COPD

Use of inhaled corticosteroids may lower the risk of lung cancer in patients with chronic obstructive pulmonary disease, and continued use may also reduce lung cancer risk, recent research from the European Respiratory Journal has shown.

“The appropriate use of [inhaled corticosteroids] ICS in [chronic obstructive pulmonary disease] COPD patients is often debated and not all patients might benefit from the use of ICS. The clinical benefits and risk of use in an individual patient must be weighed by the physician,” wrote Adam J.N. Raymakers, MSc, PhD, of the University of British Columbia’s Collaboration for Outcomes Research and Evaluation (CORE), Vancouver, B.C., and colleagues.

“This study, however, indicates that potential benefits may accrue from ICS use in COPD patients in terms of reduced lung cancer risk, and that sustained use may be associated with reduced risk of lung cancer.”

Dr. Raymakers and colleagues did an analysis of 39,676 patients with COPD (mean age, 70.7 years; 53% female) who received ICS between 1997 and 2007 and linked those patients to a registry of cancer patients in British Columbia. The linked databases included the Medical Services Plan (MSP) payment information file, Discharge Abstract Database (DAD), PharmaNet data file, and the British Columbia Cancer Registry (BCCR). The researchers determined a patient had COPD if he or she received three or more prescriptions related to COPD, while ICS exposure was analyzed in the context of a patient’s ICS exposure, cumulative duration, cumulative dose, and weighted cumulative duration and dose.

The analysis revealed 372,075 prescriptions for ICS were dispensed and 71.2% of the patients were “distinct users” of ICS, with patients filling a median of eight prescriptions at mean 5.2 years of follow-up. Fluticasone propionate was the most common ICS prescribed at a dose of 0.64 mg per day, and patients had median 60 days of ICS supplied per person.

Overall, there were 994 cases of lung cancer (2.5%), and exposure to ICS was linked to a 30% reduction in lung cancer risk (hazard ratio, 0.70; 95% confidence interval, 0.61-0.80), while recency-weighted duration of ICS exposure was linked to a 26% reduction in lung cancer risk (HR, 0.74; 95% CI, 0.66-0.87). There was a 43% reduced risk of lung cancer per gram of ICS when the data were measured by recency-weighted cumulative dosage.

In a multivariate analysis, ICS use was associated with a 30% reduction in risk of non–small cell lung cancer (HR, 0.70; 95% CI, 0.60-0.82), which the researchers said suggests ICS provides a protective effect for patients against lung cancer. “These results highlight the importance of properly identifying which patients might be at the highest risk of lung cancer, to enhance the therapeutic benefits of ICS in these COPD patients,” they wrote.

This study received funding from the Canadian Institutes of Health Research. The authors report no conflicts of interest.

SOURCE: Raymakers A, et al. Eur Respir J. 2019. doi: 10.1183/13993003.01257-2018.

Use of inhaled corticosteroids may lower the risk of lung cancer in patients with chronic obstructive pulmonary disease, and continued use may also reduce lung cancer risk, recent research from the European Respiratory Journal has shown.

“The appropriate use of [inhaled corticosteroids] ICS in [chronic obstructive pulmonary disease] COPD patients is often debated and not all patients might benefit from the use of ICS. The clinical benefits and risk of use in an individual patient must be weighed by the physician,” wrote Adam J.N. Raymakers, MSc, PhD, of the University of British Columbia’s Collaboration for Outcomes Research and Evaluation (CORE), Vancouver, B.C., and colleagues.

“This study, however, indicates that potential benefits may accrue from ICS use in COPD patients in terms of reduced lung cancer risk, and that sustained use may be associated with reduced risk of lung cancer.”

Dr. Raymakers and colleagues did an analysis of 39,676 patients with COPD (mean age, 70.7 years; 53% female) who received ICS between 1997 and 2007 and linked those patients to a registry of cancer patients in British Columbia. The linked databases included the Medical Services Plan (MSP) payment information file, Discharge Abstract Database (DAD), PharmaNet data file, and the British Columbia Cancer Registry (BCCR). The researchers determined a patient had COPD if he or she received three or more prescriptions related to COPD, while ICS exposure was analyzed in the context of a patient’s ICS exposure, cumulative duration, cumulative dose, and weighted cumulative duration and dose.

The analysis revealed 372,075 prescriptions for ICS were dispensed and 71.2% of the patients were “distinct users” of ICS, with patients filling a median of eight prescriptions at mean 5.2 years of follow-up. Fluticasone propionate was the most common ICS prescribed at a dose of 0.64 mg per day, and patients had median 60 days of ICS supplied per person.

Overall, there were 994 cases of lung cancer (2.5%), and exposure to ICS was linked to a 30% reduction in lung cancer risk (hazard ratio, 0.70; 95% confidence interval, 0.61-0.80), while recency-weighted duration of ICS exposure was linked to a 26% reduction in lung cancer risk (HR, 0.74; 95% CI, 0.66-0.87). There was a 43% reduced risk of lung cancer per gram of ICS when the data were measured by recency-weighted cumulative dosage.

In a multivariate analysis, ICS use was associated with a 30% reduction in risk of non–small cell lung cancer (HR, 0.70; 95% CI, 0.60-0.82), which the researchers said suggests ICS provides a protective effect for patients against lung cancer. “These results highlight the importance of properly identifying which patients might be at the highest risk of lung cancer, to enhance the therapeutic benefits of ICS in these COPD patients,” they wrote.

This study received funding from the Canadian Institutes of Health Research. The authors report no conflicts of interest.

SOURCE: Raymakers A, et al. Eur Respir J. 2019. doi: 10.1183/13993003.01257-2018.

Use of inhaled corticosteroids may lower the risk of lung cancer in patients with chronic obstructive pulmonary disease, and continued use may also reduce lung cancer risk, recent research from the European Respiratory Journal has shown.

“The appropriate use of [inhaled corticosteroids] ICS in [chronic obstructive pulmonary disease] COPD patients is often debated and not all patients might benefit from the use of ICS. The clinical benefits and risk of use in an individual patient must be weighed by the physician,” wrote Adam J.N. Raymakers, MSc, PhD, of the University of British Columbia’s Collaboration for Outcomes Research and Evaluation (CORE), Vancouver, B.C., and colleagues.

“This study, however, indicates that potential benefits may accrue from ICS use in COPD patients in terms of reduced lung cancer risk, and that sustained use may be associated with reduced risk of lung cancer.”

Dr. Raymakers and colleagues did an analysis of 39,676 patients with COPD (mean age, 70.7 years; 53% female) who received ICS between 1997 and 2007 and linked those patients to a registry of cancer patients in British Columbia. The linked databases included the Medical Services Plan (MSP) payment information file, Discharge Abstract Database (DAD), PharmaNet data file, and the British Columbia Cancer Registry (BCCR). The researchers determined a patient had COPD if he or she received three or more prescriptions related to COPD, while ICS exposure was analyzed in the context of a patient’s ICS exposure, cumulative duration, cumulative dose, and weighted cumulative duration and dose.

The analysis revealed 372,075 prescriptions for ICS were dispensed and 71.2% of the patients were “distinct users” of ICS, with patients filling a median of eight prescriptions at mean 5.2 years of follow-up. Fluticasone propionate was the most common ICS prescribed at a dose of 0.64 mg per day, and patients had median 60 days of ICS supplied per person.

Overall, there were 994 cases of lung cancer (2.5%), and exposure to ICS was linked to a 30% reduction in lung cancer risk (hazard ratio, 0.70; 95% confidence interval, 0.61-0.80), while recency-weighted duration of ICS exposure was linked to a 26% reduction in lung cancer risk (HR, 0.74; 95% CI, 0.66-0.87). There was a 43% reduced risk of lung cancer per gram of ICS when the data were measured by recency-weighted cumulative dosage.

In a multivariate analysis, ICS use was associated with a 30% reduction in risk of non–small cell lung cancer (HR, 0.70; 95% CI, 0.60-0.82), which the researchers said suggests ICS provides a protective effect for patients against lung cancer. “These results highlight the importance of properly identifying which patients might be at the highest risk of lung cancer, to enhance the therapeutic benefits of ICS in these COPD patients,” they wrote.

This study received funding from the Canadian Institutes of Health Research. The authors report no conflicts of interest.

SOURCE: Raymakers A, et al. Eur Respir J. 2019. doi: 10.1183/13993003.01257-2018.

Chronic obstructive pulmonary disease (COPD) prevalence among adults is strongly correlated with their state’s current smoking prevalence, according to a Centers for Disease Control and Prevention analysis of respondents to a behavioral risk factor survey.

“Population-based strategies for smoking prevention and control have the potential to decrease the prevalence of COPD in the United States,” wrote Anne G. Wheaton, PhD, of the CDC’s National Center for Chronic Disease Prevention and Health Promotion and coauthors. The study was published in the Morbidity and Mortality Weekly Report.

Dr. Wheaton and her fellow researchers analyzed data from 418,378 adult respondents to the 2017 Behavioral Risk Factor Surveillance System survey. Responses came from all 50 states and Washington, D.C.; respondents who had smoked less than 100 lifetime cigarettes were categorized as “never smoked,” while those who had smoked at least 100 cigarettes but no longer smoked were categorized as “former smokers.” Anyone who had smoked at least 100 cigarettes and currently smoked was categorized as a “current smoker.”

The age-adjusted prevalence of COPD among U.S. adults was 6.2% (95% confidence interval, 6.0%-6.3%) in 2017. Current cigarette smokers had a prevalence of 15.2% (95% CI, 14.7%-15.7%); this dipped to 7.6% (95% CI, 7.3%-8.0%) among former smokers and 2.8% (95% CI, 2.7%-2.9%) among adults who had never smoked. Patterns were visible within states: Current smokers had a state-level prevalence of COPD that was strongly correlated with state-level current smoking prevalence (Pearson correlation coefficient, 0.69; P less than .001). State-level COPD prevalence among former smokers (Pearson correlation coefficient, 0.71; P less than .001) and those who never smoked (Pearson correlation coefficient, 0.64; P less than .001) were also strongly correlated with the current smoking prevalence, indicating secondhand smoke as a risk factor for COPD.

The coauthors acknowledged the study’s limitations, including relying on self-reporting for both COPD and smoking status. They also noted that there was no way to measure exposure to secondhand smoke, other indoor or outdoor air pollutants, or respiratory infection history, “all of which might contribute to COPD risk.”

No conflicts of interest were reported.

SOURCE: Wheaton AG et al. MMWR Morb Mortal Wkly Rep. 2019 Jun 21;68(24):533-8.

Chronic obstructive pulmonary disease (COPD) prevalence among adults is strongly correlated with their state’s current smoking prevalence, according to a Centers for Disease Control and Prevention analysis of respondents to a behavioral risk factor survey.

“Population-based strategies for smoking prevention and control have the potential to decrease the prevalence of COPD in the United States,” wrote Anne G. Wheaton, PhD, of the CDC’s National Center for Chronic Disease Prevention and Health Promotion and coauthors. The study was published in the Morbidity and Mortality Weekly Report.

Dr. Wheaton and her fellow researchers analyzed data from 418,378 adult respondents to the 2017 Behavioral Risk Factor Surveillance System survey. Responses came from all 50 states and Washington, D.C.; respondents who had smoked less than 100 lifetime cigarettes were categorized as “never smoked,” while those who had smoked at least 100 cigarettes but no longer smoked were categorized as “former smokers.” Anyone who had smoked at least 100 cigarettes and currently smoked was categorized as a “current smoker.”

The age-adjusted prevalence of COPD among U.S. adults was 6.2% (95% confidence interval, 6.0%-6.3%) in 2017. Current cigarette smokers had a prevalence of 15.2% (95% CI, 14.7%-15.7%); this dipped to 7.6% (95% CI, 7.3%-8.0%) among former smokers and 2.8% (95% CI, 2.7%-2.9%) among adults who had never smoked. Patterns were visible within states: Current smokers had a state-level prevalence of COPD that was strongly correlated with state-level current smoking prevalence (Pearson correlation coefficient, 0.69; P less than .001). State-level COPD prevalence among former smokers (Pearson correlation coefficient, 0.71; P less than .001) and those who never smoked (Pearson correlation coefficient, 0.64; P less than .001) were also strongly correlated with the current smoking prevalence, indicating secondhand smoke as a risk factor for COPD.

The coauthors acknowledged the study’s limitations, including relying on self-reporting for both COPD and smoking status. They also noted that there was no way to measure exposure to secondhand smoke, other indoor or outdoor air pollutants, or respiratory infection history, “all of which might contribute to COPD risk.”

No conflicts of interest were reported.

SOURCE: Wheaton AG et al. MMWR Morb Mortal Wkly Rep. 2019 Jun 21;68(24):533-8.

Chronic obstructive pulmonary disease (COPD) prevalence among adults is strongly correlated with their state’s current smoking prevalence, according to a Centers for Disease Control and Prevention analysis of respondents to a behavioral risk factor survey.

“Population-based strategies for smoking prevention and control have the potential to decrease the prevalence of COPD in the United States,” wrote Anne G. Wheaton, PhD, of the CDC’s National Center for Chronic Disease Prevention and Health Promotion and coauthors. The study was published in the Morbidity and Mortality Weekly Report.

Dr. Wheaton and her fellow researchers analyzed data from 418,378 adult respondents to the 2017 Behavioral Risk Factor Surveillance System survey. Responses came from all 50 states and Washington, D.C.; respondents who had smoked less than 100 lifetime cigarettes were categorized as “never smoked,” while those who had smoked at least 100 cigarettes but no longer smoked were categorized as “former smokers.” Anyone who had smoked at least 100 cigarettes and currently smoked was categorized as a “current smoker.”

The age-adjusted prevalence of COPD among U.S. adults was 6.2% (95% confidence interval, 6.0%-6.3%) in 2017. Current cigarette smokers had a prevalence of 15.2% (95% CI, 14.7%-15.7%); this dipped to 7.6% (95% CI, 7.3%-8.0%) among former smokers and 2.8% (95% CI, 2.7%-2.9%) among adults who had never smoked. Patterns were visible within states: Current smokers had a state-level prevalence of COPD that was strongly correlated with state-level current smoking prevalence (Pearson correlation coefficient, 0.69; P less than .001). State-level COPD prevalence among former smokers (Pearson correlation coefficient, 0.71; P less than .001) and those who never smoked (Pearson correlation coefficient, 0.64; P less than .001) were also strongly correlated with the current smoking prevalence, indicating secondhand smoke as a risk factor for COPD.

The coauthors acknowledged the study’s limitations, including relying on self-reporting for both COPD and smoking status. They also noted that there was no way to measure exposure to secondhand smoke, other indoor or outdoor air pollutants, or respiratory infection history, “all of which might contribute to COPD risk.”

No conflicts of interest were reported.

SOURCE: Wheaton AG et al. MMWR Morb Mortal Wkly Rep. 2019 Jun 21;68(24):533-8.

SAN ANTONIO – People who smoke and have opioid use disorder have a lower likelihood of drug use several months after initiating smoking cessation treatment if they are treated with nicotine replacement therapy rather than varenicline, new research suggests.

“Differences were not due to the pretreatment differences in drug use, which were covaried,” wrote Damaris J. Rohsenow, PhD, and colleagues at Brown University’s Center for Alcohol and Addiction Studies, Providence, R.I. “Results suggest it may be preferable to offer smokers with opioid use disorder [nicotine replacement therapy] rather than varenicline, given their lower adherence and more illicit drug use days during follow-up when given varenicline compared to [nicotine replacement therapy].”

They shared their research poster at the annual meeting of the College on Problems of Drug Dependence.

About 80%-90% of patients with OUD smoke, and those patients have a particularly difficult time with smoking cessation partly because of nonadherence to cessation medications, the authors noted. Smoking increases the risk of relapse from any substance use disorder, and pain – frequently comorbid with smoking – contributes to opioid use, they added.

Though smoking treatment has been shown not to increase drug or alcohol use, varenicline and nicotine replacement therapy have different effects on a4b2 nicotinic acetylcholinergic receptors (nAChRs). The authors noted that nicotine offers greater pain inhibition via full agonist effects across multiple nAChRs, whereas varenicline has only a partial agonist effect on a single nAChR.

“Smokers may receive more rewarding dopamine effects from the full nicotine agonist,” they wrote. The researchers therefore aimed to compare responses to nicotine replacement therapy and varenicline among smokers with and without OUD.

Ninety patients without OUD and 47 patients with it were randomly assigned to receive transdermal nicotine replacement therapy with placebo capsules or varenicline capsules with a placebo patch for 12 weeks with 3- and 6-month follow-ups. At baseline, those with OUD were significantly more likely to be white and slightly younger and have twice as many drug use days than those without the disorder.

Differences also existed between those with and without OUD for comorbid alcohol use disorder (55% vs. 81%), marijuana use disorder (32% vs. 19%) and cocaine use disorder (70% vs. 55%).

Those without OUD had slightly greater medication adherence, but with only borderline significance just among those taking varenicline. Loss to follow-up, meanwhile, was significantly greater for those with OUD in both treatment groups.

Most striking was the significantly higher number of drug use days among those with OUD who took varenicline vs. all other groups. Those patients had 16.5 drug use days at 4-6 months’ follow-up, compared with 0.13 days among those with OUD using nicotine replacement therapy (P less than .026). Among those without OUD, nicotine replacement therapy patients had 5 drug use days, and varenicline patients had 2.5 drug use days.

“Given interactions between nicotine and the opioid system and given that [nicotine replacement therapy] binds to more types of nAChRs than varenicline does, it is possible that [nicotine replacement therapy] dampens desire to use opiates compared to varenicline by stimulating more nAChRs,” the authors wrote. “Increasing nicotine dose may be better for smokers with opioid use disorder,” they added, though they noted the small size of the study and the need for replication with larger populations.

The research was funded by the National Institute on Drug Abuse and the Department of Veterans Affairs. The authors reported no disclosures.

SAN ANTONIO – People who smoke and have opioid use disorder have a lower likelihood of drug use several months after initiating smoking cessation treatment if they are treated with nicotine replacement therapy rather than varenicline, new research suggests.

“Differences were not due to the pretreatment differences in drug use, which were covaried,” wrote Damaris J. Rohsenow, PhD, and colleagues at Brown University’s Center for Alcohol and Addiction Studies, Providence, R.I. “Results suggest it may be preferable to offer smokers with opioid use disorder [nicotine replacement therapy] rather than varenicline, given their lower adherence and more illicit drug use days during follow-up when given varenicline compared to [nicotine replacement therapy].”

They shared their research poster at the annual meeting of the College on Problems of Drug Dependence.

About 80%-90% of patients with OUD smoke, and those patients have a particularly difficult time with smoking cessation partly because of nonadherence to cessation medications, the authors noted. Smoking increases the risk of relapse from any substance use disorder, and pain – frequently comorbid with smoking – contributes to opioid use, they added.

Though smoking treatment has been shown not to increase drug or alcohol use, varenicline and nicotine replacement therapy have different effects on a4b2 nicotinic acetylcholinergic receptors (nAChRs). The authors noted that nicotine offers greater pain inhibition via full agonist effects across multiple nAChRs, whereas varenicline has only a partial agonist effect on a single nAChR.

“Smokers may receive more rewarding dopamine effects from the full nicotine agonist,” they wrote. The researchers therefore aimed to compare responses to nicotine replacement therapy and varenicline among smokers with and without OUD.

Ninety patients without OUD and 47 patients with it were randomly assigned to receive transdermal nicotine replacement therapy with placebo capsules or varenicline capsules with a placebo patch for 12 weeks with 3- and 6-month follow-ups. At baseline, those with OUD were significantly more likely to be white and slightly younger and have twice as many drug use days than those without the disorder.

Differences also existed between those with and without OUD for comorbid alcohol use disorder (55% vs. 81%), marijuana use disorder (32% vs. 19%) and cocaine use disorder (70% vs. 55%).

Those without OUD had slightly greater medication adherence, but with only borderline significance just among those taking varenicline. Loss to follow-up, meanwhile, was significantly greater for those with OUD in both treatment groups.

Most striking was the significantly higher number of drug use days among those with OUD who took varenicline vs. all other groups. Those patients had 16.5 drug use days at 4-6 months’ follow-up, compared with 0.13 days among those with OUD using nicotine replacement therapy (P less than .026). Among those without OUD, nicotine replacement therapy patients had 5 drug use days, and varenicline patients had 2.5 drug use days.

“Given interactions between nicotine and the opioid system and given that [nicotine replacement therapy] binds to more types of nAChRs than varenicline does, it is possible that [nicotine replacement therapy] dampens desire to use opiates compared to varenicline by stimulating more nAChRs,” the authors wrote. “Increasing nicotine dose may be better for smokers with opioid use disorder,” they added, though they noted the small size of the study and the need for replication with larger populations.

The research was funded by the National Institute on Drug Abuse and the Department of Veterans Affairs. The authors reported no disclosures.

SAN ANTONIO – People who smoke and have opioid use disorder have a lower likelihood of drug use several months after initiating smoking cessation treatment if they are treated with nicotine replacement therapy rather than varenicline, new research suggests.

“Differences were not due to the pretreatment differences in drug use, which were covaried,” wrote Damaris J. Rohsenow, PhD, and colleagues at Brown University’s Center for Alcohol and Addiction Studies, Providence, R.I. “Results suggest it may be preferable to offer smokers with opioid use disorder [nicotine replacement therapy] rather than varenicline, given their lower adherence and more illicit drug use days during follow-up when given varenicline compared to [nicotine replacement therapy].”

They shared their research poster at the annual meeting of the College on Problems of Drug Dependence.

About 80%-90% of patients with OUD smoke, and those patients have a particularly difficult time with smoking cessation partly because of nonadherence to cessation medications, the authors noted. Smoking increases the risk of relapse from any substance use disorder, and pain – frequently comorbid with smoking – contributes to opioid use, they added.

Though smoking treatment has been shown not to increase drug or alcohol use, varenicline and nicotine replacement therapy have different effects on a4b2 nicotinic acetylcholinergic receptors (nAChRs). The authors noted that nicotine offers greater pain inhibition via full agonist effects across multiple nAChRs, whereas varenicline has only a partial agonist effect on a single nAChR.

“Smokers may receive more rewarding dopamine effects from the full nicotine agonist,” they wrote. The researchers therefore aimed to compare responses to nicotine replacement therapy and varenicline among smokers with and without OUD.

Ninety patients without OUD and 47 patients with it were randomly assigned to receive transdermal nicotine replacement therapy with placebo capsules or varenicline capsules with a placebo patch for 12 weeks with 3- and 6-month follow-ups. At baseline, those with OUD were significantly more likely to be white and slightly younger and have twice as many drug use days than those without the disorder.

Differences also existed between those with and without OUD for comorbid alcohol use disorder (55% vs. 81%), marijuana use disorder (32% vs. 19%) and cocaine use disorder (70% vs. 55%).

Those without OUD had slightly greater medication adherence, but with only borderline significance just among those taking varenicline. Loss to follow-up, meanwhile, was significantly greater for those with OUD in both treatment groups.

Most striking was the significantly higher number of drug use days among those with OUD who took varenicline vs. all other groups. Those patients had 16.5 drug use days at 4-6 months’ follow-up, compared with 0.13 days among those with OUD using nicotine replacement therapy (P less than .026). Among those without OUD, nicotine replacement therapy patients had 5 drug use days, and varenicline patients had 2.5 drug use days.

“Given interactions between nicotine and the opioid system and given that [nicotine replacement therapy] binds to more types of nAChRs than varenicline does, it is possible that [nicotine replacement therapy] dampens desire to use opiates compared to varenicline by stimulating more nAChRs,” the authors wrote. “Increasing nicotine dose may be better for smokers with opioid use disorder,” they added, though they noted the small size of the study and the need for replication with larger populations.

The research was funded by the National Institute on Drug Abuse and the Department of Veterans Affairs. The authors reported no disclosures.

Poor subjective sleep quality was associated with subsequent symptomatic exacerbations of chronic obstructive pulmonary disease in an 18-month prospective study of 480 patients.

©marcociannarel/Thinkstock

“Poor sleep quality in COPD has previously been associated with reduced health-related quality of life and reduced physical activity during the day,” wrote Matthew Shorofsky, MD, of McGill University, Montreal, and associates. Their report is in CHEST. “However, to our knowledge, this is the first population-based longitudinal study evaluating exacerbation risk in relation to subjective sleep disturbances and assessing previously diagnosed and undiagnosed COPD.”

The study included participants enrolled in the Canadian Respiratory Research Network and the Canadian Cohort Obstructive Lung Disease (CanCOLD) study who had COPD, available baseline PSQI scores, and 18 months of follow-up data. The PSQI includes 19 questions on sleep quality, latency, duration, efficiency, disturbances, use of sleep medications, and daytime dysfunction. Total score ranges between 0 and 21, and a score above 5 is considered poor sleep. Online patient surveys and quarterly phone interviews were used to track symptom-based exacerbations (at least 48 hours of increased dyspnea, sputum volume, or sputum purulence) and event-based exacerbations (a symptom-based exacerbation plus the use antibiotics or corticosteroids or health services).

At baseline, 203 patients met the PSQI threshold for poor sleep quality. During follow-up, 185 patients had at least one COPD exacerbation. Poor sleep at baseline was significantly more prevalent among patients with symptoms-based COPD exacerbations (50.3%) than among patients without symptoms-based exacerbations (37.3%; P = .01). Poor baseline sleep quality remained a significant risk factor for symptom-based exacerbations of COPD even after the researchers accounted for the effect of age, gender, body mass index, smoking, depression, angina, baseline inhaled respiratory medications, forced expiratory volume in 1 second %predicted, and modified Medical Research Council (mMRC) dyspnea scale (adjusted risk ratio, 1.09; 95% confidence interval, 1.01-1.18; P =.02).

Patients with at least one symptomatic exacerbation of COPD were significantly more likely to meet the threshold for poor sleep quality on the Pittsburgh Sleep Quality Index and have significantly higher median PSQI scores compared with patients without exacerbations (6.0 [interquartile range, 3.0 to 8.0] vs. 5.0 [2.0 to 7.0]; P = .01). Poor baseline sleep quality also was associated with event-based exacerbations and with a shorter time to symptoms-based exacerbations. Sleep disturbances, such as rising to void or experiencing respiratory issues or pain during sleep, correlated most strongly with symptoms-based exacerbations.

Several factors could explain the link between poor sleep quality and COPD exacerbations, the investigators wrote. Patients with inadequately controlled COPD have more frequent and unstable respiratory symptoms, which could disrupt sleep either directly or indirectly (secondary to medication use or anxiety, for example). Conversely, sleep disruption can impede immune function and increase systemic inflammation, which might worsen COPD control and increase exacerbation risk. Poor sleep can impair memory and cognition, “potentially fostering medication nonadherence and symptom flare-up, especially in the older COPD population.” Although the link is poorly understood, patients with COPD often have comorbid obstructive sleep apnea (OSA), which is associated with COPD exacerbations, the researchers wrote. Treating OSA is associated with improved COPD morbidity and fewer exacerbations and hospitalizations.

The researchers acknowledged limitations to their study design. “Individuals with asthma or other obstructive lung diseases could not be definitively excluded; methacholine challenges were not performed. However, analyses excluding self-reported asthma were consistent with our main results. Second, because definitions of COPD exacerbation vary among studies, comparison may be limited, but CanCOLD used a standard definition, as recommended by GOLD.”

The CanCOLD study has received funding from the Canadian Respiratory Research Network, Astra Zeneca Canada, Boehringer Ingelheim Canada, GlaxoSmithKline Canada, Novartis, Merck Nycomed, Pfizer Canada, and Theratechnologies. Dr. Shorofsky had no disclosures. Several coinvestigators reported ties to GlaxoSmithKline, Novartis, Boehringer Ingelheim, Merck, Almirall, and Theratechnologies.

SOURCE: Shorofsky M et al. CHEST. 2019 May 28. doi: 10.1016/j.chest.2019.04.132.

Poor subjective sleep quality was associated with subsequent symptomatic exacerbations of chronic obstructive pulmonary disease in an 18-month prospective study of 480 patients.

©marcociannarel/Thinkstock

“Poor sleep quality in COPD has previously been associated with reduced health-related quality of life and reduced physical activity during the day,” wrote Matthew Shorofsky, MD, of McGill University, Montreal, and associates. Their report is in CHEST. “However, to our knowledge, this is the first population-based longitudinal study evaluating exacerbation risk in relation to subjective sleep disturbances and assessing previously diagnosed and undiagnosed COPD.”

The study included participants enrolled in the Canadian Respiratory Research Network and the Canadian Cohort Obstructive Lung Disease (CanCOLD) study who had COPD, available baseline PSQI scores, and 18 months of follow-up data. The PSQI includes 19 questions on sleep quality, latency, duration, efficiency, disturbances, use of sleep medications, and daytime dysfunction. Total score ranges between 0 and 21, and a score above 5 is considered poor sleep. Online patient surveys and quarterly phone interviews were used to track symptom-based exacerbations (at least 48 hours of increased dyspnea, sputum volume, or sputum purulence) and event-based exacerbations (a symptom-based exacerbation plus the use antibiotics or corticosteroids or health services).

At baseline, 203 patients met the PSQI threshold for poor sleep quality. During follow-up, 185 patients had at least one COPD exacerbation. Poor sleep at baseline was significantly more prevalent among patients with symptoms-based COPD exacerbations (50.3%) than among patients without symptoms-based exacerbations (37.3%; P = .01). Poor baseline sleep quality remained a significant risk factor for symptom-based exacerbations of COPD even after the researchers accounted for the effect of age, gender, body mass index, smoking, depression, angina, baseline inhaled respiratory medications, forced expiratory volume in 1 second %predicted, and modified Medical Research Council (mMRC) dyspnea scale (adjusted risk ratio, 1.09; 95% confidence interval, 1.01-1.18; P =.02).

Patients with at least one symptomatic exacerbation of COPD were significantly more likely to meet the threshold for poor sleep quality on the Pittsburgh Sleep Quality Index and have significantly higher median PSQI scores compared with patients without exacerbations (6.0 [interquartile range, 3.0 to 8.0] vs. 5.0 [2.0 to 7.0]; P = .01). Poor baseline sleep quality also was associated with event-based exacerbations and with a shorter time to symptoms-based exacerbations. Sleep disturbances, such as rising to void or experiencing respiratory issues or pain during sleep, correlated most strongly with symptoms-based exacerbations.

Several factors could explain the link between poor sleep quality and COPD exacerbations, the investigators wrote. Patients with inadequately controlled COPD have more frequent and unstable respiratory symptoms, which could disrupt sleep either directly or indirectly (secondary to medication use or anxiety, for example). Conversely, sleep disruption can impede immune function and increase systemic inflammation, which might worsen COPD control and increase exacerbation risk. Poor sleep can impair memory and cognition, “potentially fostering medication nonadherence and symptom flare-up, especially in the older COPD population.” Although the link is poorly understood, patients with COPD often have comorbid obstructive sleep apnea (OSA), which is associated with COPD exacerbations, the researchers wrote. Treating OSA is associated with improved COPD morbidity and fewer exacerbations and hospitalizations.

The researchers acknowledged limitations to their study design. “Individuals with asthma or other obstructive lung diseases could not be definitively excluded; methacholine challenges were not performed. However, analyses excluding self-reported asthma were consistent with our main results. Second, because definitions of COPD exacerbation vary among studies, comparison may be limited, but CanCOLD used a standard definition, as recommended by GOLD.”

The CanCOLD study has received funding from the Canadian Respiratory Research Network, Astra Zeneca Canada, Boehringer Ingelheim Canada, GlaxoSmithKline Canada, Novartis, Merck Nycomed, Pfizer Canada, and Theratechnologies. Dr. Shorofsky had no disclosures. Several coinvestigators reported ties to GlaxoSmithKline, Novartis, Boehringer Ingelheim, Merck, Almirall, and Theratechnologies.

SOURCE: Shorofsky M et al. CHEST. 2019 May 28. doi: 10.1016/j.chest.2019.04.132.

Poor subjective sleep quality was associated with subsequent symptomatic exacerbations of chronic obstructive pulmonary disease in an 18-month prospective study of 480 patients.

©marcociannarel/Thinkstock

“Poor sleep quality in COPD has previously been associated with reduced health-related quality of life and reduced physical activity during the day,” wrote Matthew Shorofsky, MD, of McGill University, Montreal, and associates. Their report is in CHEST. “However, to our knowledge, this is the first population-based longitudinal study evaluating exacerbation risk in relation to subjective sleep disturbances and assessing previously diagnosed and undiagnosed COPD.”

The study included participants enrolled in the Canadian Respiratory Research Network and the Canadian Cohort Obstructive Lung Disease (CanCOLD) study who had COPD, available baseline PSQI scores, and 18 months of follow-up data. The PSQI includes 19 questions on sleep quality, latency, duration, efficiency, disturbances, use of sleep medications, and daytime dysfunction. Total score ranges between 0 and 21, and a score above 5 is considered poor sleep. Online patient surveys and quarterly phone interviews were used to track symptom-based exacerbations (at least 48 hours of increased dyspnea, sputum volume, or sputum purulence) and event-based exacerbations (a symptom-based exacerbation plus the use antibiotics or corticosteroids or health services).

At baseline, 203 patients met the PSQI threshold for poor sleep quality. During follow-up, 185 patients had at least one COPD exacerbation. Poor sleep at baseline was significantly more prevalent among patients with symptoms-based COPD exacerbations (50.3%) than among patients without symptoms-based exacerbations (37.3%; P = .01). Poor baseline sleep quality remained a significant risk factor for symptom-based exacerbations of COPD even after the researchers accounted for the effect of age, gender, body mass index, smoking, depression, angina, baseline inhaled respiratory medications, forced expiratory volume in 1 second %predicted, and modified Medical Research Council (mMRC) dyspnea scale (adjusted risk ratio, 1.09; 95% confidence interval, 1.01-1.18; P =.02).

Patients with at least one symptomatic exacerbation of COPD were significantly more likely to meet the threshold for poor sleep quality on the Pittsburgh Sleep Quality Index and have significantly higher median PSQI scores compared with patients without exacerbations (6.0 [interquartile range, 3.0 to 8.0] vs. 5.0 [2.0 to 7.0]; P = .01). Poor baseline sleep quality also was associated with event-based exacerbations and with a shorter time to symptoms-based exacerbations. Sleep disturbances, such as rising to void or experiencing respiratory issues or pain during sleep, correlated most strongly with symptoms-based exacerbations.

Several factors could explain the link between poor sleep quality and COPD exacerbations, the investigators wrote. Patients with inadequately controlled COPD have more frequent and unstable respiratory symptoms, which could disrupt sleep either directly or indirectly (secondary to medication use or anxiety, for example). Conversely, sleep disruption can impede immune function and increase systemic inflammation, which might worsen COPD control and increase exacerbation risk. Poor sleep can impair memory and cognition, “potentially fostering medication nonadherence and symptom flare-up, especially in the older COPD population.” Although the link is poorly understood, patients with COPD often have comorbid obstructive sleep apnea (OSA), which is associated with COPD exacerbations, the researchers wrote. Treating OSA is associated with improved COPD morbidity and fewer exacerbations and hospitalizations.

The researchers acknowledged limitations to their study design. “Individuals with asthma or other obstructive lung diseases could not be definitively excluded; methacholine challenges were not performed. However, analyses excluding self-reported asthma were consistent with our main results. Second, because definitions of COPD exacerbation vary among studies, comparison may be limited, but CanCOLD used a standard definition, as recommended by GOLD.”

The CanCOLD study has received funding from the Canadian Respiratory Research Network, Astra Zeneca Canada, Boehringer Ingelheim Canada, GlaxoSmithKline Canada, Novartis, Merck Nycomed, Pfizer Canada, and Theratechnologies. Dr. Shorofsky had no disclosures. Several coinvestigators reported ties to GlaxoSmithKline, Novartis, Boehringer Ingelheim, Merck, Almirall, and Theratechnologies.

SOURCE: Shorofsky M et al. CHEST. 2019 May 28. doi: 10.1016/j.chest.2019.04.132.

Using eosinophil levels to guide steroid treatment in patients with chronic obstructive pulmonary disease (COPD) was found to be noninferior to standard treatment in terms of the number of days out of hospital and alive, new research has found.

Writing in the Lancet Respiratory Medicine, researchers reported the outcomes of a multicenter, controlled, open-label trial comparing eosinophil-guided and standard therapy with systemic corticosteroids in 318 patients with COPD.

Pradeesh Sivapalan, MD, of the respiratory medicine section of Herlev and Gentofte Hospital at the University of Copenhagen, and coauthors wrote that eosinophilic inflammation had been seen in 20%-40% of patients with acute exacerbations of COPD. Patients with higher eosinophilic blood counts were at increased risk of acute exacerbations but were also more likely to benefit from corticosteroid treatment.

In the eosinophil-guided therapy arm of the study, 159 patients received 80 mg of intravenous methylprednisolone on day 1, then from the second day were treated with 37.5 mg of prednisolone oral tablet daily ­– up to 4 days – only on days when their blood eosinophil count was at least 0.3 x 10^⁹ cells/L. In the control arm, 159 patients also received 80 mg of intravenous methylprednisolone on day 1, followed by 37.5 mg of prednisolone tablets daily for 4 days.

After 14 days, there were no significant differences between the two groups for mean days alive and out of hospital.

There were 12 more cases of readmission with COPD, including three fatalities, in the eosinophil-guided group within the first month. However the authors said these differences were not statistically significant, but “because the study was not powered to detect differences in this absolute risk range, we cannot rule out that this was an actual harm effect from the interventional strategy.”

The eosinophil-guided therapy group did show more than a 50% reduction in the median duration of systemic corticosteroid therapy, which was 2 days in the eosinophil-guided group, compared with 5 days in the control group (P less than .0001), and the differences between the two groups remained significant at days 30 and 90.

“The tested strategy was successful in reducing the exposure to systemic corticosteroids, but we cannot exclude the possibility that a more aggressive algorithm, such as a single dose of systemic corticosteroid, might have been more effective,” the authors wrote.

At the 90-day follow-up, there were no differences in the number of infections requiring antibiotic treatment, nor in dyspepsia, ulcer complications, or initiation of new proton-pump inhibitor treatment.

The study was supported by the Danish Regions Medical Fund and the Danish Council for Independent Research. Two authors declared personal fees from pharmaceutical companies outside the submitted work. No other conflicts were declared.

SOURCE: Sivapalan P et al. Lancet Respir Med. 2019, May 20. doi: 10.1016/S2213-2600(19)30176-6.

Using eosinophil levels to guide steroid treatment in patients with chronic obstructive pulmonary disease (COPD) was found to be noninferior to standard treatment in terms of the number of days out of hospital and alive, new research has found.

Writing in the Lancet Respiratory Medicine, researchers reported the outcomes of a multicenter, controlled, open-label trial comparing eosinophil-guided and standard therapy with systemic corticosteroids in 318 patients with COPD.

Pradeesh Sivapalan, MD, of the respiratory medicine section of Herlev and Gentofte Hospital at the University of Copenhagen, and coauthors wrote that eosinophilic inflammation had been seen in 20%-40% of patients with acute exacerbations of COPD. Patients with higher eosinophilic blood counts were at increased risk of acute exacerbations but were also more likely to benefit from corticosteroid treatment.

In the eosinophil-guided therapy arm of the study, 159 patients received 80 mg of intravenous methylprednisolone on day 1, then from the second day were treated with 37.5 mg of prednisolone oral tablet daily ­– up to 4 days – only on days when their blood eosinophil count was at least 0.3 x 10^⁹ cells/L. In the control arm, 159 patients also received 80 mg of intravenous methylprednisolone on day 1, followed by 37.5 mg of prednisolone tablets daily for 4 days.

After 14 days, there were no significant differences between the two groups for mean days alive and out of hospital.

There were 12 more cases of readmission with COPD, including three fatalities, in the eosinophil-guided group within the first month. However the authors said these differences were not statistically significant, but “because the study was not powered to detect differences in this absolute risk range, we cannot rule out that this was an actual harm effect from the interventional strategy.”

The eosinophil-guided therapy group did show more than a 50% reduction in the median duration of systemic corticosteroid therapy, which was 2 days in the eosinophil-guided group, compared with 5 days in the control group (P less than .0001), and the differences between the two groups remained significant at days 30 and 90.

“The tested strategy was successful in reducing the exposure to systemic corticosteroids, but we cannot exclude the possibility that a more aggressive algorithm, such as a single dose of systemic corticosteroid, might have been more effective,” the authors wrote.

At the 90-day follow-up, there were no differences in the number of infections requiring antibiotic treatment, nor in dyspepsia, ulcer complications, or initiation of new proton-pump inhibitor treatment.

The study was supported by the Danish Regions Medical Fund and the Danish Council for Independent Research. Two authors declared personal fees from pharmaceutical companies outside the submitted work. No other conflicts were declared.

SOURCE: Sivapalan P et al. Lancet Respir Med. 2019, May 20. doi: 10.1016/S2213-2600(19)30176-6.

Using eosinophil levels to guide steroid treatment in patients with chronic obstructive pulmonary disease (COPD) was found to be noninferior to standard treatment in terms of the number of days out of hospital and alive, new research has found.

Writing in the Lancet Respiratory Medicine, researchers reported the outcomes of a multicenter, controlled, open-label trial comparing eosinophil-guided and standard therapy with systemic corticosteroids in 318 patients with COPD.

Pradeesh Sivapalan, MD, of the respiratory medicine section of Herlev and Gentofte Hospital at the University of Copenhagen, and coauthors wrote that eosinophilic inflammation had been seen in 20%-40% of patients with acute exacerbations of COPD. Patients with higher eosinophilic blood counts were at increased risk of acute exacerbations but were also more likely to benefit from corticosteroid treatment.

In the eosinophil-guided therapy arm of the study, 159 patients received 80 mg of intravenous methylprednisolone on day 1, then from the second day were treated with 37.5 mg of prednisolone oral tablet daily ­– up to 4 days – only on days when their blood eosinophil count was at least 0.3 x 10^⁹ cells/L. In the control arm, 159 patients also received 80 mg of intravenous methylprednisolone on day 1, followed by 37.5 mg of prednisolone tablets daily for 4 days.

After 14 days, there were no significant differences between the two groups for mean days alive and out of hospital.

There were 12 more cases of readmission with COPD, including three fatalities, in the eosinophil-guided group within the first month. However the authors said these differences were not statistically significant, but “because the study was not powered to detect differences in this absolute risk range, we cannot rule out that this was an actual harm effect from the interventional strategy.”

The eosinophil-guided therapy group did show more than a 50% reduction in the median duration of systemic corticosteroid therapy, which was 2 days in the eosinophil-guided group, compared with 5 days in the control group (P less than .0001), and the differences between the two groups remained significant at days 30 and 90.

“The tested strategy was successful in reducing the exposure to systemic corticosteroids, but we cannot exclude the possibility that a more aggressive algorithm, such as a single dose of systemic corticosteroid, might have been more effective,” the authors wrote.

At the 90-day follow-up, there were no differences in the number of infections requiring antibiotic treatment, nor in dyspepsia, ulcer complications, or initiation of new proton-pump inhibitor treatment.

The study was supported by the Danish Regions Medical Fund and the Danish Council for Independent Research. Two authors declared personal fees from pharmaceutical companies outside the submitted work. No other conflicts were declared.

SOURCE: Sivapalan P et al. Lancet Respir Med. 2019, May 20. doi: 10.1016/S2213-2600(19)30176-6.

Atrial fibrillation is being seen with increasing frequency in patients admitted to U.S. hospitals for exacerbations of end-stage chronic obstructive pulmonary disease, based on a retrospective analysis of data from the Nationwide Inpatient Sample.

The prevalence of atrial fibrillation (AFib) among patients with end-stage chronic obstructive pulmonary disease (COPD) on home oxygen who were admitted with COPD exacerbations increased from 12.9% in 2003 to 21.3% in 2014, according to Xiaochun Xiao of the department of health statistics at Second Military Medical University in Shanghai and colleagues.

Additionally, “we found that comorbid [AFib] was associated with an increased risk of the need for mechanical ventilation, especially invasive mechanical ventilation. Moreover, comorbid [AFib] was associated with adverse clinical outcomes, including increased in-hospital death, acute respiratory failure, acute kidney injury, sepsis, and stroke,” the researchers wrote in the study published in the journal CHEST.

Patients included in the study were aged at least 18 years, were diagnosed with end-stage COPD and on home oxygen, and were hospitalized because of a COPD-related exacerbation. Based on 1,345,270 weighted hospital admissions of adults with end-stage COPD on home oxygen who met the inclusion criteria for the study, 18.2% (244,488 admissions) of patients had AFib, and the prevalence of AFib in COPD patients increased over time from 2003 (12.9%) to 2014 (21.3%; P less than .0001).

Patients with AFib, compared with patients without AFib, were older (75.5 years vs. 69.6 years; P less than .0001) and more likely to be male (50.7% vs. 59.1%; P less than .0001) and white (80.9% vs. 74.4%; P less than .0001). Patients with AFib also had higher stroke risk reflected in higher CHA₂DS₂-VASc scores (3.26 vs. 2.45; P less than .0001), and higher likelihood of in-hospital mortality and readmission reflected in Elixhauser scores greater than or equal to 4 (51.2% vs. 35.6%).

In addition, the prevalence of AFib increased with increasing income. Larger hospitals in terms of bed size, urban environment, and Medicare insurance status also were associated with a higher AFib prevalence.

AFib was associated with an increased cost of $1,415 and an increased length of stay of 0.6 days after adjustment for potential confounders. AFib also predicted risk for several adverse events, including stroke (odds ratio, 1.80; in-hospital death, [OR, 1.54]), invasive mechanical ventilation (OR, 1.37), sepsis (OR, 1.23), noninvasive mechanical ventilation (OR, 1.14), acute kidney injury (OR, 1.09), and acute respiratory failure (OR, 1.09).

The researchers noted the database could have potentially overinflated AFib prevalence, as they could not differentiate index admissions and readmissions. The database also does not contain information about secondary diagnoses codes present on admission, which could make it difficult to identify adverse events that occurred during hospitalization.

“Our findings should prompt further efforts to identify the reasons for increased [AFib] prevalence and provide better management strategies for end-stage COPD patients comorbid with [AFib],” the researchers concluded.

This study was funded by a grant from the Fourth Round of the Shanghai 3-year Action Plan on Public Health Discipline and Talent Program. The authors reported no relevant conflict of interest.

SOURCE: Xiao X et al. CHEST. 2019 Jan 23. doi: 10.1016/j.chest.2018.12.021.

Atrial fibrillation is being seen with increasing frequency in patients admitted to U.S. hospitals for exacerbations of end-stage chronic obstructive pulmonary disease, based on a retrospective analysis of data from the Nationwide Inpatient Sample.

The prevalence of atrial fibrillation (AFib) among patients with end-stage chronic obstructive pulmonary disease (COPD) on home oxygen who were admitted with COPD exacerbations increased from 12.9% in 2003 to 21.3% in 2014, according to Xiaochun Xiao of the department of health statistics at Second Military Medical University in Shanghai and colleagues.

Additionally, “we found that comorbid [AFib] was associated with an increased risk of the need for mechanical ventilation, especially invasive mechanical ventilation. Moreover, comorbid [AFib] was associated with adverse clinical outcomes, including increased in-hospital death, acute respiratory failure, acute kidney injury, sepsis, and stroke,” the researchers wrote in the study published in the journal CHEST.

Patients included in the study were aged at least 18 years, were diagnosed with end-stage COPD and on home oxygen, and were hospitalized because of a COPD-related exacerbation. Based on 1,345,270 weighted hospital admissions of adults with end-stage COPD on home oxygen who met the inclusion criteria for the study, 18.2% (244,488 admissions) of patients had AFib, and the prevalence of AFib in COPD patients increased over time from 2003 (12.9%) to 2014 (21.3%; P less than .0001).

Patients with AFib, compared with patients without AFib, were older (75.5 years vs. 69.6 years; P less than .0001) and more likely to be male (50.7% vs. 59.1%; P less than .0001) and white (80.9% vs. 74.4%; P less than .0001). Patients with AFib also had higher stroke risk reflected in higher CHA₂DS₂-VASc scores (3.26 vs. 2.45; P less than .0001), and higher likelihood of in-hospital mortality and readmission reflected in Elixhauser scores greater than or equal to 4 (51.2% vs. 35.6%).

In addition, the prevalence of AFib increased with increasing income. Larger hospitals in terms of bed size, urban environment, and Medicare insurance status also were associated with a higher AFib prevalence.

AFib was associated with an increased cost of $1,415 and an increased length of stay of 0.6 days after adjustment for potential confounders. AFib also predicted risk for several adverse events, including stroke (odds ratio, 1.80; in-hospital death, [OR, 1.54]), invasive mechanical ventilation (OR, 1.37), sepsis (OR, 1.23), noninvasive mechanical ventilation (OR, 1.14), acute kidney injury (OR, 1.09), and acute respiratory failure (OR, 1.09).

The researchers noted the database could have potentially overinflated AFib prevalence, as they could not differentiate index admissions and readmissions. The database also does not contain information about secondary diagnoses codes present on admission, which could make it difficult to identify adverse events that occurred during hospitalization.

“Our findings should prompt further efforts to identify the reasons for increased [AFib] prevalence and provide better management strategies for end-stage COPD patients comorbid with [AFib],” the researchers concluded.

This study was funded by a grant from the Fourth Round of the Shanghai 3-year Action Plan on Public Health Discipline and Talent Program. The authors reported no relevant conflict of interest.

SOURCE: Xiao X et al. CHEST. 2019 Jan 23. doi: 10.1016/j.chest.2018.12.021.

Atrial fibrillation is being seen with increasing frequency in patients admitted to U.S. hospitals for exacerbations of end-stage chronic obstructive pulmonary disease, based on a retrospective analysis of data from the Nationwide Inpatient Sample.

The prevalence of atrial fibrillation (AFib) among patients with end-stage chronic obstructive pulmonary disease (COPD) on home oxygen who were admitted with COPD exacerbations increased from 12.9% in 2003 to 21.3% in 2014, according to Xiaochun Xiao of the department of health statistics at Second Military Medical University in Shanghai and colleagues.

Additionally, “we found that comorbid [AFib] was associated with an increased risk of the need for mechanical ventilation, especially invasive mechanical ventilation. Moreover, comorbid [AFib] was associated with adverse clinical outcomes, including increased in-hospital death, acute respiratory failure, acute kidney injury, sepsis, and stroke,” the researchers wrote in the study published in the journal CHEST.

Patients included in the study were aged at least 18 years, were diagnosed with end-stage COPD and on home oxygen, and were hospitalized because of a COPD-related exacerbation. Based on 1,345,270 weighted hospital admissions of adults with end-stage COPD on home oxygen who met the inclusion criteria for the study, 18.2% (244,488 admissions) of patients had AFib, and the prevalence of AFib in COPD patients increased over time from 2003 (12.9%) to 2014 (21.3%; P less than .0001).

Patients with AFib, compared with patients without AFib, were older (75.5 years vs. 69.6 years; P less than .0001) and more likely to be male (50.7% vs. 59.1%; P less than .0001) and white (80.9% vs. 74.4%; P less than .0001). Patients with AFib also had higher stroke risk reflected in higher CHA₂DS₂-VASc scores (3.26 vs. 2.45; P less than .0001), and higher likelihood of in-hospital mortality and readmission reflected in Elixhauser scores greater than or equal to 4 (51.2% vs. 35.6%).

In addition, the prevalence of AFib increased with increasing income. Larger hospitals in terms of bed size, urban environment, and Medicare insurance status also were associated with a higher AFib prevalence.

AFib was associated with an increased cost of $1,415 and an increased length of stay of 0.6 days after adjustment for potential confounders. AFib also predicted risk for several adverse events, including stroke (odds ratio, 1.80; in-hospital death, [OR, 1.54]), invasive mechanical ventilation (OR, 1.37), sepsis (OR, 1.23), noninvasive mechanical ventilation (OR, 1.14), acute kidney injury (OR, 1.09), and acute respiratory failure (OR, 1.09).

The researchers noted the database could have potentially overinflated AFib prevalence, as they could not differentiate index admissions and readmissions. The database also does not contain information about secondary diagnoses codes present on admission, which could make it difficult to identify adverse events that occurred during hospitalization.

“Our findings should prompt further efforts to identify the reasons for increased [AFib] prevalence and provide better management strategies for end-stage COPD patients comorbid with [AFib],” the researchers concluded.

This study was funded by a grant from the Fourth Round of the Shanghai 3-year Action Plan on Public Health Discipline and Talent Program. The authors reported no relevant conflict of interest.

SOURCE: Xiao X et al. CHEST. 2019 Jan 23. doi: 10.1016/j.chest.2018.12.021.

Aclidinium bromide reduced exacerbations in adults with chronic obstructive pulmonary disease with no increased risk of major adverse cardiovascular events, compared with placebo, in a randomized trial of more than 3,000 patients.

Aclidinium, a long-acting muscarinic antagonist (LAMA), has been shown to reduce COPD exacerbation in the short term, but long-term effectiveness has not been examined, wrote Robert A. Wise, MD, of Johns Hopkins University, Baltimore, and colleagues.

ASCENT-COPD is a multicenter, double-blind, randomized, placebo-controlled, parallel-group noninferiority study conducted at 522 sites in the United States and Canada. A paper on recent data from ASCENT-COPD, published in JAMA, supports early findings reported last year at the American Thoracic Society meeting.

The researchers randomized adults with COPD to a 400-mg dose of aclidinium bromide twice daily, or placebo. The average age of the patients was 67 years; 59% were men. The median exposure time to aclidinium or placebo was 365 days during the first year of treatment, and the median exposure overall was 495 days for aclidinium patients and 478 days for placebo patients.

Of the 2,537 patients who completed the study, 69 (3.9%) in the aclidinium group and 76 (4.2%) in the placebo group experienced a major adverse cardiovascular event (MACE, defined as a composite of cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke).

In addition, annual rates of moderate to severe COPD exacerbations were significantly lower in the aclidinium patients compared with placebo patients (0.44 vs. 0.57, P less than .001).

In a secondary analysis with a definition of MACE expanded to include heart failure, arrhythmias, or cerebrovascular disease, results remained similar between the groups; events occurred in 168 aclidinium patients (9.4%) and 160 placebo patients (8.9%). The rate of COPD exacerbations requiring hospitalization was significantly lower in aclidinium patients, compared with placebo patients (0.07 vs. 0.10, P = .006).

Overall, the most common treatment-emergent adverse events were similar in the aclidinium and placebo groups, respectively; pneumonia (6.1% vs. 5.8%), urinary tract infections (5.2% vs. 5.0%), and upper respiratory tract infections (4.8% vs. 5.6%). The most common serious adverse events (in at least 1% of patients) were pneumonia, atrial fibrillation, heart failure, and coronary artery disease. Dry mouth and urinary retention were rare, and occurred in less than 1% of patients in each group.

“No patient subgroup demonstrated a difference in efficacy except when analyzed by baseline COPD severity, in which the treatment benefit was observed only in patients with FEV₁ [forced expiratory volume in 1 second] of 50% predicted or less,” the researchers noted. “This may be explained by the lower exacerbation rate seen in the placebo group in patients with moderate airway obstruction vs. severe or very severe obstruction,” they said.

“Outcomes of this trial add data to the long-standing controversy over the safety of LAMAs in COPD” and support the need for additional research, they said.

The study findings were limited by several factors including insufficient power to detect cause-specific mortality and the use of a LAMA with low risk of systemic effects, the researchers noted.

SOURCE: Wise R et al. JAMA. 2019. 321:1693-1701.

Aclidinium bromide reduced exacerbations in adults with chronic obstructive pulmonary disease with no increased risk of major adverse cardiovascular events, compared with placebo, in a randomized trial of more than 3,000 patients.

Aclidinium, a long-acting muscarinic antagonist (LAMA), has been shown to reduce COPD exacerbation in the short term, but long-term effectiveness has not been examined, wrote Robert A. Wise, MD, of Johns Hopkins University, Baltimore, and colleagues.

ASCENT-COPD is a multicenter, double-blind, randomized, placebo-controlled, parallel-group noninferiority study conducted at 522 sites in the United States and Canada. A paper on recent data from ASCENT-COPD, published in JAMA, supports early findings reported last year at the American Thoracic Society meeting.

The researchers randomized adults with COPD to a 400-mg dose of aclidinium bromide twice daily, or placebo. The average age of the patients was 67 years; 59% were men. The median exposure time to aclidinium or placebo was 365 days during the first year of treatment, and the median exposure overall was 495 days for aclidinium patients and 478 days for placebo patients.

Of the 2,537 patients who completed the study, 69 (3.9%) in the aclidinium group and 76 (4.2%) in the placebo group experienced a major adverse cardiovascular event (MACE, defined as a composite of cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke).

In addition, annual rates of moderate to severe COPD exacerbations were significantly lower in the aclidinium patients compared with placebo patients (0.44 vs. 0.57, P less than .001).

In a secondary analysis with a definition of MACE expanded to include heart failure, arrhythmias, or cerebrovascular disease, results remained similar between the groups; events occurred in 168 aclidinium patients (9.4%) and 160 placebo patients (8.9%). The rate of COPD exacerbations requiring hospitalization was significantly lower in aclidinium patients, compared with placebo patients (0.07 vs. 0.10, P = .006).

Overall, the most common treatment-emergent adverse events were similar in the aclidinium and placebo groups, respectively; pneumonia (6.1% vs. 5.8%), urinary tract infections (5.2% vs. 5.0%), and upper respiratory tract infections (4.8% vs. 5.6%). The most common serious adverse events (in at least 1% of patients) were pneumonia, atrial fibrillation, heart failure, and coronary artery disease. Dry mouth and urinary retention were rare, and occurred in less than 1% of patients in each group.

“No patient subgroup demonstrated a difference in efficacy except when analyzed by baseline COPD severity, in which the treatment benefit was observed only in patients with FEV₁ [forced expiratory volume in 1 second] of 50% predicted or less,” the researchers noted. “This may be explained by the lower exacerbation rate seen in the placebo group in patients with moderate airway obstruction vs. severe or very severe obstruction,” they said.

“Outcomes of this trial add data to the long-standing controversy over the safety of LAMAs in COPD” and support the need for additional research, they said.

The study findings were limited by several factors including insufficient power to detect cause-specific mortality and the use of a LAMA with low risk of systemic effects, the researchers noted.

SOURCE: Wise R et al. JAMA. 2019. 321:1693-1701.

Aclidinium bromide reduced exacerbations in adults with chronic obstructive pulmonary disease with no increased risk of major adverse cardiovascular events, compared with placebo, in a randomized trial of more than 3,000 patients.

Aclidinium, a long-acting muscarinic antagonist (LAMA), has been shown to reduce COPD exacerbation in the short term, but long-term effectiveness has not been examined, wrote Robert A. Wise, MD, of Johns Hopkins University, Baltimore, and colleagues.

ASCENT-COPD is a multicenter, double-blind, randomized, placebo-controlled, parallel-group noninferiority study conducted at 522 sites in the United States and Canada. A paper on recent data from ASCENT-COPD, published in JAMA, supports early findings reported last year at the American Thoracic Society meeting.

The researchers randomized adults with COPD to a 400-mg dose of aclidinium bromide twice daily, or placebo. The average age of the patients was 67 years; 59% were men. The median exposure time to aclidinium or placebo was 365 days during the first year of treatment, and the median exposure overall was 495 days for aclidinium patients and 478 days for placebo patients.

Of the 2,537 patients who completed the study, 69 (3.9%) in the aclidinium group and 76 (4.2%) in the placebo group experienced a major adverse cardiovascular event (MACE, defined as a composite of cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke).

In addition, annual rates of moderate to severe COPD exacerbations were significantly lower in the aclidinium patients compared with placebo patients (0.44 vs. 0.57, P less than .001).

In a secondary analysis with a definition of MACE expanded to include heart failure, arrhythmias, or cerebrovascular disease, results remained similar between the groups; events occurred in 168 aclidinium patients (9.4%) and 160 placebo patients (8.9%). The rate of COPD exacerbations requiring hospitalization was significantly lower in aclidinium patients, compared with placebo patients (0.07 vs. 0.10, P = .006).

Overall, the most common treatment-emergent adverse events were similar in the aclidinium and placebo groups, respectively; pneumonia (6.1% vs. 5.8%), urinary tract infections (5.2% vs. 5.0%), and upper respiratory tract infections (4.8% vs. 5.6%). The most common serious adverse events (in at least 1% of patients) were pneumonia, atrial fibrillation, heart failure, and coronary artery disease. Dry mouth and urinary retention were rare, and occurred in less than 1% of patients in each group.

“No patient subgroup demonstrated a difference in efficacy except when analyzed by baseline COPD severity, in which the treatment benefit was observed only in patients with FEV₁ [forced expiratory volume in 1 second] of 50% predicted or less,” the researchers noted. “This may be explained by the lower exacerbation rate seen in the placebo group in patients with moderate airway obstruction vs. severe or very severe obstruction,” they said.

“Outcomes of this trial add data to the long-standing controversy over the safety of LAMAs in COPD” and support the need for additional research, they said.

The study findings were limited by several factors including insufficient power to detect cause-specific mortality and the use of a LAMA with low risk of systemic effects, the researchers noted.

SOURCE: Wise R et al. JAMA. 2019. 321:1693-1701.

Women undergoing open descending thoracic aortic aneurysm (DTA) and open thoracoabdominal aortic aneurysm (TAAA) repair are not at greater risk for operative mortality than their male counterparts. However, they are at significantly greater risk for major adverse events and have significantly lower 5-year survival, according to the results of a single institution database review of 738 surgery patients.

From May 1997 to June 2017, there were 462 men (59%) and 321 women (41%) who underwent open repair of DTA or TAAA, according to Leonard N. Girardi, MD, and colleagues from Weill Cornell Medicine, New York, who performed the study published in the Journal of Vascular Surgery. The researchers used logistic regression and Cox regression analyses to assess the effect of sex on perioperative and long-term outcomes.

Demographically, women were significantly older (67.6 years vs. 62.6 years), with a significantly higher incidence of chronic obstructive pulmonary disease (47.0% vs. 35.7%) and a significantly greater percentage of patients with a forced expiratory volume in 1 second less than 50% (28.3% vs 18.2%). Degenerative aneurysms were significantly more common in women (61.7% vs. 41.6%), whereas chronic dissections significantly predominated in men (42.4% vs. 23.1%). Operative mortality was not significantly different between women and men (5.6% vs. 6.2%); however, women were significantly more likely to require a tracheostomy after surgery (10.6% vs. 5.0%).

Logistic regression found that being a woman was an independent risk factor for a composite of major adverse events (odds ratio, 2.68) and need for tracheostomy (OR, 3.73). In addition, women had significantly worse 5-year survival than men undergoing DTA or TAAA repair (59.7% vs. 66.2%, P =.025). There was no difference in overall survival between 1997-2007 and 2008-2017.

“Women and men undergoing TAAA repair have significant and consistent differences in preoperative characteristics. Despite these differences, operative mortality is similar between the two groups. However, women are at significantly increased risk of [major adverse events], especially respiratory failure, because of those differences in risk factors, including age, pulmonary function, and aneurysm etiology,” the researchers concluded.

The authors reported that they had no conflicts of interest.

[email protected]

SOURCE: Girardi LN et al. J Vasc Surg 2019;69:1028-35.

Women undergoing open descending thoracic aortic aneurysm (DTA) and open thoracoabdominal aortic aneurysm (TAAA) repair are not at greater risk for operative mortality than their male counterparts. However, they are at significantly greater risk for major adverse events and have significantly lower 5-year survival, according to the results of a single institution database review of 738 surgery patients.

From May 1997 to June 2017, there were 462 men (59%) and 321 women (41%) who underwent open repair of DTA or TAAA, according to Leonard N. Girardi, MD, and colleagues from Weill Cornell Medicine, New York, who performed the study published in the Journal of Vascular Surgery. The researchers used logistic regression and Cox regression analyses to assess the effect of sex on perioperative and long-term outcomes.

Demographically, women were significantly older (67.6 years vs. 62.6 years), with a significantly higher incidence of chronic obstructive pulmonary disease (47.0% vs. 35.7%) and a significantly greater percentage of patients with a forced expiratory volume in 1 second less than 50% (28.3% vs 18.2%). Degenerative aneurysms were significantly more common in women (61.7% vs. 41.6%), whereas chronic dissections significantly predominated in men (42.4% vs. 23.1%). Operative mortality was not significantly different between women and men (5.6% vs. 6.2%); however, women were significantly more likely to require a tracheostomy after surgery (10.6% vs. 5.0%).

Logistic regression found that being a woman was an independent risk factor for a composite of major adverse events (odds ratio, 2.68) and need for tracheostomy (OR, 3.73). In addition, women had significantly worse 5-year survival than men undergoing DTA or TAAA repair (59.7% vs. 66.2%, P =.025). There was no difference in overall survival between 1997-2007 and 2008-2017.

“Women and men undergoing TAAA repair have significant and consistent differences in preoperative characteristics. Despite these differences, operative mortality is similar between the two groups. However, women are at significantly increased risk of [major adverse events], especially respiratory failure, because of those differences in risk factors, including age, pulmonary function, and aneurysm etiology,” the researchers concluded.

The authors reported that they had no conflicts of interest.

[email protected]

SOURCE: Girardi LN et al. J Vasc Surg 2019;69:1028-35.

Women undergoing open descending thoracic aortic aneurysm (DTA) and open thoracoabdominal aortic aneurysm (TAAA) repair are not at greater risk for operative mortality than their male counterparts. However, they are at significantly greater risk for major adverse events and have significantly lower 5-year survival, according to the results of a single institution database review of 738 surgery patients.

From May 1997 to June 2017, there were 462 men (59%) and 321 women (41%) who underwent open repair of DTA or TAAA, according to Leonard N. Girardi, MD, and colleagues from Weill Cornell Medicine, New York, who performed the study published in the Journal of Vascular Surgery. The researchers used logistic regression and Cox regression analyses to assess the effect of sex on perioperative and long-term outcomes.

Demographically, women were significantly older (67.6 years vs. 62.6 years), with a significantly higher incidence of chronic obstructive pulmonary disease (47.0% vs. 35.7%) and a significantly greater percentage of patients with a forced expiratory volume in 1 second less than 50% (28.3% vs 18.2%). Degenerative aneurysms were significantly more common in women (61.7% vs. 41.6%), whereas chronic dissections significantly predominated in men (42.4% vs. 23.1%). Operative mortality was not significantly different between women and men (5.6% vs. 6.2%); however, women were significantly more likely to require a tracheostomy after surgery (10.6% vs. 5.0%).

Logistic regression found that being a woman was an independent risk factor for a composite of major adverse events (odds ratio, 2.68) and need for tracheostomy (OR, 3.73). In addition, women had significantly worse 5-year survival than men undergoing DTA or TAAA repair (59.7% vs. 66.2%, P =.025). There was no difference in overall survival between 1997-2007 and 2008-2017.

“Women and men undergoing TAAA repair have significant and consistent differences in preoperative characteristics. Despite these differences, operative mortality is similar between the two groups. However, women are at significantly increased risk of [major adverse events], especially respiratory failure, because of those differences in risk factors, including age, pulmonary function, and aneurysm etiology,” the researchers concluded.

The authors reported that they had no conflicts of interest.

[email protected]

SOURCE: Girardi LN et al. J Vasc Surg 2019;69:1028-35.

PHILADELPHIA – While triple therapy is effective for patients with chronic obstructive pulmonary disease (COPD), not all patients actually need the inhaled corticosteroid component to reduce exacerbations, a Mayo Clinic pulmonologist said at the annual meeting of the American College of Physicians.

Andrew D. Bowser/MDedge News

“When you’re increasing therapy, we can go to a dual-bronchodilator combination before adding corticosteroids,” Megan Dulohery Scrodin, MD, of Mayo Clinic, Rochester, Minn., noted in a well-attended session.

That approach came as news to many internists, at least going by results of an audience poll in which 76% of attendees picked triple therapy for a 65-year-old male with COPD and frequent exacerbations despite having used a long-acting muscarinic antagonist (LAMA). Only 10% picked what Dr. Dulohery Scrodin said was optimal: to keep the patient on the LAMA, and add a long-acting beta-agonist (LABA).

“I would encourage you to do this as a stepwise process,” Dr. Dulohery Scrodin told attendees after seeing those poll results.

For a patient with minimal symptoms and few exacerbations, the best approach is a short-acting bronchodilator plus smoking cessation, avoidance of environmental triggers, and keeping up to date with vaccinations, she said.

For patients with more severe symptoms or frequent exacerbations, adding a LAMA or LABA would be warranted, along with considering pulmonary rehabilitation.

“There’s been studies comparing long-acting muscarinic antagonists to long-acting beta agonists, and the long-acting muscarinic antagonists like tiotropium seem to be superior,” she said. “So I always do a LAMA inhaler first.”

For patients still having exacerbations despite one long-acting bronchodilator, the best approach would be to add the second bronchodilator, and if that still doesn’t work, she said, add an inhaled corticosteroid and consider a pulmonary consultation for advanced therapy.

“If the patient doesn’t need an inhaled corticosteroid, we try to avoid it and use dual bronchodilator therapy,” said Dr. Dulohery Scrodin, noting that inhaled corticosteroids are associated with increased risk of pneumonia, along with other complications such as dysphonia and oral candidiasis.

In studies, single-inhaler triple therapy with fluticasone furoate, umeclidinium, and vilanterol does seem to reduce exacerbations more than LABA/LAMA combination therapy or LABA/inhaled corticosteroid treatment, but that doesn’t necessarily mean it should be automatically chosen over dual therapy, the presenter noted.

“Similar to asthma, I would do the least amount of therapy that your patient gets under control,” she told the audience.

Dr. Dulohery Scrodin reported that she had no relevant disclosures.

PHILADELPHIA – While triple therapy is effective for patients with chronic obstructive pulmonary disease (COPD), not all patients actually need the inhaled corticosteroid component to reduce exacerbations, a Mayo Clinic pulmonologist said at the annual meeting of the American College of Physicians.

Andrew D. Bowser/MDedge News

“When you’re increasing therapy, we can go to a dual-bronchodilator combination before adding corticosteroids,” Megan Dulohery Scrodin, MD, of Mayo Clinic, Rochester, Minn., noted in a well-attended session.

That approach came as news to many internists, at least going by results of an audience poll in which 76% of attendees picked triple therapy for a 65-year-old male with COPD and frequent exacerbations despite having used a long-acting muscarinic antagonist (LAMA). Only 10% picked what Dr. Dulohery Scrodin said was optimal: to keep the patient on the LAMA, and add a long-acting beta-agonist (LABA).

“I would encourage you to do this as a stepwise process,” Dr. Dulohery Scrodin told attendees after seeing those poll results.

For a patient with minimal symptoms and few exacerbations, the best approach is a short-acting bronchodilator plus smoking cessation, avoidance of environmental triggers, and keeping up to date with vaccinations, she said.

For patients with more severe symptoms or frequent exacerbations, adding a LAMA or LABA would be warranted, along with considering pulmonary rehabilitation.

“There’s been studies comparing long-acting muscarinic antagonists to long-acting beta agonists, and the long-acting muscarinic antagonists like tiotropium seem to be superior,” she said. “So I always do a LAMA inhaler first.”

For patients still having exacerbations despite one long-acting bronchodilator, the best approach would be to add the second bronchodilator, and if that still doesn’t work, she said, add an inhaled corticosteroid and consider a pulmonary consultation for advanced therapy.

“If the patient doesn’t need an inhaled corticosteroid, we try to avoid it and use dual bronchodilator therapy,” said Dr. Dulohery Scrodin, noting that inhaled corticosteroids are associated with increased risk of pneumonia, along with other complications such as dysphonia and oral candidiasis.

In studies, single-inhaler triple therapy with fluticasone furoate, umeclidinium, and vilanterol does seem to reduce exacerbations more than LABA/LAMA combination therapy or LABA/inhaled corticosteroid treatment, but that doesn’t necessarily mean it should be automatically chosen over dual therapy, the presenter noted.

“Similar to asthma, I would do the least amount of therapy that your patient gets under control,” she told the audience.

Dr. Dulohery Scrodin reported that she had no relevant disclosures.

PHILADELPHIA – While triple therapy is effective for patients with chronic obstructive pulmonary disease (COPD), not all patients actually need the inhaled corticosteroid component to reduce exacerbations, a Mayo Clinic pulmonologist said at the annual meeting of the American College of Physicians.

Andrew D. Bowser/MDedge News

“When you’re increasing therapy, we can go to a dual-bronchodilator combination before adding corticosteroids,” Megan Dulohery Scrodin, MD, of Mayo Clinic, Rochester, Minn., noted in a well-attended session.

That approach came as news to many internists, at least going by results of an audience poll in which 76% of attendees picked triple therapy for a 65-year-old male with COPD and frequent exacerbations despite having used a long-acting muscarinic antagonist (LAMA). Only 10% picked what Dr. Dulohery Scrodin said was optimal: to keep the patient on the LAMA, and add a long-acting beta-agonist (LABA).

“I would encourage you to do this as a stepwise process,” Dr. Dulohery Scrodin told attendees after seeing those poll results.

For a patient with minimal symptoms and few exacerbations, the best approach is a short-acting bronchodilator plus smoking cessation, avoidance of environmental triggers, and keeping up to date with vaccinations, she said.

For patients with more severe symptoms or frequent exacerbations, adding a LAMA or LABA would be warranted, along with considering pulmonary rehabilitation.

“There’s been studies comparing long-acting muscarinic antagonists to long-acting beta agonists, and the long-acting muscarinic antagonists like tiotropium seem to be superior,” she said. “So I always do a LAMA inhaler first.”

For patients still having exacerbations despite one long-acting bronchodilator, the best approach would be to add the second bronchodilator, and if that still doesn’t work, she said, add an inhaled corticosteroid and consider a pulmonary consultation for advanced therapy.

“If the patient doesn’t need an inhaled corticosteroid, we try to avoid it and use dual bronchodilator therapy,” said Dr. Dulohery Scrodin, noting that inhaled corticosteroids are associated with increased risk of pneumonia, along with other complications such as dysphonia and oral candidiasis.

In studies, single-inhaler triple therapy with fluticasone furoate, umeclidinium, and vilanterol does seem to reduce exacerbations more than LABA/LAMA combination therapy or LABA/inhaled corticosteroid treatment, but that doesn’t necessarily mean it should be automatically chosen over dual therapy, the presenter noted.

“Similar to asthma, I would do the least amount of therapy that your patient gets under control,” she told the audience.

Dr. Dulohery Scrodin reported that she had no relevant disclosures.

Concerns about abatacept (Orencia)-related lung disease in patients with rheumatoid arthritis appear to be unfounded, a large U.S. database review has determined.

designer491/Thinkstock

Safety signals seen in a small subset of patients in the 2006 ASSURE study likely arose from chance, Samy Suissa, PhD, and his colleagues wrote in Seminars in Arthritis & Rheumatism. Patients in that study with preexisting chronic obstructive pulmonary disease (COPD) were 84% more likely to develop an exacerbation or other lung disorder than were those taking a placebo comparator.

The new database study contradicted that finding.

“Our study suggests that these numerical differences in ASSURE are expected results of random variation and thus compatible with chance,” Dr. Suissa of Jewish General Hospital and McGill University, both in Montreal, and his coauthors wrote. “Moreover, our findings are consistent with two studies of the safety of abatacept in the context of interstitial lung disease, albeit a different respiratory disease than COPD.”

The year-long ASSURE trial reported on the safety of abatacept in 959 patients versus 482 assigned to placebo. The safety signal arose in a subgroup of 54 patients with COPD, 37 of whom were assigned to abatacept and 17 to placebo. Among these were four serious respiratory adverse events (COPD exacerbation, worsening of COPD, bronchitis, and pneumonia) in four patients taking abatacept and none in the placebo arm.

“It is useful to note that this difference of 11% versus 0% rate is compatible with chance [exact P = .31], while the exact 95% confidence interval for the odds ratio is wide and includes unity ... The trial also reported more mild-moderate respiratory events with abatacept than with placebo [43.2% vs. 23.5%], including cough, rhonchi, COPD exacerbation, COPD, dyspnea, and nasal congestion. This difference resulted in an odds ration of 1.84,” with a wide confidence interval that included unity (0.48-8.63).

Nevertheless, these findings led to the addition of a warning in the prescribing insert: “Adult COPD patients treated with Orencia developed adverse events more frequently than those treated with placebo, including COPD exacerbations, cough, rhonchi, and dyspnea. Use of Orencia in patients with RA and COPD should be undertaken with caution and such patients should be monitored for worsening of their respiratory status.”

Dr. Suissa’s team used the U.S. MarketScan prescribing database to asses the risk of respiratory adverse events associated with abatacept, compared with other biologic disease-modifying antirheumatic drugs (DMARDs) in a real-world setting.

The cohort comprised 1,807 patients with rheumatoid arthritis and COPD who started a new prescription for abatacept, matched in time to 3,547 who initiated another biologic DMARD. The primary endpoint was the combined risk of hospitalization for COPD exacerbation, bronchitis, and hospitalized pneumonia or influenza.

The most common comparator biologic DMARDs were etanercept, adalimumab, rituximab, and infliximab.

For patients with COPD and comparator patients, the incidence rates for COPD exacerbation were 1.2 per 100 person-years with abatacept and 2.1 per 100 person-years with a different biologic DMARD; for bronchitis, the respective rates were 4.2 and 5.3; for hospitalized pneumonia or influenza, 3.6 and 2.6; and for outpatient pneumonia or flu, 14.7 and 14.4. For the combined endpoint, the incidence rate was 8.7 per 100 person-years with abatacept and 9.9 per 100 person-years with other biologic DMARDs.

The adjusted hazard ratio of the combined endpoint with abatacept versus that with other biologic DMARDs was a nonsignificant risk of 0.87. The hazard ratio with abatacept was 0.60 for hospitalized COPD; 0.80 for bronchitis; 1.39 for hospitalized pneumonia and flu; and 1.05 for outpatient pneumonia and flu. None of these associations was statistically significant.

“One exception was the risk of hospitalization for pneumonia or influenza, which was higher with abatacept among patients with more severe COPD,” at 6.99, than it was with other biologic DMARDs, the authors noted.

Dr. Suissa disclosed relationships with AstraZeneca, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, and Novartis.

[email protected]

SOURCE: Suissa S et al. Semin Arthritis Rheum. 2019 Mar 16. doi: 10.1016j.semarthrit.2019.03.007.
 

Concerns about abatacept (Orencia)-related lung disease in patients with rheumatoid arthritis appear to be unfounded, a large U.S. database review has determined.

designer491/Thinkstock

Safety signals seen in a small subset of patients in the 2006 ASSURE study likely arose from chance, Samy Suissa, PhD, and his colleagues wrote in Seminars in Arthritis & Rheumatism. Patients in that study with preexisting chronic obstructive pulmonary disease (COPD) were 84% more likely to develop an exacerbation or other lung disorder than were those taking a placebo comparator.

The new database study contradicted that finding.

“Our study suggests that these numerical differences in ASSURE are expected results of random variation and thus compatible with chance,” Dr. Suissa of Jewish General Hospital and McGill University, both in Montreal, and his coauthors wrote. “Moreover, our findings are consistent with two studies of the safety of abatacept in the context of interstitial lung disease, albeit a different respiratory disease than COPD.”

The year-long ASSURE trial reported on the safety of abatacept in 959 patients versus 482 assigned to placebo. The safety signal arose in a subgroup of 54 patients with COPD, 37 of whom were assigned to abatacept and 17 to placebo. Among these were four serious respiratory adverse events (COPD exacerbation, worsening of COPD, bronchitis, and pneumonia) in four patients taking abatacept and none in the placebo arm.

“It is useful to note that this difference of 11% versus 0% rate is compatible with chance [exact P = .31], while the exact 95% confidence interval for the odds ratio is wide and includes unity ... The trial also reported more mild-moderate respiratory events with abatacept than with placebo [43.2% vs. 23.5%], including cough, rhonchi, COPD exacerbation, COPD, dyspnea, and nasal congestion. This difference resulted in an odds ration of 1.84,” with a wide confidence interval that included unity (0.48-8.63).

Nevertheless, these findings led to the addition of a warning in the prescribing insert: “Adult COPD patients treated with Orencia developed adverse events more frequently than those treated with placebo, including COPD exacerbations, cough, rhonchi, and dyspnea. Use of Orencia in patients with RA and COPD should be undertaken with caution and such patients should be monitored for worsening of their respiratory status.”

Dr. Suissa’s team used the U.S. MarketScan prescribing database to asses the risk of respiratory adverse events associated with abatacept, compared with other biologic disease-modifying antirheumatic drugs (DMARDs) in a real-world setting.

The cohort comprised 1,807 patients with rheumatoid arthritis and COPD who started a new prescription for abatacept, matched in time to 3,547 who initiated another biologic DMARD. The primary endpoint was the combined risk of hospitalization for COPD exacerbation, bronchitis, and hospitalized pneumonia or influenza.

The most common comparator biologic DMARDs were etanercept, adalimumab, rituximab, and infliximab.

For patients with COPD and comparator patients, the incidence rates for COPD exacerbation were 1.2 per 100 person-years with abatacept and 2.1 per 100 person-years with a different biologic DMARD; for bronchitis, the respective rates were 4.2 and 5.3; for hospitalized pneumonia or influenza, 3.6 and 2.6; and for outpatient pneumonia or flu, 14.7 and 14.4. For the combined endpoint, the incidence rate was 8.7 per 100 person-years with abatacept and 9.9 per 100 person-years with other biologic DMARDs.

The adjusted hazard ratio of the combined endpoint with abatacept versus that with other biologic DMARDs was a nonsignificant risk of 0.87. The hazard ratio with abatacept was 0.60 for hospitalized COPD; 0.80 for bronchitis; 1.39 for hospitalized pneumonia and flu; and 1.05 for outpatient pneumonia and flu. None of these associations was statistically significant.

“One exception was the risk of hospitalization for pneumonia or influenza, which was higher with abatacept among patients with more severe COPD,” at 6.99, than it was with other biologic DMARDs, the authors noted.

Dr. Suissa disclosed relationships with AstraZeneca, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, and Novartis.

[email protected]

SOURCE: Suissa S et al. Semin Arthritis Rheum. 2019 Mar 16. doi: 10.1016j.semarthrit.2019.03.007.
 

Concerns about abatacept (Orencia)-related lung disease in patients with rheumatoid arthritis appear to be unfounded, a large U.S. database review has determined.

designer491/Thinkstock

Safety signals seen in a small subset of patients in the 2006 ASSURE study likely arose from chance, Samy Suissa, PhD, and his colleagues wrote in Seminars in Arthritis & Rheumatism. Patients in that study with preexisting chronic obstructive pulmonary disease (COPD) were 84% more likely to develop an exacerbation or other lung disorder than were those taking a placebo comparator.

The new database study contradicted that finding.

“Our study suggests that these numerical differences in ASSURE are expected results of random variation and thus compatible with chance,” Dr. Suissa of Jewish General Hospital and McGill University, both in Montreal, and his coauthors wrote. “Moreover, our findings are consistent with two studies of the safety of abatacept in the context of interstitial lung disease, albeit a different respiratory disease than COPD.”

The year-long ASSURE trial reported on the safety of abatacept in 959 patients versus 482 assigned to placebo. The safety signal arose in a subgroup of 54 patients with COPD, 37 of whom were assigned to abatacept and 17 to placebo. Among these were four serious respiratory adverse events (COPD exacerbation, worsening of COPD, bronchitis, and pneumonia) in four patients taking abatacept and none in the placebo arm.

“It is useful to note that this difference of 11% versus 0% rate is compatible with chance [exact P = .31], while the exact 95% confidence interval for the odds ratio is wide and includes unity ... The trial also reported more mild-moderate respiratory events with abatacept than with placebo [43.2% vs. 23.5%], including cough, rhonchi, COPD exacerbation, COPD, dyspnea, and nasal congestion. This difference resulted in an odds ration of 1.84,” with a wide confidence interval that included unity (0.48-8.63).

Nevertheless, these findings led to the addition of a warning in the prescribing insert: “Adult COPD patients treated with Orencia developed adverse events more frequently than those treated with placebo, including COPD exacerbations, cough, rhonchi, and dyspnea. Use of Orencia in patients with RA and COPD should be undertaken with caution and such patients should be monitored for worsening of their respiratory status.”

Dr. Suissa’s team used the U.S. MarketScan prescribing database to asses the risk of respiratory adverse events associated with abatacept, compared with other biologic disease-modifying antirheumatic drugs (DMARDs) in a real-world setting.

The cohort comprised 1,807 patients with rheumatoid arthritis and COPD who started a new prescription for abatacept, matched in time to 3,547 who initiated another biologic DMARD. The primary endpoint was the combined risk of hospitalization for COPD exacerbation, bronchitis, and hospitalized pneumonia or influenza.

The most common comparator biologic DMARDs were etanercept, adalimumab, rituximab, and infliximab.

For patients with COPD and comparator patients, the incidence rates for COPD exacerbation were 1.2 per 100 person-years with abatacept and 2.1 per 100 person-years with a different biologic DMARD; for bronchitis, the respective rates were 4.2 and 5.3; for hospitalized pneumonia or influenza, 3.6 and 2.6; and for outpatient pneumonia or flu, 14.7 and 14.4. For the combined endpoint, the incidence rate was 8.7 per 100 person-years with abatacept and 9.9 per 100 person-years with other biologic DMARDs.

The adjusted hazard ratio of the combined endpoint with abatacept versus that with other biologic DMARDs was a nonsignificant risk of 0.87. The hazard ratio with abatacept was 0.60 for hospitalized COPD; 0.80 for bronchitis; 1.39 for hospitalized pneumonia and flu; and 1.05 for outpatient pneumonia and flu. None of these associations was statistically significant.

“One exception was the risk of hospitalization for pneumonia or influenza, which was higher with abatacept among patients with more severe COPD,” at 6.99, than it was with other biologic DMARDs, the authors noted.

Dr. Suissa disclosed relationships with AstraZeneca, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, and Novartis.

[email protected]

SOURCE: Suissa S et al. Semin Arthritis Rheum. 2019 Mar 16. doi: 10.1016j.semarthrit.2019.03.007.