community health at the University of Texas, Galveston, and colleagues wrote.

“Patients with COPD and their physicians should judiciously assess the risks and benefits of opioids and benzodiazepines, alone and in combination, and preferentially recommend nonopioid and nonbenzodiazepine approaches for pain, sleep, and anxiety management in patients with COPD,” the investigators wrote.

The researchers performed a case-control study of 3,232 Medicare beneficiary cases of COPD patients who were aged at least 66 years. Patients were included if they experienced a hospitalization related to a COPD-related adverse event with a respiratory diagnosis in 2014 and then matched to one or two control patients (total, 6,247 patients) based on age at hospitalization, gender, COPD medication, COPD complexity, obstructive sleep apnea, and socioeconomic status. COPD complexity was assigned to three levels (low, moderate, high) and calculated using the patient’s comorbid respiratory conditions and associated medical procedures in the 12 months prior to their hospitalization.

They found that, in the 30 days before COPD-related hospitalization, use of opioids was associated with greater likelihood of hospitalization (adjusted odds ratio, 1.73; 95% confidence interval, 1.52-1.97), as was use of benzodiazepines (aOR, 1.42; 95% CI, 1.21-1.66). When patients used both opioids and benzodiazepines, they had a significantly higher risk of hospitalization, compared with patients who did not use opioids or benzodiazepines (aOR, 2.32; 95% CI, 1.94-2.77).

In the 60 days prior to hospitalization, there was also a greater likelihood of hospitalization among COPD patients who used opioids (aOR, 1.66; 95% CI, 1.47-1.88), benzodiazepines (aOR, 1.44; 95% CI, 1.24-1.67), and both opioids and benzodiazepines (aOR, 2.27; 95% CI, 1.93-2.67); at 90 days, this higher risk of hospitalization persisted among COPD patients taking opioids (aOR, 1.58; 95% CI, 1.40-1.78), benzodiazepines (aOR, 1.40; 95% CI, 1.20-1.63), and both opioids and benzodiazepines (aOR, 2.21; 95% CI, 1.88-2.59).

The researchers acknowledged that one potential limitation in the study was how COPD diagnoses were obtained through coding performed by clinicians instead of from laboratory testing. Confounding by COPD indication and severity; use of over-the-counter medication or opioids and benzodiazepines received illegally; and lack of analyses of potential confounders such as diet, alcohol use, smoking status and herbal supplement use were other limitations.

This study was supported by an award from the National Center for Advancing Translational Sciences and National Institutes of Health. Dr. Baillargeon had no disclosures.

SOURCE: Baillargeon JG et al. Ann Am Thorac Soc. 2019 Oct 1. doi: 10.1513/AnnalsATS.201901-024OC.

NEW ORLEANS – A history of recent exacerbations did not significantly affect the safety or efficacy of aclidinium bromide (Tudorza) in patients with moderate to severe chronic obstructive pulmonary disease and high cardiovascular risk, analysis of a postmarketing surveillance trial suggests.

Andrew D. Bowser/MDedge News

Regardless of exacerbation history, the long-acting muscarinic antagonist reduced the rate of moderate or severe COPD exacerbations versus placebo in this subgroup analysis of the phase IV ASCENT-COPD trial, presented here at the annual meeting of the American College of Chest Physicians.

At the same time, there were no significant increases in the risk of mortality or major cardiac adverse events (MACE) for those patients who had an exacerbation in the past year versus those who did not, according to investigator Robert A. Wise, MD.

Those findings may be reassuring, given that COPD patients commonly have comorbidities and cardiovascular risk factors, according to Dr. Wise, professor of medicine at the Johns Hopkins University, Baltimore.

“There’s a concern and some evidence that patients who have a propensity to COPD exacerbations may also have an increased risk for cardiovascular events,” Dr. Wise said in a podium presentation.

Accordingly, he and coinvestigators sought to tease out the impact of COPD exacerbations on safety as well as efficacy in the randomized, placebo-controlled ASCENT-COPD trial, which included 3,630 patients with moderate to severe COPD plus a cardiovascular disease history or multiple atherothrombotic risk factors.

Of the patients who were analyzed in the study, 1,433 patients had at least one treated COPD exacerbation in the year before screening for the study, while 2,156 had no exacerbations in the prior year, Dr. Wise said.

Top-line results of that study, published several months ago, showed that aclidinium did not increase MACE risk over 3 years, and reduced the rate of moderate to severe COPD exacerbations over the first year (JAMA. 2019 7 May 7;321[17]:1693-701).

In this latest analysis, presented at the meeting, risk of MACE with aclidinium treatment was not increased versus placebo, irrespective of whether they had exacerbations in the prior year (interaction P = .233); likewise, the risk of all-cause mortality was similar between groups (P = .154).

In terms of reduction in moderate or severe COPD exacerbations in the first year, aclidinium was superior to placebo both for the patients who had at least one or exacerbation in the prior year (rate ratio, 0.80) and those who had no exacerbations in the prior year (RR, 0.69).

“This translates into a number-needed-to-treat to prevent one exacerbation of about 11 patients for those without an exacerbation, compared to about 6 patients for those with a prior exacerbation,” Dr. Wise said in his presentation.

The ASCENT-COPD study was funded initially by Forest Laboratories and later by AstraZeneca and Circassia. Dr. Wise provided disclosures related to AstraZeneca, GlaxoSmithKline, Boehringer Ingelheim, Sunovion, Mylan/Theravance, Contrafect, Pearl, Merck, Verona, Novartis, AbbVie, Syneos, Regeneron, and Kiniksa.

SOURCE: Wise R et al. CHEST 2019. Abstract, doi: 10.1016/j.chest.2019.08.231.

NEW ORLEANS – A history of recent exacerbations did not significantly affect the safety or efficacy of aclidinium bromide (Tudorza) in patients with moderate to severe chronic obstructive pulmonary disease and high cardiovascular risk, analysis of a postmarketing surveillance trial suggests.

Andrew D. Bowser/MDedge News

Regardless of exacerbation history, the long-acting muscarinic antagonist reduced the rate of moderate or severe COPD exacerbations versus placebo in this subgroup analysis of the phase IV ASCENT-COPD trial, presented here at the annual meeting of the American College of Chest Physicians.

At the same time, there were no significant increases in the risk of mortality or major cardiac adverse events (MACE) for those patients who had an exacerbation in the past year versus those who did not, according to investigator Robert A. Wise, MD.

Those findings may be reassuring, given that COPD patients commonly have comorbidities and cardiovascular risk factors, according to Dr. Wise, professor of medicine at the Johns Hopkins University, Baltimore.

“There’s a concern and some evidence that patients who have a propensity to COPD exacerbations may also have an increased risk for cardiovascular events,” Dr. Wise said in a podium presentation.

Accordingly, he and coinvestigators sought to tease out the impact of COPD exacerbations on safety as well as efficacy in the randomized, placebo-controlled ASCENT-COPD trial, which included 3,630 patients with moderate to severe COPD plus a cardiovascular disease history or multiple atherothrombotic risk factors.

Of the patients who were analyzed in the study, 1,433 patients had at least one treated COPD exacerbation in the year before screening for the study, while 2,156 had no exacerbations in the prior year, Dr. Wise said.

Top-line results of that study, published several months ago, showed that aclidinium did not increase MACE risk over 3 years, and reduced the rate of moderate to severe COPD exacerbations over the first year (JAMA. 2019 7 May 7;321[17]:1693-701).

In this latest analysis, presented at the meeting, risk of MACE with aclidinium treatment was not increased versus placebo, irrespective of whether they had exacerbations in the prior year (interaction P = .233); likewise, the risk of all-cause mortality was similar between groups (P = .154).

In terms of reduction in moderate or severe COPD exacerbations in the first year, aclidinium was superior to placebo both for the patients who had at least one or exacerbation in the prior year (rate ratio, 0.80) and those who had no exacerbations in the prior year (RR, 0.69).

“This translates into a number-needed-to-treat to prevent one exacerbation of about 11 patients for those without an exacerbation, compared to about 6 patients for those with a prior exacerbation,” Dr. Wise said in his presentation.

The ASCENT-COPD study was funded initially by Forest Laboratories and later by AstraZeneca and Circassia. Dr. Wise provided disclosures related to AstraZeneca, GlaxoSmithKline, Boehringer Ingelheim, Sunovion, Mylan/Theravance, Contrafect, Pearl, Merck, Verona, Novartis, AbbVie, Syneos, Regeneron, and Kiniksa.

SOURCE: Wise R et al. CHEST 2019. Abstract, doi: 10.1016/j.chest.2019.08.231.

NEW ORLEANS – A history of recent exacerbations did not significantly affect the safety or efficacy of aclidinium bromide (Tudorza) in patients with moderate to severe chronic obstructive pulmonary disease and high cardiovascular risk, analysis of a postmarketing surveillance trial suggests.

Andrew D. Bowser/MDedge News

Regardless of exacerbation history, the long-acting muscarinic antagonist reduced the rate of moderate or severe COPD exacerbations versus placebo in this subgroup analysis of the phase IV ASCENT-COPD trial, presented here at the annual meeting of the American College of Chest Physicians.

At the same time, there were no significant increases in the risk of mortality or major cardiac adverse events (MACE) for those patients who had an exacerbation in the past year versus those who did not, according to investigator Robert A. Wise, MD.

Those findings may be reassuring, given that COPD patients commonly have comorbidities and cardiovascular risk factors, according to Dr. Wise, professor of medicine at the Johns Hopkins University, Baltimore.

“There’s a concern and some evidence that patients who have a propensity to COPD exacerbations may also have an increased risk for cardiovascular events,” Dr. Wise said in a podium presentation.

Accordingly, he and coinvestigators sought to tease out the impact of COPD exacerbations on safety as well as efficacy in the randomized, placebo-controlled ASCENT-COPD trial, which included 3,630 patients with moderate to severe COPD plus a cardiovascular disease history or multiple atherothrombotic risk factors.

Of the patients who were analyzed in the study, 1,433 patients had at least one treated COPD exacerbation in the year before screening for the study, while 2,156 had no exacerbations in the prior year, Dr. Wise said.

Top-line results of that study, published several months ago, showed that aclidinium did not increase MACE risk over 3 years, and reduced the rate of moderate to severe COPD exacerbations over the first year (JAMA. 2019 7 May 7;321[17]:1693-701).

In this latest analysis, presented at the meeting, risk of MACE with aclidinium treatment was not increased versus placebo, irrespective of whether they had exacerbations in the prior year (interaction P = .233); likewise, the risk of all-cause mortality was similar between groups (P = .154).

In terms of reduction in moderate or severe COPD exacerbations in the first year, aclidinium was superior to placebo both for the patients who had at least one or exacerbation in the prior year (rate ratio, 0.80) and those who had no exacerbations in the prior year (RR, 0.69).

“This translates into a number-needed-to-treat to prevent one exacerbation of about 11 patients for those without an exacerbation, compared to about 6 patients for those with a prior exacerbation,” Dr. Wise said in his presentation.

The ASCENT-COPD study was funded initially by Forest Laboratories and later by AstraZeneca and Circassia. Dr. Wise provided disclosures related to AstraZeneca, GlaxoSmithKline, Boehringer Ingelheim, Sunovion, Mylan/Theravance, Contrafect, Pearl, Merck, Verona, Novartis, AbbVie, Syneos, Regeneron, and Kiniksa.

SOURCE: Wise R et al. CHEST 2019. Abstract, doi: 10.1016/j.chest.2019.08.231.

A new study has found that beta-blocker treatment did not prevent exacerbations in patients with moderate or severe chronic obstructive pulmonary disease (COPD).

decade3d/Thinkstock

“These results differ from previously reported findings from observational studies suggesting that beta-blockers reduce the risks of exacerbation and death from any cause in patients with COPD,” wrote Mark T. Dransfield, MD, of the University of Alabama at Birmingham and coauthors. Their findings were presented at the annual meeting of the American College of Chest Physicians and also were published simultaneously in the New England Journal of Medicine.

To determine the value of beta-blockers as a potential treatment for COPD, the researchers launched a prospective randomized trial called BLOCK COPD, consisting of 532 patients with moderate or severe COPD. They were assigned to two groups: those receiving extended-release metoprolol (n = 268) and those receiving placebo (n = 264). The mean age of all patients was 65 years.

The groups saw no significant difference in median time until the first exacerbation, which was 202 days (95% confidence interval, 162-282) in the metoprolol group and 222 days (95% CI, 189-295) in the placebo group (hazard ratio, 1.05; 95% CI, 0.84-1.32; P = .66). Metoprolol was associated with a higher risk of severe or very severe exacerbations leading to hospitalization (HR, 1.91; 95% CI, 1.29-2.83). During treatment, there were 11 deaths in the metoprolol group and 5 deaths in the placebo group.

Though there was no evidence of increases in patient-reported adverse events related to metoprolol, more discontinuations did occur in the metoprolol group compared with placebo (11.2% vs. 6.1%).

The authors acknowledged their study’s limitations, chiefly including the fact that the trial was ended early “on the basis of the conditional power analyses and concern about safety.” In addition, the reduction of heart rate and blood pressure in the metoprolol group made it impossible to fully blind the study. Finally, many patients in the trial had already suffered the effects of moderate to severe COPD, including previous hospitalization and the need for supplemental oxygen, leading to uncertainty as to “whether our results would apply to patients with mild airflow obstruction or a lower exacerbation risk.”

The study was supported by a grant from the Department of Defense. The authors reported numerous potential conflicts of interest, including receiving grants, personal fees and research funds from various pharmaceutical companies and government entities.
 

SOURCE: Dransfield MT et al. CHEST 2019. 2019 Oct 20. doi: 10.1056/NEJMoa1908142.

A new study has found that beta-blocker treatment did not prevent exacerbations in patients with moderate or severe chronic obstructive pulmonary disease (COPD).

decade3d/Thinkstock

“These results differ from previously reported findings from observational studies suggesting that beta-blockers reduce the risks of exacerbation and death from any cause in patients with COPD,” wrote Mark T. Dransfield, MD, of the University of Alabama at Birmingham and coauthors. Their findings were presented at the annual meeting of the American College of Chest Physicians and also were published simultaneously in the New England Journal of Medicine.

To determine the value of beta-blockers as a potential treatment for COPD, the researchers launched a prospective randomized trial called BLOCK COPD, consisting of 532 patients with moderate or severe COPD. They were assigned to two groups: those receiving extended-release metoprolol (n = 268) and those receiving placebo (n = 264). The mean age of all patients was 65 years.

The groups saw no significant difference in median time until the first exacerbation, which was 202 days (95% confidence interval, 162-282) in the metoprolol group and 222 days (95% CI, 189-295) in the placebo group (hazard ratio, 1.05; 95% CI, 0.84-1.32; P = .66). Metoprolol was associated with a higher risk of severe or very severe exacerbations leading to hospitalization (HR, 1.91; 95% CI, 1.29-2.83). During treatment, there were 11 deaths in the metoprolol group and 5 deaths in the placebo group.

Though there was no evidence of increases in patient-reported adverse events related to metoprolol, more discontinuations did occur in the metoprolol group compared with placebo (11.2% vs. 6.1%).

The authors acknowledged their study’s limitations, chiefly including the fact that the trial was ended early “on the basis of the conditional power analyses and concern about safety.” In addition, the reduction of heart rate and blood pressure in the metoprolol group made it impossible to fully blind the study. Finally, many patients in the trial had already suffered the effects of moderate to severe COPD, including previous hospitalization and the need for supplemental oxygen, leading to uncertainty as to “whether our results would apply to patients with mild airflow obstruction or a lower exacerbation risk.”

The study was supported by a grant from the Department of Defense. The authors reported numerous potential conflicts of interest, including receiving grants, personal fees and research funds from various pharmaceutical companies and government entities.
 

SOURCE: Dransfield MT et al. CHEST 2019. 2019 Oct 20. doi: 10.1056/NEJMoa1908142.

A new study has found that beta-blocker treatment did not prevent exacerbations in patients with moderate or severe chronic obstructive pulmonary disease (COPD).

decade3d/Thinkstock

“These results differ from previously reported findings from observational studies suggesting that beta-blockers reduce the risks of exacerbation and death from any cause in patients with COPD,” wrote Mark T. Dransfield, MD, of the University of Alabama at Birmingham and coauthors. Their findings were presented at the annual meeting of the American College of Chest Physicians and also were published simultaneously in the New England Journal of Medicine.

To determine the value of beta-blockers as a potential treatment for COPD, the researchers launched a prospective randomized trial called BLOCK COPD, consisting of 532 patients with moderate or severe COPD. They were assigned to two groups: those receiving extended-release metoprolol (n = 268) and those receiving placebo (n = 264). The mean age of all patients was 65 years.

The groups saw no significant difference in median time until the first exacerbation, which was 202 days (95% confidence interval, 162-282) in the metoprolol group and 222 days (95% CI, 189-295) in the placebo group (hazard ratio, 1.05; 95% CI, 0.84-1.32; P = .66). Metoprolol was associated with a higher risk of severe or very severe exacerbations leading to hospitalization (HR, 1.91; 95% CI, 1.29-2.83). During treatment, there were 11 deaths in the metoprolol group and 5 deaths in the placebo group.

Though there was no evidence of increases in patient-reported adverse events related to metoprolol, more discontinuations did occur in the metoprolol group compared with placebo (11.2% vs. 6.1%).

The authors acknowledged their study’s limitations, chiefly including the fact that the trial was ended early “on the basis of the conditional power analyses and concern about safety.” In addition, the reduction of heart rate and blood pressure in the metoprolol group made it impossible to fully blind the study. Finally, many patients in the trial had already suffered the effects of moderate to severe COPD, including previous hospitalization and the need for supplemental oxygen, leading to uncertainty as to “whether our results would apply to patients with mild airflow obstruction or a lower exacerbation risk.”

The study was supported by a grant from the Department of Defense. The authors reported numerous potential conflicts of interest, including receiving grants, personal fees and research funds from various pharmaceutical companies and government entities.
 

SOURCE: Dransfield MT et al. CHEST 2019. 2019 Oct 20. doi: 10.1056/NEJMoa1908142.

Influenza vaccination modestly reduces the risk of hospitalizations associated with laboratory-confirmed influenza in people with chronic obstructive pulmonary disease (COPD), according to data published in the Journal of Infectious Diseases.

Cynthia Goldsmith/CDC photo #10073

“To the best of our knowledge, this is the first large, real-world population study to examine vaccine effectiveness in people with COPD using the test-negative design and influenza-specific study outcomes,” wrote Andrea S. Gershon, MD, of Sunnybrook Health Sciences Center in Toronto and colleagues. “These findings emphasize the need for more effective influenza vaccines for older COPD patients and other preventive strategies.”
 

A test-negative study design

Data suggest that 70% of COPD exacerbations are caused by infection, and influenza often is identified as the cause. Although all major COPD practice guidelines recommend seasonal influenza vaccination, the evidence indicating that vaccination reduces hospitalizations and death is limited. The inherent or corticosteroid-induced decrease in immune response to vaccination and respiratory infection among patients with COPD may reduce the effectiveness of influenza vaccination, wrote Dr. Gershon and colleagues.

The investigators used a test-negative design to evaluate how effectively influenza vaccination prevents laboratory-confirmed influenza–associated hospitalizations in community-dwelling older patients with COPD. They chose this design because it attenuates biases resulting from misclassification of infection and from differences in health care–seeking behavior between vaccinated and unvaccinated patients.

Dr. Gershon and colleagues examined health care administrative data and respiratory specimens collected from patients who had been tested for influenza during the 2010-2011 to 2015-2016 influenza seasons. Eligible patients were aged 66 years or older, had physician-diagnosed COPD, and had been tested for influenza within 3 days before and during an acute care hospitalization. The researchers determined influenza vaccination status using physician and pharmacist billing claims. They obtained demographic information through linkage with the provincial health insurance database. Multivariable logistic regression allowed Dr. Gershon and colleagues to estimate the adjusted odds ratio of influenza vaccination in people with laboratory-confirmed influenza, compared with those without.
 

Effectiveness did not vary by demographic factors

The investigators included 21,748 patients in their analysis. Of this population, 3,636 (16.7%) patients tested positive for influenza. Vaccinated patients were less likely than unvaccinated patients to test positive for influenza (15.3% vs. 18.6%). Vaccinated patients also were more likely to be older; live in an urban area; live in a higher income neighborhood; have had more outpatient visits with a physician in the previous year; have received a prescription for a COPD medication in the previous 6 months; have diabetes, asthma, or immunocompromising conditions; have a longer duration of COPD; and have had an outpatient COPD exacerbation in the previous year.

The overall unadjusted estimate of vaccine effectiveness against laboratory-confirmed influenza–associated hospitalizations was 21%. Multivariable adjustment yielded an effectiveness of 22%. When Dr. Gershon and colleagues corrected for misclassification of vaccination status among people with COPD, the effectiveness was estimated to be 43%. Vaccine effectiveness did not vary significantly according to influenza season, nor did it vary significantly by patient-specific factors such as age, sex, influenza subtype, codiagnosis of asthma, duration of COPD, previous outpatient COPD exacerbations, previous COPD hospitalization, previous receipt of inhaled corticosteroids, and previous pneumonia.

One limitation of the study was the possibility that COPD was misclassified because not all participants underwent pulmonary function testing. In addition, the estimates of vaccine effectiveness in the present study are specific to the outcome of influenza hospitalization and may not be generalizable to vaccine effectiveness estimates of outpatient outcomes, said the investigators. Finally, Dr. Gershon and colleagues could not identify the type of vaccine received.

“Given that a large pragmatic randomized controlled trial evaluating influenza vaccination would be unethical, this is likely the most robust estimate of vaccine effectiveness for hospitalizations in the COPD population to guide influenza vaccine recommendations for patients with COPD,” wrote Dr. Gershon and colleagues.

An Ontario Ministry of Health and Long-Term Care Health Systems Research Fund Capacity Grant and a Canadian Institutes of Health Research operating grant funded this research. One investigator received grants from the Canadian Institutes of Health Research during the study, and others received grants from pharmaceutical companies that were unrelated to this study.

[email protected]

SOURCE: Gershon AS et al. J Infect Dis. 2019 Sep 24. doi: 10.1093/infdis/jiz419.

Influenza vaccination modestly reduces the risk of hospitalizations associated with laboratory-confirmed influenza in people with chronic obstructive pulmonary disease (COPD), according to data published in the Journal of Infectious Diseases.

Cynthia Goldsmith/CDC photo #10073

“To the best of our knowledge, this is the first large, real-world population study to examine vaccine effectiveness in people with COPD using the test-negative design and influenza-specific study outcomes,” wrote Andrea S. Gershon, MD, of Sunnybrook Health Sciences Center in Toronto and colleagues. “These findings emphasize the need for more effective influenza vaccines for older COPD patients and other preventive strategies.”
 

A test-negative study design

Data suggest that 70% of COPD exacerbations are caused by infection, and influenza often is identified as the cause. Although all major COPD practice guidelines recommend seasonal influenza vaccination, the evidence indicating that vaccination reduces hospitalizations and death is limited. The inherent or corticosteroid-induced decrease in immune response to vaccination and respiratory infection among patients with COPD may reduce the effectiveness of influenza vaccination, wrote Dr. Gershon and colleagues.

The investigators used a test-negative design to evaluate how effectively influenza vaccination prevents laboratory-confirmed influenza–associated hospitalizations in community-dwelling older patients with COPD. They chose this design because it attenuates biases resulting from misclassification of infection and from differences in health care–seeking behavior between vaccinated and unvaccinated patients.

Dr. Gershon and colleagues examined health care administrative data and respiratory specimens collected from patients who had been tested for influenza during the 2010-2011 to 2015-2016 influenza seasons. Eligible patients were aged 66 years or older, had physician-diagnosed COPD, and had been tested for influenza within 3 days before and during an acute care hospitalization. The researchers determined influenza vaccination status using physician and pharmacist billing claims. They obtained demographic information through linkage with the provincial health insurance database. Multivariable logistic regression allowed Dr. Gershon and colleagues to estimate the adjusted odds ratio of influenza vaccination in people with laboratory-confirmed influenza, compared with those without.
 

Effectiveness did not vary by demographic factors

The investigators included 21,748 patients in their analysis. Of this population, 3,636 (16.7%) patients tested positive for influenza. Vaccinated patients were less likely than unvaccinated patients to test positive for influenza (15.3% vs. 18.6%). Vaccinated patients also were more likely to be older; live in an urban area; live in a higher income neighborhood; have had more outpatient visits with a physician in the previous year; have received a prescription for a COPD medication in the previous 6 months; have diabetes, asthma, or immunocompromising conditions; have a longer duration of COPD; and have had an outpatient COPD exacerbation in the previous year.

The overall unadjusted estimate of vaccine effectiveness against laboratory-confirmed influenza–associated hospitalizations was 21%. Multivariable adjustment yielded an effectiveness of 22%. When Dr. Gershon and colleagues corrected for misclassification of vaccination status among people with COPD, the effectiveness was estimated to be 43%. Vaccine effectiveness did not vary significantly according to influenza season, nor did it vary significantly by patient-specific factors such as age, sex, influenza subtype, codiagnosis of asthma, duration of COPD, previous outpatient COPD exacerbations, previous COPD hospitalization, previous receipt of inhaled corticosteroids, and previous pneumonia.

One limitation of the study was the possibility that COPD was misclassified because not all participants underwent pulmonary function testing. In addition, the estimates of vaccine effectiveness in the present study are specific to the outcome of influenza hospitalization and may not be generalizable to vaccine effectiveness estimates of outpatient outcomes, said the investigators. Finally, Dr. Gershon and colleagues could not identify the type of vaccine received.

“Given that a large pragmatic randomized controlled trial evaluating influenza vaccination would be unethical, this is likely the most robust estimate of vaccine effectiveness for hospitalizations in the COPD population to guide influenza vaccine recommendations for patients with COPD,” wrote Dr. Gershon and colleagues.

An Ontario Ministry of Health and Long-Term Care Health Systems Research Fund Capacity Grant and a Canadian Institutes of Health Research operating grant funded this research. One investigator received grants from the Canadian Institutes of Health Research during the study, and others received grants from pharmaceutical companies that were unrelated to this study.

[email protected]

SOURCE: Gershon AS et al. J Infect Dis. 2019 Sep 24. doi: 10.1093/infdis/jiz419.

Influenza vaccination modestly reduces the risk of hospitalizations associated with laboratory-confirmed influenza in people with chronic obstructive pulmonary disease (COPD), according to data published in the Journal of Infectious Diseases.

Cynthia Goldsmith/CDC photo #10073

“To the best of our knowledge, this is the first large, real-world population study to examine vaccine effectiveness in people with COPD using the test-negative design and influenza-specific study outcomes,” wrote Andrea S. Gershon, MD, of Sunnybrook Health Sciences Center in Toronto and colleagues. “These findings emphasize the need for more effective influenza vaccines for older COPD patients and other preventive strategies.”
 

A test-negative study design

Data suggest that 70% of COPD exacerbations are caused by infection, and influenza often is identified as the cause. Although all major COPD practice guidelines recommend seasonal influenza vaccination, the evidence indicating that vaccination reduces hospitalizations and death is limited. The inherent or corticosteroid-induced decrease in immune response to vaccination and respiratory infection among patients with COPD may reduce the effectiveness of influenza vaccination, wrote Dr. Gershon and colleagues.

The investigators used a test-negative design to evaluate how effectively influenza vaccination prevents laboratory-confirmed influenza–associated hospitalizations in community-dwelling older patients with COPD. They chose this design because it attenuates biases resulting from misclassification of infection and from differences in health care–seeking behavior between vaccinated and unvaccinated patients.

Dr. Gershon and colleagues examined health care administrative data and respiratory specimens collected from patients who had been tested for influenza during the 2010-2011 to 2015-2016 influenza seasons. Eligible patients were aged 66 years or older, had physician-diagnosed COPD, and had been tested for influenza within 3 days before and during an acute care hospitalization. The researchers determined influenza vaccination status using physician and pharmacist billing claims. They obtained demographic information through linkage with the provincial health insurance database. Multivariable logistic regression allowed Dr. Gershon and colleagues to estimate the adjusted odds ratio of influenza vaccination in people with laboratory-confirmed influenza, compared with those without.
 

Effectiveness did not vary by demographic factors

The investigators included 21,748 patients in their analysis. Of this population, 3,636 (16.7%) patients tested positive for influenza. Vaccinated patients were less likely than unvaccinated patients to test positive for influenza (15.3% vs. 18.6%). Vaccinated patients also were more likely to be older; live in an urban area; live in a higher income neighborhood; have had more outpatient visits with a physician in the previous year; have received a prescription for a COPD medication in the previous 6 months; have diabetes, asthma, or immunocompromising conditions; have a longer duration of COPD; and have had an outpatient COPD exacerbation in the previous year.

The overall unadjusted estimate of vaccine effectiveness against laboratory-confirmed influenza–associated hospitalizations was 21%. Multivariable adjustment yielded an effectiveness of 22%. When Dr. Gershon and colleagues corrected for misclassification of vaccination status among people with COPD, the effectiveness was estimated to be 43%. Vaccine effectiveness did not vary significantly according to influenza season, nor did it vary significantly by patient-specific factors such as age, sex, influenza subtype, codiagnosis of asthma, duration of COPD, previous outpatient COPD exacerbations, previous COPD hospitalization, previous receipt of inhaled corticosteroids, and previous pneumonia.

One limitation of the study was the possibility that COPD was misclassified because not all participants underwent pulmonary function testing. In addition, the estimates of vaccine effectiveness in the present study are specific to the outcome of influenza hospitalization and may not be generalizable to vaccine effectiveness estimates of outpatient outcomes, said the investigators. Finally, Dr. Gershon and colleagues could not identify the type of vaccine received.

“Given that a large pragmatic randomized controlled trial evaluating influenza vaccination would be unethical, this is likely the most robust estimate of vaccine effectiveness for hospitalizations in the COPD population to guide influenza vaccine recommendations for patients with COPD,” wrote Dr. Gershon and colleagues.

An Ontario Ministry of Health and Long-Term Care Health Systems Research Fund Capacity Grant and a Canadian Institutes of Health Research operating grant funded this research. One investigator received grants from the Canadian Institutes of Health Research during the study, and others received grants from pharmaceutical companies that were unrelated to this study.

[email protected]

SOURCE: Gershon AS et al. J Infect Dis. 2019 Sep 24. doi: 10.1093/infdis/jiz419.