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Obesity and lung disease: Much more than BMI
The diverse effects of obesity on lung health and disease are increasingly being teased apart, with researchers honing in on the impact of metabolic dysfunction, circulating inflammatory factors produced by adipose tissue, lipid handling, and other factors – in addition to body mass index – that are associated with the obese state.
“The bird’s eye view is that obesity completely changes lung health. It’s something we’ve only recently begun to appreciate,” said Anne E. Dixon, MA, BM, BCh, director of the Vermont Lung Center at the University of Vermont, Burlington, who is focused on the research field of obesity and lung disease.
Structural, mechanical effects of obesity on lung function are better known and appreciated. Accumulation of fat in the mediastinum and abdominal and thoracic cavities causes reductions in lung volume, in functional residual capacity, and in the compliance of the lungs, chest wall, and entire respiratory system, for instance.
Yet obesity is more than a state of increased BMI, and “what we’ve begun to understand is that [its impact on the lungs and respiratory health] is much more complicated than just a mechanical problem,” said Dr. Dixon, also director of pulmonary and critical care medicine at the University of Vermont Medical Center and professor of medicine at the medical college.
With obesity, adipose tissue changes not only in quantity, but in function, producing proinflammatory cytokines and hormones – such as leptin, tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 – that can have direct effects on the lung. Insulin resistance, which is common with obesity, is also seemingly deleterious. And obesity-associated changes in immune function, lipid handling, diet, and the gut microbiome may also impact lung health and disease, she said.
Dr. Dixon, who wrote about these changes in a 2018 review article in the journal CHEST and another 2019 piece in Expert Review of Respiratory Medicine, has developed a research program focused on obesity and lung disease and has edited a book and organized international conferences on the topic. (CHEST 2018;153[3]:702-9 and Exper Rev Respir Med. 2018;12[9]:755-67.)
“The more I do, the more I realize that there are multiple obesity-associated changes involved, and that [our current high level of] obesity is like a huge population-level natural experiment ... on lung health,” she told this news organization.
Associations between lung disease and the metabolic and other disturbances of obesity are most established in asthma research and have taken hold in the realm of sleep-disordered breathing. But as the prevalence of obesity continues to grow, its role in other lung diseases such as chronic obstructive pulmonary disorder (COPD) and, most recently, pulmonary arterial hypertension (PAH), is getting attention in academia.
And certainly, COVID-19 has highlighted an “urgent need” to better understand how obesity increases susceptibility to severe viral infections, Dr. Dixon added.
Here are some glimpses into current thinking and some examples of research that may have preventive and therapeutic implications in the future:
OSA and OHS
“With sleep apnea we tend to focus on anatomic considerations, but there may be relationships or interactions between obesity and neuromuscular function and neuroventilatory control,” Susheel P. Patil, MD, PhD, director of the sleep medicine program for University Hospitals and assistant professor at Case Western Reserve University, Cleveland, said in an interview.
Some studies suggest, for instance, that TNF-alpha can increase obstructive sleep apnea (OSA) susceptibility and severity through its neuroventilatory modulating properties during sleep. And the potential for additional proinflammatory cytokines produced by adipose tissue to similarly affect upper airway neuroventilatory control is an “intriguing line” of inquiry for researchers in the sleep apnea space, he said.
Leptin is of interest particularly in obesity hypoventilation syndrome (OHS), which is characterized by chronic daytime hypercapnia. Best known as a satiety hormone, leptin is produced by adipose tissue and suppresses appetite at the central nervous system level. But it has long been known that leptin also affects ventilation and the control of breathing.
When transported across the blood-brain barrier, leptin increases the hypercapnic ventilatory response, Babak Mokhlesi, MD, MSc, codirector of the Rush Lung Center and chief of pulmonary, critical care, and sleep medicine at Rush University Medical Center in Chicago, said in an interview.
Research suggests that patients with OHS may have resistance to leptin at the central nervous system level – with leptin not reaching the sites of ventilatory control. This is a “prevailing theory” and could explain why these patients “do not augment their ventilation to maintain homeostasis, normal levels of CO2,” Dr. Mokhlesi said.
“Why some patients with severe obesity develop CO2 retention while others do not is not fully understood,” he said, noting that patients with OHS can normalize their CO2 quickly when instructed to take deep breaths. “What we know is that the centers in the brain responsible for augmenting ventilation when CO2 goes up are somehow blunted.”
In a study of obese mice led by Vsevolod Y. Polotsky, MD, PhD, of Johns Hopkins University, Baltimore – and highlighted by Dr. Mokhlesi as an example of important, recent research – leptin delivered intranasally alleviated hypoventilation (and upper-airway obstruction), while intraperitoneally administered leptin did not, seemingly overcoming “central leptin deficiency.” (Am J Respir Crit Care Med. 2019;199[6]:773-83).
“This proved that there is some level of resistance in this animal model ... and has potential for therapeutics in the future,” Dr. Mokhlesi said.
Understanding the role of insulin resistance in OSA is another research focus. Some data suggest that insulin resistance, which is more common in obesity, is more prevalent in populations with OSA, Dr. Patil said. Researchers have discussed a bidirectional relationship for years, but it’s likely that insulin resistance is a precursor, he said.
In a mechanistic study published in 2016, Dr. Patil and his coinvestigators found that obese individuals with insulin resistance but without frank diabetes or sleep apnea demonstrated preclinical elevations in pharyngeal collapsibility during sleep. The findings suggest that insulin resistance could play a causal role in OSA pathogenesis by “generating requisite elevations in pharyngeal collapsibility,” they wrote (Eur. Respir J. 2016;47[6]:1718-26).
More recently, Dr. Patil noted in the interview, there is increasing appreciation in academia that the type of fat may be important to predicting OSA. “Visceral fat has a completely different cytokine-secretion profile than subcutaneous fat ... it is the more metabolically active fat that may secondarily impact upper airway function though a neuroinflammatory mechanism,” he said. “That is one of the working hypotheses today.”
Asthma
Research has so roundly suggested that metabolic dysfunction contributes to severe, poorly controlled asthma that there’s recent and growing interest in targeting metabolic dysfunction as part of the treatment of obese asthma, said Dr. Dixon, whose own research in obesity and lung disease has focused on asthma.
Data from animal models and some epidemiologic studies have suggested that drugs used to treat type 2 diabetes mellitus, such as glucagon-like peptide receptor-1 (GLPR-1) agonists and metformin, may help control asthma. In one recent study – cited by Dr. Dixon in a 2022 review of obesity and asthma – people with obesity and asthma who were prescribed GLPR-1 agonists for diabetes had fewer asthma exacerbations compared with those who took other medications for diabetes (Semin Respir Crit Care Med. 2022 Feb 17. doi: 10.1055/s-0042-1742384).
There is also research interest in targeting the pro-inflammatory adipokine interleukin 6 (IL-6), since increased circulating levels of IL-6 correlate with asthma severity, and in addressing oxidative stress in asthma through treatment with a mitochondrially targeted antioxidant, she said. Oxidative stress is increased in the airways of people with obesity, and researchers believe it may contribute to the pathophysiology of obese asthma through effects on airway nitric oxide levels.
(Her own research work at the University of Vermont has found associations between poor asthma control and high levels of leptin, and similar associations involving low levels of adiponectin, an anti-inflammatory adipokine that has been shown to downregulate eosinophil recruitment in the airways.)
Weight loss has been shown in mostly small, single-center studies to improve asthma control, but short of weight loss, researchers are also investigating the role of poor dietary quality. Thus far, data suggest that it’s the composition of the diet, and not just its contribution to weight gain, that could be impactful, Dr. Dixon said.
More basic research questions cited by Dr. Dixon include the extent to which adipose tissue inflammation causes inflammation in the lungs. “It’s a little unclear whether all the metabolic dysfunction associated with poor asthma control is causing inflammation in the lungs,” she said, though “we’ve done some work here that shows mediators produced by the adipose tissue could be impacting production of inflammatory mediators by the airway epithelium.”
Overall, she said, “the big questions [in asthma] are, how does adipose tissue affect the airway? Is it through direct effects? Through effects on the immune system? And obesity is affected by diet and the gut microbiome – how can these be [impacting] the airway?”
Obesity “is associated with so many changes – the gut, the immune system, and metabolic dysfunction, in addition to airway mechanics,” she said, “that I no longer think, as I did when I came to this, that it’s just one thing. It’s probably all of these things together.”
In the meantime, questions about potential shared pathways for the development of obesity and asthma remain. “Obesity is a risk factor for developing asthma, but it’s also entirely possible that asthma is a risk factor for developing obesity,” she said. (Some data from pediatric populations, she noted, suggest that nonobese children with asthma are at increased risk of developing obesity.)
Also important, Dr. Dixon said, is “emerging literature in the last 5-10 years” that suggests that people with obesity are more susceptible to the effects of air pollution. Research involving inner-city schoolchildren with asthma, for instance, has shown that those with obesity had worse symptoms with air pollution exposure than did those who were not obese.
Pulmonary arterial hypertension
Some research has looked at adipose tissue–produced substances in PAH, but the most well-established association in obesity and PAH involves insulin resistance.
“I don’t think we’re certain as a community that obesity [in general] is the problem – it’s not itself considered a risk factor for PAH,” Anna R. Hemnes, MD, associate professor of medicine at Vanderbilt University Medical Center in Nashville, Tenn., said in an interview. She noted that it’s “hard to dissect obesity” apart.
Researchers are “more confident,” she said, “that insulin resistance – one feature of obesity [in some people] – is associated with worse outcomes in PAH.” Metabolic disease resembling insulin resistance is common in PAH and is believed to contribute to pulmonary vascular disease and right ventricular (RV) failure – the main cause of mortality in PAH – at least in part because of increased oxidative stress.
Dr. Hemnes led a mechanistic phase II clinical trial of metformin in PAH in which the drug was associated with improved RV fractional area change and reduced RV lipid deposition (J Am Heart Assoc. 2020;9[22]:e018349), and she’s now leading a National Institutes of Health–funded multicenter trial looking at the impact of metformin and an exercise intervention on 6-minute walk distance and World Health Organization functional class in PAH.
At the Rush Lung Center, in the meantime, Dr. Mokhlesi is utilizing animal models of OSA and OHS to explore the effect of hypoxia and nighttime hypercapnia on the development of PAH. “I think the jury is still out as to whether obesity itself is a major risk factor, but if so, by what mechanism?” he said. “Is it worsening [sleep-disordered breathing], which then worsens PAH?”
COPD
The focus in COPD has traditionally been on underweight, but the relationship between obesity and COPD has increasingly been recognized in the last 10-15 years, said Frits M. E. Franssen, MD, PhD, of CIRO, a research institute in Horn, the Netherlands, that treats COPD and other chronic lung diseases, and of the department of respiratory medicine at Maastricht University.
Researchers like Dr. Franssen are trying, for one, to understand obesity’s impact on COPD pathophysiology and to tease apart the impact of both conditions on disease severity and patient-related outcomes such as exercise capacity and exercise-related symptoms.
When Dr. Franssen’s group compared responses to weight-bearing exercise (6-min. walk test) and weight-supported exercise (cycling) in obese and normal weight COPD patients matched for age, gender, and degree of airflow limitation, the researchers found that walking capacity was significantly reduced while cycling capacity was preserved in the obese group (Respirology. 2016;21[3]:483-8).
Exercise-related symptoms (dyspnea and leg fatigue) were largely comparable between the obese and normal-weight COPD patients in both exercise modalities. However, in other studies, dyspnea ratings during cycling – at any given level of ventilation – have been lower in obese patients, indicating that “additional fat mass may have a beneficial effect on lung functioning [in non–weight-bearing exercise],” he said in an interview.
Dr. Franssen’s group also has assessed body composition in overweight and obese patients with COPD and found that a significant number have low muscle mass. These patients had worse lung function, exercise tolerance, and muscle strength compared to patients with comparable BMI and normal muscle mass (Respir Res. 2021 Mar 25. doi: 10.1186/s12931-021-01689-w).
“We’d always thought that obese patients have normal muscle mass ... but now we know it can be dramatically low,” he said. In assessing obesity and formulating any weight loss plans, “we’re now interested not only in weight but in the distribution of fat mass and fat-free mass ... and in maintaining muscle mass in patients who are [prescribed dietary interventions].”
Paradoxically, in patients with severe COPD, obesity is associated with prolonged survival, while in patients with mild to moderate COPD, obesity is associated with increased mortality risk, he noted.
The impact of adipose tissue and the chronic inflammation and metabolic disturbances that characterize obesity are currently largely unexplored, he said. Researchers have not yet studied what optimal weights may be for patients with COPD. “And we’re interested in the questions, are body weight and body composition the result of the disease, or [are they] determining the type of COPD one will get?” Dr. Franssen said.
Patients with COPD who are obese have “more of the phenotype of chronic bronchitis,” he noted, “while typical emphysema patients are normally underweight.”
The diverse effects of obesity on lung health and disease are increasingly being teased apart, with researchers honing in on the impact of metabolic dysfunction, circulating inflammatory factors produced by adipose tissue, lipid handling, and other factors – in addition to body mass index – that are associated with the obese state.
“The bird’s eye view is that obesity completely changes lung health. It’s something we’ve only recently begun to appreciate,” said Anne E. Dixon, MA, BM, BCh, director of the Vermont Lung Center at the University of Vermont, Burlington, who is focused on the research field of obesity and lung disease.
Structural, mechanical effects of obesity on lung function are better known and appreciated. Accumulation of fat in the mediastinum and abdominal and thoracic cavities causes reductions in lung volume, in functional residual capacity, and in the compliance of the lungs, chest wall, and entire respiratory system, for instance.
Yet obesity is more than a state of increased BMI, and “what we’ve begun to understand is that [its impact on the lungs and respiratory health] is much more complicated than just a mechanical problem,” said Dr. Dixon, also director of pulmonary and critical care medicine at the University of Vermont Medical Center and professor of medicine at the medical college.
With obesity, adipose tissue changes not only in quantity, but in function, producing proinflammatory cytokines and hormones – such as leptin, tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 – that can have direct effects on the lung. Insulin resistance, which is common with obesity, is also seemingly deleterious. And obesity-associated changes in immune function, lipid handling, diet, and the gut microbiome may also impact lung health and disease, she said.
Dr. Dixon, who wrote about these changes in a 2018 review article in the journal CHEST and another 2019 piece in Expert Review of Respiratory Medicine, has developed a research program focused on obesity and lung disease and has edited a book and organized international conferences on the topic. (CHEST 2018;153[3]:702-9 and Exper Rev Respir Med. 2018;12[9]:755-67.)
“The more I do, the more I realize that there are multiple obesity-associated changes involved, and that [our current high level of] obesity is like a huge population-level natural experiment ... on lung health,” she told this news organization.
Associations between lung disease and the metabolic and other disturbances of obesity are most established in asthma research and have taken hold in the realm of sleep-disordered breathing. But as the prevalence of obesity continues to grow, its role in other lung diseases such as chronic obstructive pulmonary disorder (COPD) and, most recently, pulmonary arterial hypertension (PAH), is getting attention in academia.
And certainly, COVID-19 has highlighted an “urgent need” to better understand how obesity increases susceptibility to severe viral infections, Dr. Dixon added.
Here are some glimpses into current thinking and some examples of research that may have preventive and therapeutic implications in the future:
OSA and OHS
“With sleep apnea we tend to focus on anatomic considerations, but there may be relationships or interactions between obesity and neuromuscular function and neuroventilatory control,” Susheel P. Patil, MD, PhD, director of the sleep medicine program for University Hospitals and assistant professor at Case Western Reserve University, Cleveland, said in an interview.
Some studies suggest, for instance, that TNF-alpha can increase obstructive sleep apnea (OSA) susceptibility and severity through its neuroventilatory modulating properties during sleep. And the potential for additional proinflammatory cytokines produced by adipose tissue to similarly affect upper airway neuroventilatory control is an “intriguing line” of inquiry for researchers in the sleep apnea space, he said.
Leptin is of interest particularly in obesity hypoventilation syndrome (OHS), which is characterized by chronic daytime hypercapnia. Best known as a satiety hormone, leptin is produced by adipose tissue and suppresses appetite at the central nervous system level. But it has long been known that leptin also affects ventilation and the control of breathing.
When transported across the blood-brain barrier, leptin increases the hypercapnic ventilatory response, Babak Mokhlesi, MD, MSc, codirector of the Rush Lung Center and chief of pulmonary, critical care, and sleep medicine at Rush University Medical Center in Chicago, said in an interview.
Research suggests that patients with OHS may have resistance to leptin at the central nervous system level – with leptin not reaching the sites of ventilatory control. This is a “prevailing theory” and could explain why these patients “do not augment their ventilation to maintain homeostasis, normal levels of CO2,” Dr. Mokhlesi said.
“Why some patients with severe obesity develop CO2 retention while others do not is not fully understood,” he said, noting that patients with OHS can normalize their CO2 quickly when instructed to take deep breaths. “What we know is that the centers in the brain responsible for augmenting ventilation when CO2 goes up are somehow blunted.”
In a study of obese mice led by Vsevolod Y. Polotsky, MD, PhD, of Johns Hopkins University, Baltimore – and highlighted by Dr. Mokhlesi as an example of important, recent research – leptin delivered intranasally alleviated hypoventilation (and upper-airway obstruction), while intraperitoneally administered leptin did not, seemingly overcoming “central leptin deficiency.” (Am J Respir Crit Care Med. 2019;199[6]:773-83).
“This proved that there is some level of resistance in this animal model ... and has potential for therapeutics in the future,” Dr. Mokhlesi said.
Understanding the role of insulin resistance in OSA is another research focus. Some data suggest that insulin resistance, which is more common in obesity, is more prevalent in populations with OSA, Dr. Patil said. Researchers have discussed a bidirectional relationship for years, but it’s likely that insulin resistance is a precursor, he said.
In a mechanistic study published in 2016, Dr. Patil and his coinvestigators found that obese individuals with insulin resistance but without frank diabetes or sleep apnea demonstrated preclinical elevations in pharyngeal collapsibility during sleep. The findings suggest that insulin resistance could play a causal role in OSA pathogenesis by “generating requisite elevations in pharyngeal collapsibility,” they wrote (Eur. Respir J. 2016;47[6]:1718-26).
More recently, Dr. Patil noted in the interview, there is increasing appreciation in academia that the type of fat may be important to predicting OSA. “Visceral fat has a completely different cytokine-secretion profile than subcutaneous fat ... it is the more metabolically active fat that may secondarily impact upper airway function though a neuroinflammatory mechanism,” he said. “That is one of the working hypotheses today.”
Asthma
Research has so roundly suggested that metabolic dysfunction contributes to severe, poorly controlled asthma that there’s recent and growing interest in targeting metabolic dysfunction as part of the treatment of obese asthma, said Dr. Dixon, whose own research in obesity and lung disease has focused on asthma.
Data from animal models and some epidemiologic studies have suggested that drugs used to treat type 2 diabetes mellitus, such as glucagon-like peptide receptor-1 (GLPR-1) agonists and metformin, may help control asthma. In one recent study – cited by Dr. Dixon in a 2022 review of obesity and asthma – people with obesity and asthma who were prescribed GLPR-1 agonists for diabetes had fewer asthma exacerbations compared with those who took other medications for diabetes (Semin Respir Crit Care Med. 2022 Feb 17. doi: 10.1055/s-0042-1742384).
There is also research interest in targeting the pro-inflammatory adipokine interleukin 6 (IL-6), since increased circulating levels of IL-6 correlate with asthma severity, and in addressing oxidative stress in asthma through treatment with a mitochondrially targeted antioxidant, she said. Oxidative stress is increased in the airways of people with obesity, and researchers believe it may contribute to the pathophysiology of obese asthma through effects on airway nitric oxide levels.
(Her own research work at the University of Vermont has found associations between poor asthma control and high levels of leptin, and similar associations involving low levels of adiponectin, an anti-inflammatory adipokine that has been shown to downregulate eosinophil recruitment in the airways.)
Weight loss has been shown in mostly small, single-center studies to improve asthma control, but short of weight loss, researchers are also investigating the role of poor dietary quality. Thus far, data suggest that it’s the composition of the diet, and not just its contribution to weight gain, that could be impactful, Dr. Dixon said.
More basic research questions cited by Dr. Dixon include the extent to which adipose tissue inflammation causes inflammation in the lungs. “It’s a little unclear whether all the metabolic dysfunction associated with poor asthma control is causing inflammation in the lungs,” she said, though “we’ve done some work here that shows mediators produced by the adipose tissue could be impacting production of inflammatory mediators by the airway epithelium.”
Overall, she said, “the big questions [in asthma] are, how does adipose tissue affect the airway? Is it through direct effects? Through effects on the immune system? And obesity is affected by diet and the gut microbiome – how can these be [impacting] the airway?”
Obesity “is associated with so many changes – the gut, the immune system, and metabolic dysfunction, in addition to airway mechanics,” she said, “that I no longer think, as I did when I came to this, that it’s just one thing. It’s probably all of these things together.”
In the meantime, questions about potential shared pathways for the development of obesity and asthma remain. “Obesity is a risk factor for developing asthma, but it’s also entirely possible that asthma is a risk factor for developing obesity,” she said. (Some data from pediatric populations, she noted, suggest that nonobese children with asthma are at increased risk of developing obesity.)
Also important, Dr. Dixon said, is “emerging literature in the last 5-10 years” that suggests that people with obesity are more susceptible to the effects of air pollution. Research involving inner-city schoolchildren with asthma, for instance, has shown that those with obesity had worse symptoms with air pollution exposure than did those who were not obese.
Pulmonary arterial hypertension
Some research has looked at adipose tissue–produced substances in PAH, but the most well-established association in obesity and PAH involves insulin resistance.
“I don’t think we’re certain as a community that obesity [in general] is the problem – it’s not itself considered a risk factor for PAH,” Anna R. Hemnes, MD, associate professor of medicine at Vanderbilt University Medical Center in Nashville, Tenn., said in an interview. She noted that it’s “hard to dissect obesity” apart.
Researchers are “more confident,” she said, “that insulin resistance – one feature of obesity [in some people] – is associated with worse outcomes in PAH.” Metabolic disease resembling insulin resistance is common in PAH and is believed to contribute to pulmonary vascular disease and right ventricular (RV) failure – the main cause of mortality in PAH – at least in part because of increased oxidative stress.
Dr. Hemnes led a mechanistic phase II clinical trial of metformin in PAH in which the drug was associated with improved RV fractional area change and reduced RV lipid deposition (J Am Heart Assoc. 2020;9[22]:e018349), and she’s now leading a National Institutes of Health–funded multicenter trial looking at the impact of metformin and an exercise intervention on 6-minute walk distance and World Health Organization functional class in PAH.
At the Rush Lung Center, in the meantime, Dr. Mokhlesi is utilizing animal models of OSA and OHS to explore the effect of hypoxia and nighttime hypercapnia on the development of PAH. “I think the jury is still out as to whether obesity itself is a major risk factor, but if so, by what mechanism?” he said. “Is it worsening [sleep-disordered breathing], which then worsens PAH?”
COPD
The focus in COPD has traditionally been on underweight, but the relationship between obesity and COPD has increasingly been recognized in the last 10-15 years, said Frits M. E. Franssen, MD, PhD, of CIRO, a research institute in Horn, the Netherlands, that treats COPD and other chronic lung diseases, and of the department of respiratory medicine at Maastricht University.
Researchers like Dr. Franssen are trying, for one, to understand obesity’s impact on COPD pathophysiology and to tease apart the impact of both conditions on disease severity and patient-related outcomes such as exercise capacity and exercise-related symptoms.
When Dr. Franssen’s group compared responses to weight-bearing exercise (6-min. walk test) and weight-supported exercise (cycling) in obese and normal weight COPD patients matched for age, gender, and degree of airflow limitation, the researchers found that walking capacity was significantly reduced while cycling capacity was preserved in the obese group (Respirology. 2016;21[3]:483-8).
Exercise-related symptoms (dyspnea and leg fatigue) were largely comparable between the obese and normal-weight COPD patients in both exercise modalities. However, in other studies, dyspnea ratings during cycling – at any given level of ventilation – have been lower in obese patients, indicating that “additional fat mass may have a beneficial effect on lung functioning [in non–weight-bearing exercise],” he said in an interview.
Dr. Franssen’s group also has assessed body composition in overweight and obese patients with COPD and found that a significant number have low muscle mass. These patients had worse lung function, exercise tolerance, and muscle strength compared to patients with comparable BMI and normal muscle mass (Respir Res. 2021 Mar 25. doi: 10.1186/s12931-021-01689-w).
“We’d always thought that obese patients have normal muscle mass ... but now we know it can be dramatically low,” he said. In assessing obesity and formulating any weight loss plans, “we’re now interested not only in weight but in the distribution of fat mass and fat-free mass ... and in maintaining muscle mass in patients who are [prescribed dietary interventions].”
Paradoxically, in patients with severe COPD, obesity is associated with prolonged survival, while in patients with mild to moderate COPD, obesity is associated with increased mortality risk, he noted.
The impact of adipose tissue and the chronic inflammation and metabolic disturbances that characterize obesity are currently largely unexplored, he said. Researchers have not yet studied what optimal weights may be for patients with COPD. “And we’re interested in the questions, are body weight and body composition the result of the disease, or [are they] determining the type of COPD one will get?” Dr. Franssen said.
Patients with COPD who are obese have “more of the phenotype of chronic bronchitis,” he noted, “while typical emphysema patients are normally underweight.”
The diverse effects of obesity on lung health and disease are increasingly being teased apart, with researchers honing in on the impact of metabolic dysfunction, circulating inflammatory factors produced by adipose tissue, lipid handling, and other factors – in addition to body mass index – that are associated with the obese state.
“The bird’s eye view is that obesity completely changes lung health. It’s something we’ve only recently begun to appreciate,” said Anne E. Dixon, MA, BM, BCh, director of the Vermont Lung Center at the University of Vermont, Burlington, who is focused on the research field of obesity and lung disease.
Structural, mechanical effects of obesity on lung function are better known and appreciated. Accumulation of fat in the mediastinum and abdominal and thoracic cavities causes reductions in lung volume, in functional residual capacity, and in the compliance of the lungs, chest wall, and entire respiratory system, for instance.
Yet obesity is more than a state of increased BMI, and “what we’ve begun to understand is that [its impact on the lungs and respiratory health] is much more complicated than just a mechanical problem,” said Dr. Dixon, also director of pulmonary and critical care medicine at the University of Vermont Medical Center and professor of medicine at the medical college.
With obesity, adipose tissue changes not only in quantity, but in function, producing proinflammatory cytokines and hormones – such as leptin, tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 – that can have direct effects on the lung. Insulin resistance, which is common with obesity, is also seemingly deleterious. And obesity-associated changes in immune function, lipid handling, diet, and the gut microbiome may also impact lung health and disease, she said.
Dr. Dixon, who wrote about these changes in a 2018 review article in the journal CHEST and another 2019 piece in Expert Review of Respiratory Medicine, has developed a research program focused on obesity and lung disease and has edited a book and organized international conferences on the topic. (CHEST 2018;153[3]:702-9 and Exper Rev Respir Med. 2018;12[9]:755-67.)
“The more I do, the more I realize that there are multiple obesity-associated changes involved, and that [our current high level of] obesity is like a huge population-level natural experiment ... on lung health,” she told this news organization.
Associations between lung disease and the metabolic and other disturbances of obesity are most established in asthma research and have taken hold in the realm of sleep-disordered breathing. But as the prevalence of obesity continues to grow, its role in other lung diseases such as chronic obstructive pulmonary disorder (COPD) and, most recently, pulmonary arterial hypertension (PAH), is getting attention in academia.
And certainly, COVID-19 has highlighted an “urgent need” to better understand how obesity increases susceptibility to severe viral infections, Dr. Dixon added.
Here are some glimpses into current thinking and some examples of research that may have preventive and therapeutic implications in the future:
OSA and OHS
“With sleep apnea we tend to focus on anatomic considerations, but there may be relationships or interactions between obesity and neuromuscular function and neuroventilatory control,” Susheel P. Patil, MD, PhD, director of the sleep medicine program for University Hospitals and assistant professor at Case Western Reserve University, Cleveland, said in an interview.
Some studies suggest, for instance, that TNF-alpha can increase obstructive sleep apnea (OSA) susceptibility and severity through its neuroventilatory modulating properties during sleep. And the potential for additional proinflammatory cytokines produced by adipose tissue to similarly affect upper airway neuroventilatory control is an “intriguing line” of inquiry for researchers in the sleep apnea space, he said.
Leptin is of interest particularly in obesity hypoventilation syndrome (OHS), which is characterized by chronic daytime hypercapnia. Best known as a satiety hormone, leptin is produced by adipose tissue and suppresses appetite at the central nervous system level. But it has long been known that leptin also affects ventilation and the control of breathing.
When transported across the blood-brain barrier, leptin increases the hypercapnic ventilatory response, Babak Mokhlesi, MD, MSc, codirector of the Rush Lung Center and chief of pulmonary, critical care, and sleep medicine at Rush University Medical Center in Chicago, said in an interview.
Research suggests that patients with OHS may have resistance to leptin at the central nervous system level – with leptin not reaching the sites of ventilatory control. This is a “prevailing theory” and could explain why these patients “do not augment their ventilation to maintain homeostasis, normal levels of CO2,” Dr. Mokhlesi said.
“Why some patients with severe obesity develop CO2 retention while others do not is not fully understood,” he said, noting that patients with OHS can normalize their CO2 quickly when instructed to take deep breaths. “What we know is that the centers in the brain responsible for augmenting ventilation when CO2 goes up are somehow blunted.”
In a study of obese mice led by Vsevolod Y. Polotsky, MD, PhD, of Johns Hopkins University, Baltimore – and highlighted by Dr. Mokhlesi as an example of important, recent research – leptin delivered intranasally alleviated hypoventilation (and upper-airway obstruction), while intraperitoneally administered leptin did not, seemingly overcoming “central leptin deficiency.” (Am J Respir Crit Care Med. 2019;199[6]:773-83).
“This proved that there is some level of resistance in this animal model ... and has potential for therapeutics in the future,” Dr. Mokhlesi said.
Understanding the role of insulin resistance in OSA is another research focus. Some data suggest that insulin resistance, which is more common in obesity, is more prevalent in populations with OSA, Dr. Patil said. Researchers have discussed a bidirectional relationship for years, but it’s likely that insulin resistance is a precursor, he said.
In a mechanistic study published in 2016, Dr. Patil and his coinvestigators found that obese individuals with insulin resistance but without frank diabetes or sleep apnea demonstrated preclinical elevations in pharyngeal collapsibility during sleep. The findings suggest that insulin resistance could play a causal role in OSA pathogenesis by “generating requisite elevations in pharyngeal collapsibility,” they wrote (Eur. Respir J. 2016;47[6]:1718-26).
More recently, Dr. Patil noted in the interview, there is increasing appreciation in academia that the type of fat may be important to predicting OSA. “Visceral fat has a completely different cytokine-secretion profile than subcutaneous fat ... it is the more metabolically active fat that may secondarily impact upper airway function though a neuroinflammatory mechanism,” he said. “That is one of the working hypotheses today.”
Asthma
Research has so roundly suggested that metabolic dysfunction contributes to severe, poorly controlled asthma that there’s recent and growing interest in targeting metabolic dysfunction as part of the treatment of obese asthma, said Dr. Dixon, whose own research in obesity and lung disease has focused on asthma.
Data from animal models and some epidemiologic studies have suggested that drugs used to treat type 2 diabetes mellitus, such as glucagon-like peptide receptor-1 (GLPR-1) agonists and metformin, may help control asthma. In one recent study – cited by Dr. Dixon in a 2022 review of obesity and asthma – people with obesity and asthma who were prescribed GLPR-1 agonists for diabetes had fewer asthma exacerbations compared with those who took other medications for diabetes (Semin Respir Crit Care Med. 2022 Feb 17. doi: 10.1055/s-0042-1742384).
There is also research interest in targeting the pro-inflammatory adipokine interleukin 6 (IL-6), since increased circulating levels of IL-6 correlate with asthma severity, and in addressing oxidative stress in asthma through treatment with a mitochondrially targeted antioxidant, she said. Oxidative stress is increased in the airways of people with obesity, and researchers believe it may contribute to the pathophysiology of obese asthma through effects on airway nitric oxide levels.
(Her own research work at the University of Vermont has found associations between poor asthma control and high levels of leptin, and similar associations involving low levels of adiponectin, an anti-inflammatory adipokine that has been shown to downregulate eosinophil recruitment in the airways.)
Weight loss has been shown in mostly small, single-center studies to improve asthma control, but short of weight loss, researchers are also investigating the role of poor dietary quality. Thus far, data suggest that it’s the composition of the diet, and not just its contribution to weight gain, that could be impactful, Dr. Dixon said.
More basic research questions cited by Dr. Dixon include the extent to which adipose tissue inflammation causes inflammation in the lungs. “It’s a little unclear whether all the metabolic dysfunction associated with poor asthma control is causing inflammation in the lungs,” she said, though “we’ve done some work here that shows mediators produced by the adipose tissue could be impacting production of inflammatory mediators by the airway epithelium.”
Overall, she said, “the big questions [in asthma] are, how does adipose tissue affect the airway? Is it through direct effects? Through effects on the immune system? And obesity is affected by diet and the gut microbiome – how can these be [impacting] the airway?”
Obesity “is associated with so many changes – the gut, the immune system, and metabolic dysfunction, in addition to airway mechanics,” she said, “that I no longer think, as I did when I came to this, that it’s just one thing. It’s probably all of these things together.”
In the meantime, questions about potential shared pathways for the development of obesity and asthma remain. “Obesity is a risk factor for developing asthma, but it’s also entirely possible that asthma is a risk factor for developing obesity,” she said. (Some data from pediatric populations, she noted, suggest that nonobese children with asthma are at increased risk of developing obesity.)
Also important, Dr. Dixon said, is “emerging literature in the last 5-10 years” that suggests that people with obesity are more susceptible to the effects of air pollution. Research involving inner-city schoolchildren with asthma, for instance, has shown that those with obesity had worse symptoms with air pollution exposure than did those who were not obese.
Pulmonary arterial hypertension
Some research has looked at adipose tissue–produced substances in PAH, but the most well-established association in obesity and PAH involves insulin resistance.
“I don’t think we’re certain as a community that obesity [in general] is the problem – it’s not itself considered a risk factor for PAH,” Anna R. Hemnes, MD, associate professor of medicine at Vanderbilt University Medical Center in Nashville, Tenn., said in an interview. She noted that it’s “hard to dissect obesity” apart.
Researchers are “more confident,” she said, “that insulin resistance – one feature of obesity [in some people] – is associated with worse outcomes in PAH.” Metabolic disease resembling insulin resistance is common in PAH and is believed to contribute to pulmonary vascular disease and right ventricular (RV) failure – the main cause of mortality in PAH – at least in part because of increased oxidative stress.
Dr. Hemnes led a mechanistic phase II clinical trial of metformin in PAH in which the drug was associated with improved RV fractional area change and reduced RV lipid deposition (J Am Heart Assoc. 2020;9[22]:e018349), and she’s now leading a National Institutes of Health–funded multicenter trial looking at the impact of metformin and an exercise intervention on 6-minute walk distance and World Health Organization functional class in PAH.
At the Rush Lung Center, in the meantime, Dr. Mokhlesi is utilizing animal models of OSA and OHS to explore the effect of hypoxia and nighttime hypercapnia on the development of PAH. “I think the jury is still out as to whether obesity itself is a major risk factor, but if so, by what mechanism?” he said. “Is it worsening [sleep-disordered breathing], which then worsens PAH?”
COPD
The focus in COPD has traditionally been on underweight, but the relationship between obesity and COPD has increasingly been recognized in the last 10-15 years, said Frits M. E. Franssen, MD, PhD, of CIRO, a research institute in Horn, the Netherlands, that treats COPD and other chronic lung diseases, and of the department of respiratory medicine at Maastricht University.
Researchers like Dr. Franssen are trying, for one, to understand obesity’s impact on COPD pathophysiology and to tease apart the impact of both conditions on disease severity and patient-related outcomes such as exercise capacity and exercise-related symptoms.
When Dr. Franssen’s group compared responses to weight-bearing exercise (6-min. walk test) and weight-supported exercise (cycling) in obese and normal weight COPD patients matched for age, gender, and degree of airflow limitation, the researchers found that walking capacity was significantly reduced while cycling capacity was preserved in the obese group (Respirology. 2016;21[3]:483-8).
Exercise-related symptoms (dyspnea and leg fatigue) were largely comparable between the obese and normal-weight COPD patients in both exercise modalities. However, in other studies, dyspnea ratings during cycling – at any given level of ventilation – have been lower in obese patients, indicating that “additional fat mass may have a beneficial effect on lung functioning [in non–weight-bearing exercise],” he said in an interview.
Dr. Franssen’s group also has assessed body composition in overweight and obese patients with COPD and found that a significant number have low muscle mass. These patients had worse lung function, exercise tolerance, and muscle strength compared to patients with comparable BMI and normal muscle mass (Respir Res. 2021 Mar 25. doi: 10.1186/s12931-021-01689-w).
“We’d always thought that obese patients have normal muscle mass ... but now we know it can be dramatically low,” he said. In assessing obesity and formulating any weight loss plans, “we’re now interested not only in weight but in the distribution of fat mass and fat-free mass ... and in maintaining muscle mass in patients who are [prescribed dietary interventions].”
Paradoxically, in patients with severe COPD, obesity is associated with prolonged survival, while in patients with mild to moderate COPD, obesity is associated with increased mortality risk, he noted.
The impact of adipose tissue and the chronic inflammation and metabolic disturbances that characterize obesity are currently largely unexplored, he said. Researchers have not yet studied what optimal weights may be for patients with COPD. “And we’re interested in the questions, are body weight and body composition the result of the disease, or [are they] determining the type of COPD one will get?” Dr. Franssen said.
Patients with COPD who are obese have “more of the phenotype of chronic bronchitis,” he noted, “while typical emphysema patients are normally underweight.”
Cannabis vaping continues its rise in teens
More teenagers in the United States reported cannabis use with vaping in 2019, compared with 2017, while cannabis use without vaping declined, based on annual survey data from more than 50,000 teens.
“With vaping prevalence rising so quickly among teens, getting a clearer picture of how cannabis use is shifting helps inform prevention and cessation efforts,” corresponding author Noah T. Kreski, MPH, of Columbia University, New York, said in an interview.
“In just 2 years, the most common cannabis use pattern changed from ‘occasional use without vaping’ to ‘frequent use with vaping,’ said Mx. Kreski, who uses the honorific Mx. and the pronouns they/them. “Knowing that, as well as the high overlap of cannabis vaping with nicotine use and binge drinking, adds to the urgency of reducing adolescent vaping.”
To quantify the trends in cannabis vaping, the researchers reviewed data from Monitoring the Future, an annual survey of high school students across the United States. The study population included 51,052 individuals; approximately 49% were male and 49% were non-Hispanic White. The researchers examined frequency of cannabis use, trends across demographic groups, and concurrent use of cannabis and other substances such as alcohol and tobacco. The findings were published in the journal Addiction.
Frequent cannabis use was defined as six or more times in the past 30 days; occasional use was defined as one to five times in the past 30 days.
Frequent cannabis use with vaping increased from 2.1% in 2017 to 5.4% in 2019. Occasional cannabis use with vaping also increased, though less dramatically, from less than 2% in 2017 to approximately 3.5% in 2019.
By contrast, both frequent and occasional cannabis use without vaping declined from 2017 to 2019 (from 3.8% to 2.1% and from 6.9% to 4.4%, respectively).
Overall, the prevalence of any level of cannabis use increased from 13.9% in 2017 to 15.4% in 2019. Both males and females showed a similar increase in reported frequent cannabis use with vaping of approximately 3%.
The results document that vaping cannabis has become more common than smoking alone among U.S. teens across almost all demographic groups, and across sex, race, urbanicity, and level of parent education; however, the increased was especially marked among Hispanic/Latinx teens and those of lower socioeconomic status, the researchers wrote.
The researchers also examined the associations between cannabis use with and without vaping and concurrent nicotine and alcohol use. Overall, the strongest association was between smoking or vaping nicotine and vaping cannabis; teens who smoked or vaped nicotine were 42 times more likely than nonnicotine users to report vaping cannabis in the past 30 days (adjusted odds ratio, 42.28). In addition, more occasions of binge drinking were more strongly associated with cannabis use with vaping (up to 10 times more likely), compared with cannabis use without vaping, (aORs, 4.48-10.09).
The study findings were limited by several factors, including the lack of questions on tetrahydrocannabinol (THC) or cannabidiol content of the cannabis products used, although evidence suggests that the potency of cannabis products in the United States is increasing, the researchers noted. Other limitations included the cross-sectional design, which prevents making associations about causality, and lack of data on the quantity of cannabis used; only data on frequency of use were recorded.
However, the results reflect a rise in cannabis use with vaping among teens in the United States, along with an increased risk of tobacco use, e-cigarette use, and binge drinking, the researchers said.
As cannabis legalization expands across the United States, policies are needed to deter use among adolescents, the researchers wrote. “These policies should be crafted to reduce an emphasis on criminalization in preference for public health promotion given the history of unequal application of punitive consequences of drug use for racialized minorities in the United States. As products, delivery systems, potency, and marketing proliferate within a for-profit industry, increased attention to youth trends, including investment in sustained and evidence-based prevention and intervention, is increasingly necessary.”
The take-home message for clinicians is to ask whether your patients are vaping, because the prevalence is not only up, but fairly universal, Mx. Kreski said. “Have a discussion that covers a broad range of substance use topics and informs teens of the potential risks of vaping, while avoiding stigma.”
The message for parents is “to talk to your kids about the risks of vaping,” said Mx. Kreski. “Prioritize open communication rather than punishment, and work together with your teens to prevent or reduce vaping.” The message for teens: “Understand that vaping has risks. You should feel empowered to talk to your parents or doctor about those risks. While it may seem like everyone’s vaping, the majority don’t. Keeping communication open between parents/caregivers, teens, and health care providers is one of the best ways to address these trends in vaping.”
Beware more powerful cannabis products
“While drug use in general is declining in adolescents, marijuana use remains very common,” Kelly A. Curran, MD, of the University of Oklahoma Health Sciences Center, Oklahoma City, said in an interview.
“There is growing evidence that marijuana is now the first drug used by adolescents – replacing alcohol and nicotine – and frequent use can lead to substance abuse,” said Dr. Curran, who specializes in adolescent medicine but was involved in the study. “Cannabis use patterns have evolved over time. As I frequently tell my patients and their families, new strains and hybrids of marijuana have higher potencies of THC. Many adolescents are eschewing smoking and in its place using marijuana concentrates (wax, oil, shatter) via vape, dab pen, or rig. Use of these methods puts adolescents at high risk of social and health complications such as [e-cigarette or vaping use-associated lung injury], cannabis hyperemesis syndrome, and psychosis – and understanding these patterns and associated drug use helps health care professionals and parents keep adolescents safe.”
The take-home message for clinicians is that marijuana use via vaping continues to rise and to become more common than “traditional” marijuana smoking, Dr. Curran said. “This increase is across genders, in nearly all race/ethnicities (especially in Latinx youth), and in youth from lower socioeconomic status.” Vaping marijuana is associated with other substance abuse, so health care professionals should include questions about different forms of marijuana use, such as vape, dab pen, or rig, when working with patients, and counsel patients and families about the risks associated with use of any of these products.
The study was supported by the National Center for Injury Prevention and Control and by the National Institute on Drug Abuse. The researchers had no financial conflicts to disclose. Dr. Curran had no financial conflicts to disclose and serves on the editorial advisory board of Pediatric News.
More teenagers in the United States reported cannabis use with vaping in 2019, compared with 2017, while cannabis use without vaping declined, based on annual survey data from more than 50,000 teens.
“With vaping prevalence rising so quickly among teens, getting a clearer picture of how cannabis use is shifting helps inform prevention and cessation efforts,” corresponding author Noah T. Kreski, MPH, of Columbia University, New York, said in an interview.
“In just 2 years, the most common cannabis use pattern changed from ‘occasional use without vaping’ to ‘frequent use with vaping,’ said Mx. Kreski, who uses the honorific Mx. and the pronouns they/them. “Knowing that, as well as the high overlap of cannabis vaping with nicotine use and binge drinking, adds to the urgency of reducing adolescent vaping.”
To quantify the trends in cannabis vaping, the researchers reviewed data from Monitoring the Future, an annual survey of high school students across the United States. The study population included 51,052 individuals; approximately 49% were male and 49% were non-Hispanic White. The researchers examined frequency of cannabis use, trends across demographic groups, and concurrent use of cannabis and other substances such as alcohol and tobacco. The findings were published in the journal Addiction.
Frequent cannabis use was defined as six or more times in the past 30 days; occasional use was defined as one to five times in the past 30 days.
Frequent cannabis use with vaping increased from 2.1% in 2017 to 5.4% in 2019. Occasional cannabis use with vaping also increased, though less dramatically, from less than 2% in 2017 to approximately 3.5% in 2019.
By contrast, both frequent and occasional cannabis use without vaping declined from 2017 to 2019 (from 3.8% to 2.1% and from 6.9% to 4.4%, respectively).
Overall, the prevalence of any level of cannabis use increased from 13.9% in 2017 to 15.4% in 2019. Both males and females showed a similar increase in reported frequent cannabis use with vaping of approximately 3%.
The results document that vaping cannabis has become more common than smoking alone among U.S. teens across almost all demographic groups, and across sex, race, urbanicity, and level of parent education; however, the increased was especially marked among Hispanic/Latinx teens and those of lower socioeconomic status, the researchers wrote.
The researchers also examined the associations between cannabis use with and without vaping and concurrent nicotine and alcohol use. Overall, the strongest association was between smoking or vaping nicotine and vaping cannabis; teens who smoked or vaped nicotine were 42 times more likely than nonnicotine users to report vaping cannabis in the past 30 days (adjusted odds ratio, 42.28). In addition, more occasions of binge drinking were more strongly associated with cannabis use with vaping (up to 10 times more likely), compared with cannabis use without vaping, (aORs, 4.48-10.09).
The study findings were limited by several factors, including the lack of questions on tetrahydrocannabinol (THC) or cannabidiol content of the cannabis products used, although evidence suggests that the potency of cannabis products in the United States is increasing, the researchers noted. Other limitations included the cross-sectional design, which prevents making associations about causality, and lack of data on the quantity of cannabis used; only data on frequency of use were recorded.
However, the results reflect a rise in cannabis use with vaping among teens in the United States, along with an increased risk of tobacco use, e-cigarette use, and binge drinking, the researchers said.
As cannabis legalization expands across the United States, policies are needed to deter use among adolescents, the researchers wrote. “These policies should be crafted to reduce an emphasis on criminalization in preference for public health promotion given the history of unequal application of punitive consequences of drug use for racialized minorities in the United States. As products, delivery systems, potency, and marketing proliferate within a for-profit industry, increased attention to youth trends, including investment in sustained and evidence-based prevention and intervention, is increasingly necessary.”
The take-home message for clinicians is to ask whether your patients are vaping, because the prevalence is not only up, but fairly universal, Mx. Kreski said. “Have a discussion that covers a broad range of substance use topics and informs teens of the potential risks of vaping, while avoiding stigma.”
The message for parents is “to talk to your kids about the risks of vaping,” said Mx. Kreski. “Prioritize open communication rather than punishment, and work together with your teens to prevent or reduce vaping.” The message for teens: “Understand that vaping has risks. You should feel empowered to talk to your parents or doctor about those risks. While it may seem like everyone’s vaping, the majority don’t. Keeping communication open between parents/caregivers, teens, and health care providers is one of the best ways to address these trends in vaping.”
Beware more powerful cannabis products
“While drug use in general is declining in adolescents, marijuana use remains very common,” Kelly A. Curran, MD, of the University of Oklahoma Health Sciences Center, Oklahoma City, said in an interview.
“There is growing evidence that marijuana is now the first drug used by adolescents – replacing alcohol and nicotine – and frequent use can lead to substance abuse,” said Dr. Curran, who specializes in adolescent medicine but was involved in the study. “Cannabis use patterns have evolved over time. As I frequently tell my patients and their families, new strains and hybrids of marijuana have higher potencies of THC. Many adolescents are eschewing smoking and in its place using marijuana concentrates (wax, oil, shatter) via vape, dab pen, or rig. Use of these methods puts adolescents at high risk of social and health complications such as [e-cigarette or vaping use-associated lung injury], cannabis hyperemesis syndrome, and psychosis – and understanding these patterns and associated drug use helps health care professionals and parents keep adolescents safe.”
The take-home message for clinicians is that marijuana use via vaping continues to rise and to become more common than “traditional” marijuana smoking, Dr. Curran said. “This increase is across genders, in nearly all race/ethnicities (especially in Latinx youth), and in youth from lower socioeconomic status.” Vaping marijuana is associated with other substance abuse, so health care professionals should include questions about different forms of marijuana use, such as vape, dab pen, or rig, when working with patients, and counsel patients and families about the risks associated with use of any of these products.
The study was supported by the National Center for Injury Prevention and Control and by the National Institute on Drug Abuse. The researchers had no financial conflicts to disclose. Dr. Curran had no financial conflicts to disclose and serves on the editorial advisory board of Pediatric News.
More teenagers in the United States reported cannabis use with vaping in 2019, compared with 2017, while cannabis use without vaping declined, based on annual survey data from more than 50,000 teens.
“With vaping prevalence rising so quickly among teens, getting a clearer picture of how cannabis use is shifting helps inform prevention and cessation efforts,” corresponding author Noah T. Kreski, MPH, of Columbia University, New York, said in an interview.
“In just 2 years, the most common cannabis use pattern changed from ‘occasional use without vaping’ to ‘frequent use with vaping,’ said Mx. Kreski, who uses the honorific Mx. and the pronouns they/them. “Knowing that, as well as the high overlap of cannabis vaping with nicotine use and binge drinking, adds to the urgency of reducing adolescent vaping.”
To quantify the trends in cannabis vaping, the researchers reviewed data from Monitoring the Future, an annual survey of high school students across the United States. The study population included 51,052 individuals; approximately 49% were male and 49% were non-Hispanic White. The researchers examined frequency of cannabis use, trends across demographic groups, and concurrent use of cannabis and other substances such as alcohol and tobacco. The findings were published in the journal Addiction.
Frequent cannabis use was defined as six or more times in the past 30 days; occasional use was defined as one to five times in the past 30 days.
Frequent cannabis use with vaping increased from 2.1% in 2017 to 5.4% in 2019. Occasional cannabis use with vaping also increased, though less dramatically, from less than 2% in 2017 to approximately 3.5% in 2019.
By contrast, both frequent and occasional cannabis use without vaping declined from 2017 to 2019 (from 3.8% to 2.1% and from 6.9% to 4.4%, respectively).
Overall, the prevalence of any level of cannabis use increased from 13.9% in 2017 to 15.4% in 2019. Both males and females showed a similar increase in reported frequent cannabis use with vaping of approximately 3%.
The results document that vaping cannabis has become more common than smoking alone among U.S. teens across almost all demographic groups, and across sex, race, urbanicity, and level of parent education; however, the increased was especially marked among Hispanic/Latinx teens and those of lower socioeconomic status, the researchers wrote.
The researchers also examined the associations between cannabis use with and without vaping and concurrent nicotine and alcohol use. Overall, the strongest association was between smoking or vaping nicotine and vaping cannabis; teens who smoked or vaped nicotine were 42 times more likely than nonnicotine users to report vaping cannabis in the past 30 days (adjusted odds ratio, 42.28). In addition, more occasions of binge drinking were more strongly associated with cannabis use with vaping (up to 10 times more likely), compared with cannabis use without vaping, (aORs, 4.48-10.09).
The study findings were limited by several factors, including the lack of questions on tetrahydrocannabinol (THC) or cannabidiol content of the cannabis products used, although evidence suggests that the potency of cannabis products in the United States is increasing, the researchers noted. Other limitations included the cross-sectional design, which prevents making associations about causality, and lack of data on the quantity of cannabis used; only data on frequency of use were recorded.
However, the results reflect a rise in cannabis use with vaping among teens in the United States, along with an increased risk of tobacco use, e-cigarette use, and binge drinking, the researchers said.
As cannabis legalization expands across the United States, policies are needed to deter use among adolescents, the researchers wrote. “These policies should be crafted to reduce an emphasis on criminalization in preference for public health promotion given the history of unequal application of punitive consequences of drug use for racialized minorities in the United States. As products, delivery systems, potency, and marketing proliferate within a for-profit industry, increased attention to youth trends, including investment in sustained and evidence-based prevention and intervention, is increasingly necessary.”
The take-home message for clinicians is to ask whether your patients are vaping, because the prevalence is not only up, but fairly universal, Mx. Kreski said. “Have a discussion that covers a broad range of substance use topics and informs teens of the potential risks of vaping, while avoiding stigma.”
The message for parents is “to talk to your kids about the risks of vaping,” said Mx. Kreski. “Prioritize open communication rather than punishment, and work together with your teens to prevent or reduce vaping.” The message for teens: “Understand that vaping has risks. You should feel empowered to talk to your parents or doctor about those risks. While it may seem like everyone’s vaping, the majority don’t. Keeping communication open between parents/caregivers, teens, and health care providers is one of the best ways to address these trends in vaping.”
Beware more powerful cannabis products
“While drug use in general is declining in adolescents, marijuana use remains very common,” Kelly A. Curran, MD, of the University of Oklahoma Health Sciences Center, Oklahoma City, said in an interview.
“There is growing evidence that marijuana is now the first drug used by adolescents – replacing alcohol and nicotine – and frequent use can lead to substance abuse,” said Dr. Curran, who specializes in adolescent medicine but was involved in the study. “Cannabis use patterns have evolved over time. As I frequently tell my patients and their families, new strains and hybrids of marijuana have higher potencies of THC. Many adolescents are eschewing smoking and in its place using marijuana concentrates (wax, oil, shatter) via vape, dab pen, or rig. Use of these methods puts adolescents at high risk of social and health complications such as [e-cigarette or vaping use-associated lung injury], cannabis hyperemesis syndrome, and psychosis – and understanding these patterns and associated drug use helps health care professionals and parents keep adolescents safe.”
The take-home message for clinicians is that marijuana use via vaping continues to rise and to become more common than “traditional” marijuana smoking, Dr. Curran said. “This increase is across genders, in nearly all race/ethnicities (especially in Latinx youth), and in youth from lower socioeconomic status.” Vaping marijuana is associated with other substance abuse, so health care professionals should include questions about different forms of marijuana use, such as vape, dab pen, or rig, when working with patients, and counsel patients and families about the risks associated with use of any of these products.
The study was supported by the National Center for Injury Prevention and Control and by the National Institute on Drug Abuse. The researchers had no financial conflicts to disclose. Dr. Curran had no financial conflicts to disclose and serves on the editorial advisory board of Pediatric News.
FROM ADDICTION
Race-based spirometry may lead to missed diagnoses
SAN FRANCISCO – It may be time to move beyond relying largely on spirometry to distinguish between healthy and abnormal lung function in diverse populations.
That conclusion comes from investigators who looked at patients with ostensibly normal spirometry values in a large population-based study and found that using standard equations to adjust for racial differences in lung-function measures appeared to miss emphysema in a significant proportion of Black patients.
“Our traditional measures of lung health based on spirometry may be under-recognizing impaired respiratory health in Black adults and particularly Black men,” said lead author Gabrielle Liu, MD, a fellow in the division of pulmonary and critical care medicine at the Northwestern University Feinberg School of Medicine, Chicago.
“CT imaging may be useful in the evaluation of those with suspected impaired respiratory health and normal spirometry,” she said in an oral abstract session at the American Thoracic Society International Conference 2022.
Dr. Liu and colleagues studied the association between self-identified race and visually identified emphysema among 2,674 participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study. The patients had CT scans at a mean age of 50 and spirometry at a mean age of 55.
Racial differences
The investigators found that among men with forced expiratory volume in 1 second (FEV1) ranging from 100% to 120% of predicted according to race-adjusted formulas, 14.6% of Black men had emphysema, compared with only 1.7% of White men (P < .001). Respective emphysema rates in Black women and White women were 3.8% and 1.9%; this difference was not statistically significant.
Among patients with FEV1 80% to 99% of predicted according to race-specific measures, 15.5% of Black men had emphysema, compared with 4% of White men (P < .001). Respective rates of emphysema were 6.9% for Black women versus 3.2% for White women (P = .025).
When the investigators applied race-neutral spirometry reference equations to the same population, they found that it attenuated but did not completely eliminate the racial disparity in emphysema prevalence among patients with FEV1, ranging from 80% to 120% of predicted.
Relic of the past
The results suggest that race-based adjustments of spirometry measures are a relic of less enlightened times, said Adam Gaffney, MD, MPH, assistant professor of medicine at Harvard Medical School, Boston, and a pulmonologist and critical care physician at Cambridge Health Alliance, Massachusetts.
“If the average lower lung function of Black people is being driven by adversity, structural racism, and deprivation, that means that race-specific equations are normalizing that adversity,” he said in an interview.
“In my opinion, it is time to move beyond race-based equations in clinical pulmonary medicine, particularly in the context of patients with established lung disease in whom use of race-based equations might actually lead to undertreatment,” said Dr. Gaffney, who was not involved in the study.
Dr. Liu agreed that it’s time to move to race-neutral measures and that the whole concept of race-based differences is flawed.
“The long-standing structural inequities in health likely made the reference populations have lower lung function than among Whites,” she told this news organization.
Dr. Liu said that evaluation of lung function should not rely on spirometry alone, but should also include – when appropriate – CT scans, as well as improved understanding of how symptoms may be predictive for poor outcomes.
The study was supported by grants from the National Institutes of Health. Dr. Liu and Dr. Gaffney have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
SAN FRANCISCO – It may be time to move beyond relying largely on spirometry to distinguish between healthy and abnormal lung function in diverse populations.
That conclusion comes from investigators who looked at patients with ostensibly normal spirometry values in a large population-based study and found that using standard equations to adjust for racial differences in lung-function measures appeared to miss emphysema in a significant proportion of Black patients.
“Our traditional measures of lung health based on spirometry may be under-recognizing impaired respiratory health in Black adults and particularly Black men,” said lead author Gabrielle Liu, MD, a fellow in the division of pulmonary and critical care medicine at the Northwestern University Feinberg School of Medicine, Chicago.
“CT imaging may be useful in the evaluation of those with suspected impaired respiratory health and normal spirometry,” she said in an oral abstract session at the American Thoracic Society International Conference 2022.
Dr. Liu and colleagues studied the association between self-identified race and visually identified emphysema among 2,674 participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study. The patients had CT scans at a mean age of 50 and spirometry at a mean age of 55.
Racial differences
The investigators found that among men with forced expiratory volume in 1 second (FEV1) ranging from 100% to 120% of predicted according to race-adjusted formulas, 14.6% of Black men had emphysema, compared with only 1.7% of White men (P < .001). Respective emphysema rates in Black women and White women were 3.8% and 1.9%; this difference was not statistically significant.
Among patients with FEV1 80% to 99% of predicted according to race-specific measures, 15.5% of Black men had emphysema, compared with 4% of White men (P < .001). Respective rates of emphysema were 6.9% for Black women versus 3.2% for White women (P = .025).
When the investigators applied race-neutral spirometry reference equations to the same population, they found that it attenuated but did not completely eliminate the racial disparity in emphysema prevalence among patients with FEV1, ranging from 80% to 120% of predicted.
Relic of the past
The results suggest that race-based adjustments of spirometry measures are a relic of less enlightened times, said Adam Gaffney, MD, MPH, assistant professor of medicine at Harvard Medical School, Boston, and a pulmonologist and critical care physician at Cambridge Health Alliance, Massachusetts.
“If the average lower lung function of Black people is being driven by adversity, structural racism, and deprivation, that means that race-specific equations are normalizing that adversity,” he said in an interview.
“In my opinion, it is time to move beyond race-based equations in clinical pulmonary medicine, particularly in the context of patients with established lung disease in whom use of race-based equations might actually lead to undertreatment,” said Dr. Gaffney, who was not involved in the study.
Dr. Liu agreed that it’s time to move to race-neutral measures and that the whole concept of race-based differences is flawed.
“The long-standing structural inequities in health likely made the reference populations have lower lung function than among Whites,” she told this news organization.
Dr. Liu said that evaluation of lung function should not rely on spirometry alone, but should also include – when appropriate – CT scans, as well as improved understanding of how symptoms may be predictive for poor outcomes.
The study was supported by grants from the National Institutes of Health. Dr. Liu and Dr. Gaffney have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
SAN FRANCISCO – It may be time to move beyond relying largely on spirometry to distinguish between healthy and abnormal lung function in diverse populations.
That conclusion comes from investigators who looked at patients with ostensibly normal spirometry values in a large population-based study and found that using standard equations to adjust for racial differences in lung-function measures appeared to miss emphysema in a significant proportion of Black patients.
“Our traditional measures of lung health based on spirometry may be under-recognizing impaired respiratory health in Black adults and particularly Black men,” said lead author Gabrielle Liu, MD, a fellow in the division of pulmonary and critical care medicine at the Northwestern University Feinberg School of Medicine, Chicago.
“CT imaging may be useful in the evaluation of those with suspected impaired respiratory health and normal spirometry,” she said in an oral abstract session at the American Thoracic Society International Conference 2022.
Dr. Liu and colleagues studied the association between self-identified race and visually identified emphysema among 2,674 participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study. The patients had CT scans at a mean age of 50 and spirometry at a mean age of 55.
Racial differences
The investigators found that among men with forced expiratory volume in 1 second (FEV1) ranging from 100% to 120% of predicted according to race-adjusted formulas, 14.6% of Black men had emphysema, compared with only 1.7% of White men (P < .001). Respective emphysema rates in Black women and White women were 3.8% and 1.9%; this difference was not statistically significant.
Among patients with FEV1 80% to 99% of predicted according to race-specific measures, 15.5% of Black men had emphysema, compared with 4% of White men (P < .001). Respective rates of emphysema were 6.9% for Black women versus 3.2% for White women (P = .025).
When the investigators applied race-neutral spirometry reference equations to the same population, they found that it attenuated but did not completely eliminate the racial disparity in emphysema prevalence among patients with FEV1, ranging from 80% to 120% of predicted.
Relic of the past
The results suggest that race-based adjustments of spirometry measures are a relic of less enlightened times, said Adam Gaffney, MD, MPH, assistant professor of medicine at Harvard Medical School, Boston, and a pulmonologist and critical care physician at Cambridge Health Alliance, Massachusetts.
“If the average lower lung function of Black people is being driven by adversity, structural racism, and deprivation, that means that race-specific equations are normalizing that adversity,” he said in an interview.
“In my opinion, it is time to move beyond race-based equations in clinical pulmonary medicine, particularly in the context of patients with established lung disease in whom use of race-based equations might actually lead to undertreatment,” said Dr. Gaffney, who was not involved in the study.
Dr. Liu agreed that it’s time to move to race-neutral measures and that the whole concept of race-based differences is flawed.
“The long-standing structural inequities in health likely made the reference populations have lower lung function than among Whites,” she told this news organization.
Dr. Liu said that evaluation of lung function should not rely on spirometry alone, but should also include – when appropriate – CT scans, as well as improved understanding of how symptoms may be predictive for poor outcomes.
The study was supported by grants from the National Institutes of Health. Dr. Liu and Dr. Gaffney have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM ATS 2022
Most COVID-19 survivors return to work within 2 years
The burden of persistent COVID-19 symptoms appeared to improve over time, but a higher percentage of former patients reported poor health, compared with the general population. This suggests that some patients need more time to completely recover from COVID-19, wrote the authors of the new study, which was published in The Lancet Respiratory Medicine. Previous research has shown that the health effects of COVID-19 last for up to a year, but data from longer-term studies are limited, said Lixue Huang, MD, of Capital Medical University, Beijing, one of the study authors, and colleagues.
Methods and results
In the new study, the researchers reviewed data from 1,192 adult patients who were discharged from the hospital after surviving COVID-19 between Jan. 7, 2020, and May 29, 2020. The researchers measured the participants’ health outcomes at 6 months, 12 months, and 2 years after their onset of symptoms. A community-based dataset of 3,383 adults with no history of COVID-19 served as controls to measure the recovery of the COVID-19 patients. The median age of the patients at the time of hospital discharge was 57 years, and 46% were women. The median follow-up time after the onset of symptoms was 185 days, 349 days, and 685 days for the 6-month, 12-month, and 2-year visits, respectively. The researchers measured health outcomes using a 6-min walking distance (6MWD) test, laboratory tests, and questionnaires about symptoms, mental health, health-related quality of life, returning to work, and health care use since leaving the hospital.
Overall, the proportion of COVID-19 survivors with at least one symptom decreased from 68% at 6 months to 55% at 2 years (P < .0001). The most frequent symptoms were fatigue and muscle weakness, reported by approximately one-third of the patients (31%); sleep problems also were reported by 31% of the patients.
The proportion of individuals with poor results on the 6MWD decreased continuously over time, not only in COVID-19 survivors overall, but also in three subgroups of varying initial disease severity. Of the 494 survivors who reported working before becoming ill, 438 (89%) had returned to their original jobs 2 years later. The most common reasons for not returning to work were decreased physical function, unwillingness to return, and unemployment, the researchers noted.
However, at 2 years, COVID-19 survivors reported more pain and discomfort, as well as more anxiety and depression, compared with the controls (23% vs. 5% and 12% vs. 5%, respectively).
In addition, significantly more survivors who needed high levels of respiratory support while hospitalized had lung diffusion impairment (65%), reduced residual volume (62%), and total lung capacity (39%), compared with matched controls (36%, 20%, and 6%, respectively) at 2 years.
Long-COVID concerns
Approximately half of the survivors had symptoms of long COVID at 2 years. These individuals were more likely to report pain or discomfort or anxiety or depression, as well as mobility problems, compared to survivors without long COVID. Participants with long-COVID symptoms were more than twice as likely to have an outpatient clinic visit (odds ratio, 2.82), and not quite twice as likely to be rehospitalized (OR, 1.64).
“We found that [health-related quality of life], exercise capacity, and mental health continued to improve throughout the 2 years regardless of initial disease severity, but about half still had symptomatic sequelae at 2 years,” the researchers wrote in their paper.
Findings can inform doctor-patient discussions
“We are increasingly recognizing that the health effects of COVID-19 may persist beyond acute illness, therefore this is a timely study to assess the long-term impact of COVID-19 with a long follow-up period,” said Suman Pal, MD, an internal medicine physician at the University of New Mexico, Albuquerque, in an interview.
The findings are consistent with the existing literature, said Dr. Pal, who was not involved in the study. The data from the study “can help clinicians have discussions regarding expected recovery and long-term prognosis for patients with COVID-19,” he noted.
What patients should know is that “studies such as this can help COVID-19 survivors understand and monitor persistent symptoms they may experience, and bring them to the attention of their clinicians,” said Dr. Pal.
However, “As a single-center study with high attrition of subjects during the study period, the findings may not be generalizable,” Dr. Pal emphasized. “Larger-scale studies and patient registries distributed over different geographical areas and time periods will help obtain a better understanding of the nature and prevalence of long COVID,” he said.
The study findings were limited by several factors, including the lack of formerly hospitalized controls with respiratory infections other than COVID-19 to determine which outcomes are COVID-19 specific, the researchers noted. Other limitations included the use of data from only patients at a single center, and from the early stages of the pandemic, as well as the use of self-reports for comorbidities and health outcomes, they said.
However, the results represent the longest-known published longitudinal follow-up of patients who recovered from acute COVID-19, the researchers emphasized. Study strengths included the large sample size, longitudinal design, and long-term follow-up with non-COVID controls to determine outcomes. The researchers noted their plans to conduct annual follow-ups in the current study population. They added that more research is needed to explore rehabilitation programs to promote recovery for COVID-19 survivors and to reduce the effects of long COVID.
The study was supported by the Chinese Academy of Medical Sciences, National Natural Science Foundation of China, National Key Research and Development Program of China, National Administration of Traditional Chinese Medicine, Major Projects of National Science and Technology on New Drug Creation and Development of Pulmonary Tuberculosis, China Evergrande Group, Jack Ma Foundation, Sino Biopharmaceutical, Ping An Insurance (Group), and New Sunshine Charity Foundation. The researchers and Dr. Pal had no financial conflicts to disclose.
This article was updated on 5/16/2022.
The burden of persistent COVID-19 symptoms appeared to improve over time, but a higher percentage of former patients reported poor health, compared with the general population. This suggests that some patients need more time to completely recover from COVID-19, wrote the authors of the new study, which was published in The Lancet Respiratory Medicine. Previous research has shown that the health effects of COVID-19 last for up to a year, but data from longer-term studies are limited, said Lixue Huang, MD, of Capital Medical University, Beijing, one of the study authors, and colleagues.
Methods and results
In the new study, the researchers reviewed data from 1,192 adult patients who were discharged from the hospital after surviving COVID-19 between Jan. 7, 2020, and May 29, 2020. The researchers measured the participants’ health outcomes at 6 months, 12 months, and 2 years after their onset of symptoms. A community-based dataset of 3,383 adults with no history of COVID-19 served as controls to measure the recovery of the COVID-19 patients. The median age of the patients at the time of hospital discharge was 57 years, and 46% were women. The median follow-up time after the onset of symptoms was 185 days, 349 days, and 685 days for the 6-month, 12-month, and 2-year visits, respectively. The researchers measured health outcomes using a 6-min walking distance (6MWD) test, laboratory tests, and questionnaires about symptoms, mental health, health-related quality of life, returning to work, and health care use since leaving the hospital.
Overall, the proportion of COVID-19 survivors with at least one symptom decreased from 68% at 6 months to 55% at 2 years (P < .0001). The most frequent symptoms were fatigue and muscle weakness, reported by approximately one-third of the patients (31%); sleep problems also were reported by 31% of the patients.
The proportion of individuals with poor results on the 6MWD decreased continuously over time, not only in COVID-19 survivors overall, but also in three subgroups of varying initial disease severity. Of the 494 survivors who reported working before becoming ill, 438 (89%) had returned to their original jobs 2 years later. The most common reasons for not returning to work were decreased physical function, unwillingness to return, and unemployment, the researchers noted.
However, at 2 years, COVID-19 survivors reported more pain and discomfort, as well as more anxiety and depression, compared with the controls (23% vs. 5% and 12% vs. 5%, respectively).
In addition, significantly more survivors who needed high levels of respiratory support while hospitalized had lung diffusion impairment (65%), reduced residual volume (62%), and total lung capacity (39%), compared with matched controls (36%, 20%, and 6%, respectively) at 2 years.
Long-COVID concerns
Approximately half of the survivors had symptoms of long COVID at 2 years. These individuals were more likely to report pain or discomfort or anxiety or depression, as well as mobility problems, compared to survivors without long COVID. Participants with long-COVID symptoms were more than twice as likely to have an outpatient clinic visit (odds ratio, 2.82), and not quite twice as likely to be rehospitalized (OR, 1.64).
“We found that [health-related quality of life], exercise capacity, and mental health continued to improve throughout the 2 years regardless of initial disease severity, but about half still had symptomatic sequelae at 2 years,” the researchers wrote in their paper.
Findings can inform doctor-patient discussions
“We are increasingly recognizing that the health effects of COVID-19 may persist beyond acute illness, therefore this is a timely study to assess the long-term impact of COVID-19 with a long follow-up period,” said Suman Pal, MD, an internal medicine physician at the University of New Mexico, Albuquerque, in an interview.
The findings are consistent with the existing literature, said Dr. Pal, who was not involved in the study. The data from the study “can help clinicians have discussions regarding expected recovery and long-term prognosis for patients with COVID-19,” he noted.
What patients should know is that “studies such as this can help COVID-19 survivors understand and monitor persistent symptoms they may experience, and bring them to the attention of their clinicians,” said Dr. Pal.
However, “As a single-center study with high attrition of subjects during the study period, the findings may not be generalizable,” Dr. Pal emphasized. “Larger-scale studies and patient registries distributed over different geographical areas and time periods will help obtain a better understanding of the nature and prevalence of long COVID,” he said.
The study findings were limited by several factors, including the lack of formerly hospitalized controls with respiratory infections other than COVID-19 to determine which outcomes are COVID-19 specific, the researchers noted. Other limitations included the use of data from only patients at a single center, and from the early stages of the pandemic, as well as the use of self-reports for comorbidities and health outcomes, they said.
However, the results represent the longest-known published longitudinal follow-up of patients who recovered from acute COVID-19, the researchers emphasized. Study strengths included the large sample size, longitudinal design, and long-term follow-up with non-COVID controls to determine outcomes. The researchers noted their plans to conduct annual follow-ups in the current study population. They added that more research is needed to explore rehabilitation programs to promote recovery for COVID-19 survivors and to reduce the effects of long COVID.
The study was supported by the Chinese Academy of Medical Sciences, National Natural Science Foundation of China, National Key Research and Development Program of China, National Administration of Traditional Chinese Medicine, Major Projects of National Science and Technology on New Drug Creation and Development of Pulmonary Tuberculosis, China Evergrande Group, Jack Ma Foundation, Sino Biopharmaceutical, Ping An Insurance (Group), and New Sunshine Charity Foundation. The researchers and Dr. Pal had no financial conflicts to disclose.
This article was updated on 5/16/2022.
The burden of persistent COVID-19 symptoms appeared to improve over time, but a higher percentage of former patients reported poor health, compared with the general population. This suggests that some patients need more time to completely recover from COVID-19, wrote the authors of the new study, which was published in The Lancet Respiratory Medicine. Previous research has shown that the health effects of COVID-19 last for up to a year, but data from longer-term studies are limited, said Lixue Huang, MD, of Capital Medical University, Beijing, one of the study authors, and colleagues.
Methods and results
In the new study, the researchers reviewed data from 1,192 adult patients who were discharged from the hospital after surviving COVID-19 between Jan. 7, 2020, and May 29, 2020. The researchers measured the participants’ health outcomes at 6 months, 12 months, and 2 years after their onset of symptoms. A community-based dataset of 3,383 adults with no history of COVID-19 served as controls to measure the recovery of the COVID-19 patients. The median age of the patients at the time of hospital discharge was 57 years, and 46% were women. The median follow-up time after the onset of symptoms was 185 days, 349 days, and 685 days for the 6-month, 12-month, and 2-year visits, respectively. The researchers measured health outcomes using a 6-min walking distance (6MWD) test, laboratory tests, and questionnaires about symptoms, mental health, health-related quality of life, returning to work, and health care use since leaving the hospital.
Overall, the proportion of COVID-19 survivors with at least one symptom decreased from 68% at 6 months to 55% at 2 years (P < .0001). The most frequent symptoms were fatigue and muscle weakness, reported by approximately one-third of the patients (31%); sleep problems also were reported by 31% of the patients.
The proportion of individuals with poor results on the 6MWD decreased continuously over time, not only in COVID-19 survivors overall, but also in three subgroups of varying initial disease severity. Of the 494 survivors who reported working before becoming ill, 438 (89%) had returned to their original jobs 2 years later. The most common reasons for not returning to work were decreased physical function, unwillingness to return, and unemployment, the researchers noted.
However, at 2 years, COVID-19 survivors reported more pain and discomfort, as well as more anxiety and depression, compared with the controls (23% vs. 5% and 12% vs. 5%, respectively).
In addition, significantly more survivors who needed high levels of respiratory support while hospitalized had lung diffusion impairment (65%), reduced residual volume (62%), and total lung capacity (39%), compared with matched controls (36%, 20%, and 6%, respectively) at 2 years.
Long-COVID concerns
Approximately half of the survivors had symptoms of long COVID at 2 years. These individuals were more likely to report pain or discomfort or anxiety or depression, as well as mobility problems, compared to survivors without long COVID. Participants with long-COVID symptoms were more than twice as likely to have an outpatient clinic visit (odds ratio, 2.82), and not quite twice as likely to be rehospitalized (OR, 1.64).
“We found that [health-related quality of life], exercise capacity, and mental health continued to improve throughout the 2 years regardless of initial disease severity, but about half still had symptomatic sequelae at 2 years,” the researchers wrote in their paper.
Findings can inform doctor-patient discussions
“We are increasingly recognizing that the health effects of COVID-19 may persist beyond acute illness, therefore this is a timely study to assess the long-term impact of COVID-19 with a long follow-up period,” said Suman Pal, MD, an internal medicine physician at the University of New Mexico, Albuquerque, in an interview.
The findings are consistent with the existing literature, said Dr. Pal, who was not involved in the study. The data from the study “can help clinicians have discussions regarding expected recovery and long-term prognosis for patients with COVID-19,” he noted.
What patients should know is that “studies such as this can help COVID-19 survivors understand and monitor persistent symptoms they may experience, and bring them to the attention of their clinicians,” said Dr. Pal.
However, “As a single-center study with high attrition of subjects during the study period, the findings may not be generalizable,” Dr. Pal emphasized. “Larger-scale studies and patient registries distributed over different geographical areas and time periods will help obtain a better understanding of the nature and prevalence of long COVID,” he said.
The study findings were limited by several factors, including the lack of formerly hospitalized controls with respiratory infections other than COVID-19 to determine which outcomes are COVID-19 specific, the researchers noted. Other limitations included the use of data from only patients at a single center, and from the early stages of the pandemic, as well as the use of self-reports for comorbidities and health outcomes, they said.
However, the results represent the longest-known published longitudinal follow-up of patients who recovered from acute COVID-19, the researchers emphasized. Study strengths included the large sample size, longitudinal design, and long-term follow-up with non-COVID controls to determine outcomes. The researchers noted their plans to conduct annual follow-ups in the current study population. They added that more research is needed to explore rehabilitation programs to promote recovery for COVID-19 survivors and to reduce the effects of long COVID.
The study was supported by the Chinese Academy of Medical Sciences, National Natural Science Foundation of China, National Key Research and Development Program of China, National Administration of Traditional Chinese Medicine, Major Projects of National Science and Technology on New Drug Creation and Development of Pulmonary Tuberculosis, China Evergrande Group, Jack Ma Foundation, Sino Biopharmaceutical, Ping An Insurance (Group), and New Sunshine Charity Foundation. The researchers and Dr. Pal had no financial conflicts to disclose.
This article was updated on 5/16/2022.
FROM THE LANCET RESPIRATORY MEDICINE
Myositis guidelines aim to standardize adult and pediatric care
All patients with idiopathic inflammatory myopathies (IIM) should be screened for swallowing difficulties, according to the first evidence-based guideline to be produced.
The guideline, which has been developed by a working group of the British Society for Rheumatology (BSR), also advises that all diagnosed patients should have their myositis antibody levels checked and have their overall well-being assessed. Other recommendations for all patients include the use of glucocorticoids to reduce muscle inflammation and conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) for long-term treatment.
“Finally, now, we’re able to standardize the way we treat adults and children with IIM,” senior guideline author Hector Chinoy, PhD, said at the society’s annual meeting.
It has been a long labor of love, however, taking 4 years to get the guideline published, said Dr. Chinoy, professor of rheumatology and neuromuscular disease at the University of Manchester (England), and a consultant at Salford (England) Royal Hospital.
“We’re not covering diagnosis, classification, or the investigation of suspected IIM,” said Dr. Chinoy. Inclusion body myositis also is not included.
Altogether, there are 13 recommendations that have been developed using a PICO (patient or population, intervention, comparison, outcome) format, graded based on the quality of the available evidence, and then voted on by the working group members to give a score of the strength of agreement. Dr. Chinoy noted that there was a checklist included in the Supplementary Data section of the guideline to help follow the recommendations.
“The target audience for the guideline reflects the variety of clinicians caring for patients with IIM,” Dr. Chinoy said. So that is not just pediatric and adult rheumatologists, but also neurologists, dermatologists, respiratory physicians, oncologists, gastroenterologists, cardiologists, and of course other health care professionals. This includes rheumatology and neurology nurses, psychologists, speech and language therapists, and podiatrists, as well as rheumatology specialist pharmacists, physiotherapists, and occupational therapists.
With reference to the latter, Liza McCann, MBBS, who co-led the development of the guideline, said in a statement released by the BSR that the guideline “highlights the importance of exercise, led and monitored by specialist physiotherapists and occupational therapists.”
Dr. McCann, a consultant pediatric rheumatologist at Alder Hey Hospital, Liverpool, England, and Honorary Clinical Lecturer at the University of Liverpool, added that the guidelines also cover “the need to address psychological wellbeing as an integral part of treatment, in parallel with pharmacological therapies.”
Recommendation highlights
Some of the highlights of the recommendations include the use of high-dose glucocorticoids to manage skeletal muscle inflammation at the time of treatment induction, with specific guidance on the different doses to use in adults and in children. There also is guidance on the use of csDMARDs in both populations and what to use if there is refractory disease – with the strongest evidence supporting the use of intravenous immunoglobulin (IVIG) or cyclophosphamide, and possibly rituximab and abatacept.
“There is insufficient evidence to recommend JAK inhibition,” Dr. Chinoy said. The data search used to develop the guideline had a cutoff of October 2020, but even now there is only anecdotal evidence from case studies, he added.
Importantly, the guidelines recognize that childhood IIM differs from adult disease and call for children to be managed by pediatric specialists.
“Routine assessment of dysphagia should be considered in all patients,” Dr. Chinoy said, “so ask the question.” The recommendation is that a swallowing assessment should involve a speech and language therapist or gastroenterologist, and that IVIG be considered for active disease and dysphagia that is resistant to other treatments.
There also are recommendations to screen adult patients for interstitial lung disease, consider fracture risk, and screen adult patients for cancer if they have specific risk factors that include older age at onset, male gender, dysphagia, and rapid disease onset, among others.
Separate cancer screening guidelines on cards
“Around one in four patients with myositis will develop cancer within the 3 years either before or after myositis onset,” Alexander Oldroyd, MBChB, PhD, said in a separate presentation at the BSR annual meeting.
“It’s a hugely increased risk compared to the general population, and a great worry for patients,” he added. Exactly why there is an increased risk is not known, but “there’s a big link between the biological onset of cancer and myositis.”
Dr. Oldroyd, who is an NIHR Academic Clinical Lecturer at the University of Manchester in England and a coauthor of the BSR myositis guideline, is part of a special interest group set up by the International Myositis Assessment and Clinical Studies Group (IMACS) that is in the process of developing separate guidelines for cancer screening in people newly diagnosed with IIM.
The aim was to produce evidence-based recommendations that were both “pragmatic and practical,” that could help clinicians answer patient’s questions on their risk and how best and how often to screen them, Dr. Oldroyd explained. Importantly, IMACS has endeavored to create recommendations that should be applicable across different countries and health care systems.
“We had to acknowledge that there’s not a lot of evidence base there,” Dr. Oldroyd said, noting that he and colleagues conducted a systematic literature review and meta-analysis and used a Delphi process to draft 20 recommendations. These cover identifying risk factors for cancer in people with myositis and categorizing people into low, medium, and high-risk categories. The recommendations also cover what should constitute basic and enhanced screening, and how often someone should be screened.
Moreover, the authors make recommendations on the use of imaging modalities such as PET and CT scans, as well as upper and lower gastrointestinal endoscopy and naso-endoscopy.
“As rheumatologists, we don’t talk about cancer a lot,” Dr. Oldroyd said. “We pick up a lot of incidental cancers, but we don’t usually talk about cancer screening with patients.” That’s something that needs to change, he said.
“It’s important – just get it out in the open, talk to people about it,” Dr. Oldroyd said.
“Tell them what you’re wanting to do, how you’re wanting to investigate for it, clearly communicate their risk,” he said. “But also acknowledge the limited evidence as well, and clearly communicate the results.”
Dr. Chinoy acknowledged he had received fees for presentations (UCB, Biogen), consultancy (Alexion, Novartis, Eli Lilly, Orphazyme, AstraZeneca), or grant support (Eli Lilly, UCB) that had been paid via his institution for the purpose of furthering myositis research. Dr. Oldroyd had no conflicts of interest to disclose.
All patients with idiopathic inflammatory myopathies (IIM) should be screened for swallowing difficulties, according to the first evidence-based guideline to be produced.
The guideline, which has been developed by a working group of the British Society for Rheumatology (BSR), also advises that all diagnosed patients should have their myositis antibody levels checked and have their overall well-being assessed. Other recommendations for all patients include the use of glucocorticoids to reduce muscle inflammation and conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) for long-term treatment.
“Finally, now, we’re able to standardize the way we treat adults and children with IIM,” senior guideline author Hector Chinoy, PhD, said at the society’s annual meeting.
It has been a long labor of love, however, taking 4 years to get the guideline published, said Dr. Chinoy, professor of rheumatology and neuromuscular disease at the University of Manchester (England), and a consultant at Salford (England) Royal Hospital.
“We’re not covering diagnosis, classification, or the investigation of suspected IIM,” said Dr. Chinoy. Inclusion body myositis also is not included.
Altogether, there are 13 recommendations that have been developed using a PICO (patient or population, intervention, comparison, outcome) format, graded based on the quality of the available evidence, and then voted on by the working group members to give a score of the strength of agreement. Dr. Chinoy noted that there was a checklist included in the Supplementary Data section of the guideline to help follow the recommendations.
“The target audience for the guideline reflects the variety of clinicians caring for patients with IIM,” Dr. Chinoy said. So that is not just pediatric and adult rheumatologists, but also neurologists, dermatologists, respiratory physicians, oncologists, gastroenterologists, cardiologists, and of course other health care professionals. This includes rheumatology and neurology nurses, psychologists, speech and language therapists, and podiatrists, as well as rheumatology specialist pharmacists, physiotherapists, and occupational therapists.
With reference to the latter, Liza McCann, MBBS, who co-led the development of the guideline, said in a statement released by the BSR that the guideline “highlights the importance of exercise, led and monitored by specialist physiotherapists and occupational therapists.”
Dr. McCann, a consultant pediatric rheumatologist at Alder Hey Hospital, Liverpool, England, and Honorary Clinical Lecturer at the University of Liverpool, added that the guidelines also cover “the need to address psychological wellbeing as an integral part of treatment, in parallel with pharmacological therapies.”
Recommendation highlights
Some of the highlights of the recommendations include the use of high-dose glucocorticoids to manage skeletal muscle inflammation at the time of treatment induction, with specific guidance on the different doses to use in adults and in children. There also is guidance on the use of csDMARDs in both populations and what to use if there is refractory disease – with the strongest evidence supporting the use of intravenous immunoglobulin (IVIG) or cyclophosphamide, and possibly rituximab and abatacept.
“There is insufficient evidence to recommend JAK inhibition,” Dr. Chinoy said. The data search used to develop the guideline had a cutoff of October 2020, but even now there is only anecdotal evidence from case studies, he added.
Importantly, the guidelines recognize that childhood IIM differs from adult disease and call for children to be managed by pediatric specialists.
“Routine assessment of dysphagia should be considered in all patients,” Dr. Chinoy said, “so ask the question.” The recommendation is that a swallowing assessment should involve a speech and language therapist or gastroenterologist, and that IVIG be considered for active disease and dysphagia that is resistant to other treatments.
There also are recommendations to screen adult patients for interstitial lung disease, consider fracture risk, and screen adult patients for cancer if they have specific risk factors that include older age at onset, male gender, dysphagia, and rapid disease onset, among others.
Separate cancer screening guidelines on cards
“Around one in four patients with myositis will develop cancer within the 3 years either before or after myositis onset,” Alexander Oldroyd, MBChB, PhD, said in a separate presentation at the BSR annual meeting.
“It’s a hugely increased risk compared to the general population, and a great worry for patients,” he added. Exactly why there is an increased risk is not known, but “there’s a big link between the biological onset of cancer and myositis.”
Dr. Oldroyd, who is an NIHR Academic Clinical Lecturer at the University of Manchester in England and a coauthor of the BSR myositis guideline, is part of a special interest group set up by the International Myositis Assessment and Clinical Studies Group (IMACS) that is in the process of developing separate guidelines for cancer screening in people newly diagnosed with IIM.
The aim was to produce evidence-based recommendations that were both “pragmatic and practical,” that could help clinicians answer patient’s questions on their risk and how best and how often to screen them, Dr. Oldroyd explained. Importantly, IMACS has endeavored to create recommendations that should be applicable across different countries and health care systems.
“We had to acknowledge that there’s not a lot of evidence base there,” Dr. Oldroyd said, noting that he and colleagues conducted a systematic literature review and meta-analysis and used a Delphi process to draft 20 recommendations. These cover identifying risk factors for cancer in people with myositis and categorizing people into low, medium, and high-risk categories. The recommendations also cover what should constitute basic and enhanced screening, and how often someone should be screened.
Moreover, the authors make recommendations on the use of imaging modalities such as PET and CT scans, as well as upper and lower gastrointestinal endoscopy and naso-endoscopy.
“As rheumatologists, we don’t talk about cancer a lot,” Dr. Oldroyd said. “We pick up a lot of incidental cancers, but we don’t usually talk about cancer screening with patients.” That’s something that needs to change, he said.
“It’s important – just get it out in the open, talk to people about it,” Dr. Oldroyd said.
“Tell them what you’re wanting to do, how you’re wanting to investigate for it, clearly communicate their risk,” he said. “But also acknowledge the limited evidence as well, and clearly communicate the results.”
Dr. Chinoy acknowledged he had received fees for presentations (UCB, Biogen), consultancy (Alexion, Novartis, Eli Lilly, Orphazyme, AstraZeneca), or grant support (Eli Lilly, UCB) that had been paid via his institution for the purpose of furthering myositis research. Dr. Oldroyd had no conflicts of interest to disclose.
All patients with idiopathic inflammatory myopathies (IIM) should be screened for swallowing difficulties, according to the first evidence-based guideline to be produced.
The guideline, which has been developed by a working group of the British Society for Rheumatology (BSR), also advises that all diagnosed patients should have their myositis antibody levels checked and have their overall well-being assessed. Other recommendations for all patients include the use of glucocorticoids to reduce muscle inflammation and conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) for long-term treatment.
“Finally, now, we’re able to standardize the way we treat adults and children with IIM,” senior guideline author Hector Chinoy, PhD, said at the society’s annual meeting.
It has been a long labor of love, however, taking 4 years to get the guideline published, said Dr. Chinoy, professor of rheumatology and neuromuscular disease at the University of Manchester (England), and a consultant at Salford (England) Royal Hospital.
“We’re not covering diagnosis, classification, or the investigation of suspected IIM,” said Dr. Chinoy. Inclusion body myositis also is not included.
Altogether, there are 13 recommendations that have been developed using a PICO (patient or population, intervention, comparison, outcome) format, graded based on the quality of the available evidence, and then voted on by the working group members to give a score of the strength of agreement. Dr. Chinoy noted that there was a checklist included in the Supplementary Data section of the guideline to help follow the recommendations.
“The target audience for the guideline reflects the variety of clinicians caring for patients with IIM,” Dr. Chinoy said. So that is not just pediatric and adult rheumatologists, but also neurologists, dermatologists, respiratory physicians, oncologists, gastroenterologists, cardiologists, and of course other health care professionals. This includes rheumatology and neurology nurses, psychologists, speech and language therapists, and podiatrists, as well as rheumatology specialist pharmacists, physiotherapists, and occupational therapists.
With reference to the latter, Liza McCann, MBBS, who co-led the development of the guideline, said in a statement released by the BSR that the guideline “highlights the importance of exercise, led and monitored by specialist physiotherapists and occupational therapists.”
Dr. McCann, a consultant pediatric rheumatologist at Alder Hey Hospital, Liverpool, England, and Honorary Clinical Lecturer at the University of Liverpool, added that the guidelines also cover “the need to address psychological wellbeing as an integral part of treatment, in parallel with pharmacological therapies.”
Recommendation highlights
Some of the highlights of the recommendations include the use of high-dose glucocorticoids to manage skeletal muscle inflammation at the time of treatment induction, with specific guidance on the different doses to use in adults and in children. There also is guidance on the use of csDMARDs in both populations and what to use if there is refractory disease – with the strongest evidence supporting the use of intravenous immunoglobulin (IVIG) or cyclophosphamide, and possibly rituximab and abatacept.
“There is insufficient evidence to recommend JAK inhibition,” Dr. Chinoy said. The data search used to develop the guideline had a cutoff of October 2020, but even now there is only anecdotal evidence from case studies, he added.
Importantly, the guidelines recognize that childhood IIM differs from adult disease and call for children to be managed by pediatric specialists.
“Routine assessment of dysphagia should be considered in all patients,” Dr. Chinoy said, “so ask the question.” The recommendation is that a swallowing assessment should involve a speech and language therapist or gastroenterologist, and that IVIG be considered for active disease and dysphagia that is resistant to other treatments.
There also are recommendations to screen adult patients for interstitial lung disease, consider fracture risk, and screen adult patients for cancer if they have specific risk factors that include older age at onset, male gender, dysphagia, and rapid disease onset, among others.
Separate cancer screening guidelines on cards
“Around one in four patients with myositis will develop cancer within the 3 years either before or after myositis onset,” Alexander Oldroyd, MBChB, PhD, said in a separate presentation at the BSR annual meeting.
“It’s a hugely increased risk compared to the general population, and a great worry for patients,” he added. Exactly why there is an increased risk is not known, but “there’s a big link between the biological onset of cancer and myositis.”
Dr. Oldroyd, who is an NIHR Academic Clinical Lecturer at the University of Manchester in England and a coauthor of the BSR myositis guideline, is part of a special interest group set up by the International Myositis Assessment and Clinical Studies Group (IMACS) that is in the process of developing separate guidelines for cancer screening in people newly diagnosed with IIM.
The aim was to produce evidence-based recommendations that were both “pragmatic and practical,” that could help clinicians answer patient’s questions on their risk and how best and how often to screen them, Dr. Oldroyd explained. Importantly, IMACS has endeavored to create recommendations that should be applicable across different countries and health care systems.
“We had to acknowledge that there’s not a lot of evidence base there,” Dr. Oldroyd said, noting that he and colleagues conducted a systematic literature review and meta-analysis and used a Delphi process to draft 20 recommendations. These cover identifying risk factors for cancer in people with myositis and categorizing people into low, medium, and high-risk categories. The recommendations also cover what should constitute basic and enhanced screening, and how often someone should be screened.
Moreover, the authors make recommendations on the use of imaging modalities such as PET and CT scans, as well as upper and lower gastrointestinal endoscopy and naso-endoscopy.
“As rheumatologists, we don’t talk about cancer a lot,” Dr. Oldroyd said. “We pick up a lot of incidental cancers, but we don’t usually talk about cancer screening with patients.” That’s something that needs to change, he said.
“It’s important – just get it out in the open, talk to people about it,” Dr. Oldroyd said.
“Tell them what you’re wanting to do, how you’re wanting to investigate for it, clearly communicate their risk,” he said. “But also acknowledge the limited evidence as well, and clearly communicate the results.”
Dr. Chinoy acknowledged he had received fees for presentations (UCB, Biogen), consultancy (Alexion, Novartis, Eli Lilly, Orphazyme, AstraZeneca), or grant support (Eli Lilly, UCB) that had been paid via his institution for the purpose of furthering myositis research. Dr. Oldroyd had no conflicts of interest to disclose.
FROM BSR 2022
Reduced exercise capacity predicted mortality in COPD
Reduced exercise capacity and peak ventilation were significant predictors of early mortality in adults with chronic obstructive pulmonary disease, based on data from 126 individuals.
Cardiopulmonary exercise testing (CPET) is a common assessment for cardiorespiratory disease patients, but its role as a predictor of clinically relevant outcomes in chronic obstructive pulmonary disease (COPD) has not been investigated, and data on changes in exercise capacity over time in COPD patients are limited, wrote Cassia da Luz Goulart, MD, of the Federal University of São Carlos, Brazil, and colleagues.
The researchers hypothesized that CPET threshold values could be used as predictors of mortality in COPD.
In a prospective study published in Respiratory Medicine, the researchers identified 126 adults with COPD who were followed for 42 months. At study entry, each patient completed a clinical evaluation, followed by a pulmonary function test and CPET. The average age of the patients was 65 years, and 73% were men. All patients were on optimal medical management for COPD.
The researchers recorded data on peak oxygen consumption (VO2, mL/min), VCO2 (mL/min), minute ventilation (VE, L/min), the oxygen uptake efficiency slope (OUES), and ventilatory efficiency (the VE/VCO2 slope).
The participants performed CPET on a cycle ergometer, with breath-by-breath analysis measured throughout the test using a computer-based system.
A total of 48 patients (38%) died during the 42-month follow-up period. Overall, the significant predictors of mortality were VE/VCO2 slope of 30 or higher, peak VE of 25.7 L/min, and peak VO2 ≤ 13.8 mLO2 kg–1 min–1 were strong predictors of mortality in COPD patients in a Cox regression analysis.
When comparing the 78 survivors to the 48 nonsurvivors, the researchers found that the nonsurvivors were significantly more likely to be women, with worse lung function, inspiratory muscle weakness, and poorer CPET responses (P < .050 for all).
“The VE peak response is directly related to the FEV1 in COPD patients, factors such as dyspnea and increased leg discomfort negatively impact the VE response during exercise,” the researchers wrote in their discussion of the findings. In this context, our results may hold clinical utility in refining the prognostic accuracy when a patient with COPD has a VE peak ≤ 25.7 L/min,” they explained.
The study findings were limited by the inability to assess complete pulmonary function in the COPD patients, and the assessment only of three CPET measures, the researchers noted.
However, the results support the use of CPET as a clinical assessment tool for COPD patients, they said. “Moreover, therapeutic approaches, such as cardiopulmonary rehabilitation, may consider focusing on improving these metabolic and ventilatory markers as an indicator of clinical improvement and prognosis in patients with COPD,” they added.
The study was supported by the Fundação de Amparo a Pesquisa do Estado de São Paulo, Brazil, and by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior-Brasil. The researchers had no financial conflicts to disclose.
Reduced exercise capacity and peak ventilation were significant predictors of early mortality in adults with chronic obstructive pulmonary disease, based on data from 126 individuals.
Cardiopulmonary exercise testing (CPET) is a common assessment for cardiorespiratory disease patients, but its role as a predictor of clinically relevant outcomes in chronic obstructive pulmonary disease (COPD) has not been investigated, and data on changes in exercise capacity over time in COPD patients are limited, wrote Cassia da Luz Goulart, MD, of the Federal University of São Carlos, Brazil, and colleagues.
The researchers hypothesized that CPET threshold values could be used as predictors of mortality in COPD.
In a prospective study published in Respiratory Medicine, the researchers identified 126 adults with COPD who were followed for 42 months. At study entry, each patient completed a clinical evaluation, followed by a pulmonary function test and CPET. The average age of the patients was 65 years, and 73% were men. All patients were on optimal medical management for COPD.
The researchers recorded data on peak oxygen consumption (VO2, mL/min), VCO2 (mL/min), minute ventilation (VE, L/min), the oxygen uptake efficiency slope (OUES), and ventilatory efficiency (the VE/VCO2 slope).
The participants performed CPET on a cycle ergometer, with breath-by-breath analysis measured throughout the test using a computer-based system.
A total of 48 patients (38%) died during the 42-month follow-up period. Overall, the significant predictors of mortality were VE/VCO2 slope of 30 or higher, peak VE of 25.7 L/min, and peak VO2 ≤ 13.8 mLO2 kg–1 min–1 were strong predictors of mortality in COPD patients in a Cox regression analysis.
When comparing the 78 survivors to the 48 nonsurvivors, the researchers found that the nonsurvivors were significantly more likely to be women, with worse lung function, inspiratory muscle weakness, and poorer CPET responses (P < .050 for all).
“The VE peak response is directly related to the FEV1 in COPD patients, factors such as dyspnea and increased leg discomfort negatively impact the VE response during exercise,” the researchers wrote in their discussion of the findings. In this context, our results may hold clinical utility in refining the prognostic accuracy when a patient with COPD has a VE peak ≤ 25.7 L/min,” they explained.
The study findings were limited by the inability to assess complete pulmonary function in the COPD patients, and the assessment only of three CPET measures, the researchers noted.
However, the results support the use of CPET as a clinical assessment tool for COPD patients, they said. “Moreover, therapeutic approaches, such as cardiopulmonary rehabilitation, may consider focusing on improving these metabolic and ventilatory markers as an indicator of clinical improvement and prognosis in patients with COPD,” they added.
The study was supported by the Fundação de Amparo a Pesquisa do Estado de São Paulo, Brazil, and by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior-Brasil. The researchers had no financial conflicts to disclose.
Reduced exercise capacity and peak ventilation were significant predictors of early mortality in adults with chronic obstructive pulmonary disease, based on data from 126 individuals.
Cardiopulmonary exercise testing (CPET) is a common assessment for cardiorespiratory disease patients, but its role as a predictor of clinically relevant outcomes in chronic obstructive pulmonary disease (COPD) has not been investigated, and data on changes in exercise capacity over time in COPD patients are limited, wrote Cassia da Luz Goulart, MD, of the Federal University of São Carlos, Brazil, and colleagues.
The researchers hypothesized that CPET threshold values could be used as predictors of mortality in COPD.
In a prospective study published in Respiratory Medicine, the researchers identified 126 adults with COPD who were followed for 42 months. At study entry, each patient completed a clinical evaluation, followed by a pulmonary function test and CPET. The average age of the patients was 65 years, and 73% were men. All patients were on optimal medical management for COPD.
The researchers recorded data on peak oxygen consumption (VO2, mL/min), VCO2 (mL/min), minute ventilation (VE, L/min), the oxygen uptake efficiency slope (OUES), and ventilatory efficiency (the VE/VCO2 slope).
The participants performed CPET on a cycle ergometer, with breath-by-breath analysis measured throughout the test using a computer-based system.
A total of 48 patients (38%) died during the 42-month follow-up period. Overall, the significant predictors of mortality were VE/VCO2 slope of 30 or higher, peak VE of 25.7 L/min, and peak VO2 ≤ 13.8 mLO2 kg–1 min–1 were strong predictors of mortality in COPD patients in a Cox regression analysis.
When comparing the 78 survivors to the 48 nonsurvivors, the researchers found that the nonsurvivors were significantly more likely to be women, with worse lung function, inspiratory muscle weakness, and poorer CPET responses (P < .050 for all).
“The VE peak response is directly related to the FEV1 in COPD patients, factors such as dyspnea and increased leg discomfort negatively impact the VE response during exercise,” the researchers wrote in their discussion of the findings. In this context, our results may hold clinical utility in refining the prognostic accuracy when a patient with COPD has a VE peak ≤ 25.7 L/min,” they explained.
The study findings were limited by the inability to assess complete pulmonary function in the COPD patients, and the assessment only of three CPET measures, the researchers noted.
However, the results support the use of CPET as a clinical assessment tool for COPD patients, they said. “Moreover, therapeutic approaches, such as cardiopulmonary rehabilitation, may consider focusing on improving these metabolic and ventilatory markers as an indicator of clinical improvement and prognosis in patients with COPD,” they added.
The study was supported by the Fundação de Amparo a Pesquisa do Estado de São Paulo, Brazil, and by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior-Brasil. The researchers had no financial conflicts to disclose.
FROM RESPIRATORY MEDICINE
Bronchoscopic lung reduction boosts survival in severe COPD
Bronchoscopic lung volume reduction significantly increased survival in patients with severe chronic obstructive pulmonary disease, based on data from more than 1,400 individuals.
Previous studies have shown that patients with severe chronic obstructive pulmonary disease (COPD) can benefit from treatment with bronchoscopic lung volume reduction (BLVR) involving lung volume reduction coils or endobronchial valves (EBVs) in terms of improved pulmonary function, lung volume, exercise capacity, and quality of life.
However, data on the impact of the procedure on patient survival are limited, and most previous studies have been small, wrote Jorine E. Hartman, MD, of the University of Groningen, the Netherlands, and colleagues.
In a study published in Respiratory Medicine, the researchers reviewed data from 1,471 patients with severe COPD who had consultations for BLVR at a single center between June 2006 and July 2019. Of these, 483 (33%) underwent a BLVR treatment.
The follow-up period ranged from 633 days to 5,401 days. During this time, 531 patients died (35%); 165 of these (34%) were in the BLVR group.
Overall, the median survival of BLVR patients was significantly longer, compared with those who did not have the procedure, for a difference of approximately 1.7 years (3,133 days vs. 2,503 days, P < .001). No significant differences in survival were noted in BLVR patients treated with coils or EBVs.
The average age of the study population at baseline was 61 years, and 63% were women. Overall, patients treated with BLVR were more likely to be younger and female, with fewer COPD exacerbations but worse pulmonary function, as well as lower body mass index and more evidence of emphysema than the untreated patients, the researchers noted. Patients treated with BLVR also were more likely than untreated patients to have a history of myocardial infarction, percutaneous coronary intervention, or stroke.
However, BLVR was a significant independent predictor of survival after controlling for multiple variables, including age, sex, and disease severity, the researchers noted.
The current study supports existing literature on the value of BLVR for severe COPD but stands out from previous studies by comparing patients who underwent BLVR with those who did not, the researchers noted in their discussion of the findings.
The study findings were limited by several factors, including the fact that the non-treated patients were not eligible for treatment for various reasons that might have impacted survival, the researchers noted. Another limitation was the lack of data on cause of death and other medical events and treatments during the follow-up period, they said.
However, the results were strengthened by the large sample size and long-term follow-up and suggest that “reducing lung volume in patients with COPD and severe hyperinflation and reduced life expectancy may lead to a survival benefit,” they concluded.
The study received no outside funding. Dr. Hartman had no financial conflicts to disclose.
Bronchoscopic lung volume reduction significantly increased survival in patients with severe chronic obstructive pulmonary disease, based on data from more than 1,400 individuals.
Previous studies have shown that patients with severe chronic obstructive pulmonary disease (COPD) can benefit from treatment with bronchoscopic lung volume reduction (BLVR) involving lung volume reduction coils or endobronchial valves (EBVs) in terms of improved pulmonary function, lung volume, exercise capacity, and quality of life.
However, data on the impact of the procedure on patient survival are limited, and most previous studies have been small, wrote Jorine E. Hartman, MD, of the University of Groningen, the Netherlands, and colleagues.
In a study published in Respiratory Medicine, the researchers reviewed data from 1,471 patients with severe COPD who had consultations for BLVR at a single center between June 2006 and July 2019. Of these, 483 (33%) underwent a BLVR treatment.
The follow-up period ranged from 633 days to 5,401 days. During this time, 531 patients died (35%); 165 of these (34%) were in the BLVR group.
Overall, the median survival of BLVR patients was significantly longer, compared with those who did not have the procedure, for a difference of approximately 1.7 years (3,133 days vs. 2,503 days, P < .001). No significant differences in survival were noted in BLVR patients treated with coils or EBVs.
The average age of the study population at baseline was 61 years, and 63% were women. Overall, patients treated with BLVR were more likely to be younger and female, with fewer COPD exacerbations but worse pulmonary function, as well as lower body mass index and more evidence of emphysema than the untreated patients, the researchers noted. Patients treated with BLVR also were more likely than untreated patients to have a history of myocardial infarction, percutaneous coronary intervention, or stroke.
However, BLVR was a significant independent predictor of survival after controlling for multiple variables, including age, sex, and disease severity, the researchers noted.
The current study supports existing literature on the value of BLVR for severe COPD but stands out from previous studies by comparing patients who underwent BLVR with those who did not, the researchers noted in their discussion of the findings.
The study findings were limited by several factors, including the fact that the non-treated patients were not eligible for treatment for various reasons that might have impacted survival, the researchers noted. Another limitation was the lack of data on cause of death and other medical events and treatments during the follow-up period, they said.
However, the results were strengthened by the large sample size and long-term follow-up and suggest that “reducing lung volume in patients with COPD and severe hyperinflation and reduced life expectancy may lead to a survival benefit,” they concluded.
The study received no outside funding. Dr. Hartman had no financial conflicts to disclose.
Bronchoscopic lung volume reduction significantly increased survival in patients with severe chronic obstructive pulmonary disease, based on data from more than 1,400 individuals.
Previous studies have shown that patients with severe chronic obstructive pulmonary disease (COPD) can benefit from treatment with bronchoscopic lung volume reduction (BLVR) involving lung volume reduction coils or endobronchial valves (EBVs) in terms of improved pulmonary function, lung volume, exercise capacity, and quality of life.
However, data on the impact of the procedure on patient survival are limited, and most previous studies have been small, wrote Jorine E. Hartman, MD, of the University of Groningen, the Netherlands, and colleagues.
In a study published in Respiratory Medicine, the researchers reviewed data from 1,471 patients with severe COPD who had consultations for BLVR at a single center between June 2006 and July 2019. Of these, 483 (33%) underwent a BLVR treatment.
The follow-up period ranged from 633 days to 5,401 days. During this time, 531 patients died (35%); 165 of these (34%) were in the BLVR group.
Overall, the median survival of BLVR patients was significantly longer, compared with those who did not have the procedure, for a difference of approximately 1.7 years (3,133 days vs. 2,503 days, P < .001). No significant differences in survival were noted in BLVR patients treated with coils or EBVs.
The average age of the study population at baseline was 61 years, and 63% were women. Overall, patients treated with BLVR were more likely to be younger and female, with fewer COPD exacerbations but worse pulmonary function, as well as lower body mass index and more evidence of emphysema than the untreated patients, the researchers noted. Patients treated with BLVR also were more likely than untreated patients to have a history of myocardial infarction, percutaneous coronary intervention, or stroke.
However, BLVR was a significant independent predictor of survival after controlling for multiple variables, including age, sex, and disease severity, the researchers noted.
The current study supports existing literature on the value of BLVR for severe COPD but stands out from previous studies by comparing patients who underwent BLVR with those who did not, the researchers noted in their discussion of the findings.
The study findings were limited by several factors, including the fact that the non-treated patients were not eligible for treatment for various reasons that might have impacted survival, the researchers noted. Another limitation was the lack of data on cause of death and other medical events and treatments during the follow-up period, they said.
However, the results were strengthened by the large sample size and long-term follow-up and suggest that “reducing lung volume in patients with COPD and severe hyperinflation and reduced life expectancy may lead to a survival benefit,” they concluded.
The study received no outside funding. Dr. Hartman had no financial conflicts to disclose.
FROM RESPIRATORY MEDICINE
Medical education programs tell how climate change affects health
Ms. Manivannan, copresident of Emory Medical Students for Climate Action, was in the first class of Emory’s medical students to experience the birth of a refined curriculum – lobbied for and partially created by students themselves. The new course of study addresses the myriad ways climate affects health: from air pollution and its effects on the lungs and cardiovascular system to heat-related kidney disease.
“We have known that climate has affected health for decades,” Ms. Manivannan said in a recent interview. “The narrative used to be that icebergs were melting and in 2050 polar bears would be extinct. The piece that’s different now is people are linking climate to increases in asthma and various diseases. We have a way to directly communicate that it’s not a far-off thing. It’s happening to your friends and family right now.”
Hospitals, medical schools, and public health programs are stepping up to educate the next generation of doctors as well as veteran medical workers on one of the most widespread, insidious health threats of our time – climate change – and specific ways it could affect their patients.
Although climate change may seem to many Americans like a distant threat, Marilyn Howarth, MD, a pediatrician in Philadelphia, is trying to make sure physicians are better prepared to treat a growing number of health problems associated with global warming.
“There isn’t a lot of education for pediatricians and internists on environmental health issues. It has not been a standard part of education in medical school or residency training,” Dr. Howarth, deputy director of the new Philadelphia Regional Center for Children’s Environmental Health, said. “With increasing attention on our climate, we really recognize there’s a real gap in physician knowledge, both in pediatric and adult care.”
Scientists have found that climate change can alter just about every system within the human body. Studies show that more extreme weather events, such as heat waves, thunderstorms, and floods, can worsen asthma and produce more pollen and mold, triggering debilitating respiratory problems.
According to the American Lung Association, ultrafine particles of air pollution can be inhaled and then travel throughout the bloodstream, wreaking havoc on organs and increasing risk of heart attack and stroke. Various types of air pollution also cause changes to the climate by trapping heat in the atmosphere, which leads to problems such as rising sea levels and extreme weather. Plus, in a new study published in Nature, scientists warn that warming climates are forcing animals to migrate to different areas, raising the risk that new infectious diseases will hop from animals – such as bats – to humans, a process called “zoonotic spillover” that many researchers believe is responsible for the COVID-19 pandemic.
The Philadelphia Regional Center for Children’s Environmental Health
One of the latest initiatives aimed at disseminating information about children’s health to health care providers is the Philadelphia Regional Center for Children’s Environmental Health, part of Children’s Hospital of Philadelphia and Penn Medicine. CHOP and Penn Medicine are jointly funding this center’s work, which will include educating health care providers on how to better screen for climate-caused health risks and treat related conditions, such as lead poisoning and asthma.
Outreach will focus on providers who treat patients with illnesses that researchers have linked to climate change, Dr. Howarth said. The center will offer clinicians access to seminars and webinars, along with online resources to help doctors treat environmental illnesses. For example, doctors at CHOP’s Poison Control Center are developing a toolkit for physicians to treat patients with elevated levels of lead in the blood. Scientists have linked extreme weather events related to climate change to flooding that pushes metals away from river banks where they were previously contained, allowing them to more easily contaminate homes, soils, and yards.
The initiative builds on CHOP’s Community Asthma Prevention Program (CAPP), which was launched in 1997 by Tyra Bryant-Stephens, MD, its current medical director. CAPP deploys community health workers into homes armed with supplies and tips for managing asthma. The new center will use similar tactics to provide education and resources to patients. The goal is to reach as many at-risk local children as possible.
Future generation of doctors fuel growth in climate change education
Lisa Doggett, MD, cofounder and president of the board of directors of Texas Physicians for Social Responsibility, announced in March that the University of Texas at Austin, Baylor College of Medicine, Houston, and the University of Texas Southwestern in Dallas have all decided to begin offering a course on environmental threats. Emory’s new curriculum has become more comprehensive every year since its start – thanks in part to the input of students like Ms. Manivannan. Faculty members tasked her with approving the new additions to the curriculum on how climate affects health, which in 2019 had consisted of a few slides about issues such as extreme heat exposure and air pollution and their effects on childbirth outcomes.
Material on climate change has now been woven into 13 courses. It is discussed at length in relation to pulmonology, cardiology, and gastropulmonology, for example, said Rebecca Philipsborn, MD, MPA, FAAP, faculty lead for the environmental and health curriculum at Emory.
The curriculum has only been incorporated into Emory’s program for the past 2 years. Dr. Philipsborn said the school plans to expand it to the clinical years to help trainees learn to treat conditions such as pediatric asthma.
“In the past few years, there has been so much momentum, and part of that is a testament to already seeing effects of climate change and how they affect delivery of health care,” she said.
At least one medical journal has recently ramped up its efforts to educate physicians on the links between health issues and climate change. Editors of Family Practice, from Oxford University Press, have announced that they plan to publish a special Climate Crisis and Primary Health Care issue in September.
Of course, not all climate initiatives in medicine are new. A select few have existed for decades.
But only now are physicians widely seeing the links between health and environment, according to Aaron Bernstein, MD, MPH, interim director of the Center for Climate, Health, and the Global Environment (C-CHANGE) at Harvard School of Public Health, Boston.
C-CHANGE, founded in 1996, was the first center in the world to focus on the health effects of environmental change.
“It’s taken 20 years, but what we’re seeing, I think, is the fruits of education,” Dr. Bernstein said. “There’s clearly a wave building here, and I think it really started with education and people younger than the people in charge calling them into account.”
Like the Philadelphia center, Harvard’s program conducts research on climate and health and educates people from high schoolers to health care veterans. Dr. Bernstein helps lead Climate MD, a program that aims to prepare health care workers for climate crises. The Climate MD team has published several articles in peer-reviewed journals on how to better treat patients struggling with environmental health problems. For example, an article on mapping patients in hurricane zones helped shed light on how systems can identify climate-vulnerable patients using public data.
They also developed a tool to help pediatricians provide “climate-informed primary care” – guidance on how to assess whether children are at risk of any harmful environmental exposures, a feature that is not part of standard pediatric visits.
Like the other programs, Climate MD uses community outreach to treat as many local patients as possible. Staff work with providers at more than 100 health clinics, particularly in areas where climate change disproportionately affects residents.
The next major step is to bring some of this into clinical practice, Dr. Bernstein said. In February 2020, C-CHANGE held its first symposium to address that issue.
“The key is to understand climate issues from a provider’s perspective,” he said. “Then those issues can really be brought to the bedside.”
A version of this article first appeared on Medscape.com.
Ms. Manivannan, copresident of Emory Medical Students for Climate Action, was in the first class of Emory’s medical students to experience the birth of a refined curriculum – lobbied for and partially created by students themselves. The new course of study addresses the myriad ways climate affects health: from air pollution and its effects on the lungs and cardiovascular system to heat-related kidney disease.
“We have known that climate has affected health for decades,” Ms. Manivannan said in a recent interview. “The narrative used to be that icebergs were melting and in 2050 polar bears would be extinct. The piece that’s different now is people are linking climate to increases in asthma and various diseases. We have a way to directly communicate that it’s not a far-off thing. It’s happening to your friends and family right now.”
Hospitals, medical schools, and public health programs are stepping up to educate the next generation of doctors as well as veteran medical workers on one of the most widespread, insidious health threats of our time – climate change – and specific ways it could affect their patients.
Although climate change may seem to many Americans like a distant threat, Marilyn Howarth, MD, a pediatrician in Philadelphia, is trying to make sure physicians are better prepared to treat a growing number of health problems associated with global warming.
“There isn’t a lot of education for pediatricians and internists on environmental health issues. It has not been a standard part of education in medical school or residency training,” Dr. Howarth, deputy director of the new Philadelphia Regional Center for Children’s Environmental Health, said. “With increasing attention on our climate, we really recognize there’s a real gap in physician knowledge, both in pediatric and adult care.”
Scientists have found that climate change can alter just about every system within the human body. Studies show that more extreme weather events, such as heat waves, thunderstorms, and floods, can worsen asthma and produce more pollen and mold, triggering debilitating respiratory problems.
According to the American Lung Association, ultrafine particles of air pollution can be inhaled and then travel throughout the bloodstream, wreaking havoc on organs and increasing risk of heart attack and stroke. Various types of air pollution also cause changes to the climate by trapping heat in the atmosphere, which leads to problems such as rising sea levels and extreme weather. Plus, in a new study published in Nature, scientists warn that warming climates are forcing animals to migrate to different areas, raising the risk that new infectious diseases will hop from animals – such as bats – to humans, a process called “zoonotic spillover” that many researchers believe is responsible for the COVID-19 pandemic.
The Philadelphia Regional Center for Children’s Environmental Health
One of the latest initiatives aimed at disseminating information about children’s health to health care providers is the Philadelphia Regional Center for Children’s Environmental Health, part of Children’s Hospital of Philadelphia and Penn Medicine. CHOP and Penn Medicine are jointly funding this center’s work, which will include educating health care providers on how to better screen for climate-caused health risks and treat related conditions, such as lead poisoning and asthma.
Outreach will focus on providers who treat patients with illnesses that researchers have linked to climate change, Dr. Howarth said. The center will offer clinicians access to seminars and webinars, along with online resources to help doctors treat environmental illnesses. For example, doctors at CHOP’s Poison Control Center are developing a toolkit for physicians to treat patients with elevated levels of lead in the blood. Scientists have linked extreme weather events related to climate change to flooding that pushes metals away from river banks where they were previously contained, allowing them to more easily contaminate homes, soils, and yards.
The initiative builds on CHOP’s Community Asthma Prevention Program (CAPP), which was launched in 1997 by Tyra Bryant-Stephens, MD, its current medical director. CAPP deploys community health workers into homes armed with supplies and tips for managing asthma. The new center will use similar tactics to provide education and resources to patients. The goal is to reach as many at-risk local children as possible.
Future generation of doctors fuel growth in climate change education
Lisa Doggett, MD, cofounder and president of the board of directors of Texas Physicians for Social Responsibility, announced in March that the University of Texas at Austin, Baylor College of Medicine, Houston, and the University of Texas Southwestern in Dallas have all decided to begin offering a course on environmental threats. Emory’s new curriculum has become more comprehensive every year since its start – thanks in part to the input of students like Ms. Manivannan. Faculty members tasked her with approving the new additions to the curriculum on how climate affects health, which in 2019 had consisted of a few slides about issues such as extreme heat exposure and air pollution and their effects on childbirth outcomes.
Material on climate change has now been woven into 13 courses. It is discussed at length in relation to pulmonology, cardiology, and gastropulmonology, for example, said Rebecca Philipsborn, MD, MPA, FAAP, faculty lead for the environmental and health curriculum at Emory.
The curriculum has only been incorporated into Emory’s program for the past 2 years. Dr. Philipsborn said the school plans to expand it to the clinical years to help trainees learn to treat conditions such as pediatric asthma.
“In the past few years, there has been so much momentum, and part of that is a testament to already seeing effects of climate change and how they affect delivery of health care,” she said.
At least one medical journal has recently ramped up its efforts to educate physicians on the links between health issues and climate change. Editors of Family Practice, from Oxford University Press, have announced that they plan to publish a special Climate Crisis and Primary Health Care issue in September.
Of course, not all climate initiatives in medicine are new. A select few have existed for decades.
But only now are physicians widely seeing the links between health and environment, according to Aaron Bernstein, MD, MPH, interim director of the Center for Climate, Health, and the Global Environment (C-CHANGE) at Harvard School of Public Health, Boston.
C-CHANGE, founded in 1996, was the first center in the world to focus on the health effects of environmental change.
“It’s taken 20 years, but what we’re seeing, I think, is the fruits of education,” Dr. Bernstein said. “There’s clearly a wave building here, and I think it really started with education and people younger than the people in charge calling them into account.”
Like the Philadelphia center, Harvard’s program conducts research on climate and health and educates people from high schoolers to health care veterans. Dr. Bernstein helps lead Climate MD, a program that aims to prepare health care workers for climate crises. The Climate MD team has published several articles in peer-reviewed journals on how to better treat patients struggling with environmental health problems. For example, an article on mapping patients in hurricane zones helped shed light on how systems can identify climate-vulnerable patients using public data.
They also developed a tool to help pediatricians provide “climate-informed primary care” – guidance on how to assess whether children are at risk of any harmful environmental exposures, a feature that is not part of standard pediatric visits.
Like the other programs, Climate MD uses community outreach to treat as many local patients as possible. Staff work with providers at more than 100 health clinics, particularly in areas where climate change disproportionately affects residents.
The next major step is to bring some of this into clinical practice, Dr. Bernstein said. In February 2020, C-CHANGE held its first symposium to address that issue.
“The key is to understand climate issues from a provider’s perspective,” he said. “Then those issues can really be brought to the bedside.”
A version of this article first appeared on Medscape.com.
Ms. Manivannan, copresident of Emory Medical Students for Climate Action, was in the first class of Emory’s medical students to experience the birth of a refined curriculum – lobbied for and partially created by students themselves. The new course of study addresses the myriad ways climate affects health: from air pollution and its effects on the lungs and cardiovascular system to heat-related kidney disease.
“We have known that climate has affected health for decades,” Ms. Manivannan said in a recent interview. “The narrative used to be that icebergs were melting and in 2050 polar bears would be extinct. The piece that’s different now is people are linking climate to increases in asthma and various diseases. We have a way to directly communicate that it’s not a far-off thing. It’s happening to your friends and family right now.”
Hospitals, medical schools, and public health programs are stepping up to educate the next generation of doctors as well as veteran medical workers on one of the most widespread, insidious health threats of our time – climate change – and specific ways it could affect their patients.
Although climate change may seem to many Americans like a distant threat, Marilyn Howarth, MD, a pediatrician in Philadelphia, is trying to make sure physicians are better prepared to treat a growing number of health problems associated with global warming.
“There isn’t a lot of education for pediatricians and internists on environmental health issues. It has not been a standard part of education in medical school or residency training,” Dr. Howarth, deputy director of the new Philadelphia Regional Center for Children’s Environmental Health, said. “With increasing attention on our climate, we really recognize there’s a real gap in physician knowledge, both in pediatric and adult care.”
Scientists have found that climate change can alter just about every system within the human body. Studies show that more extreme weather events, such as heat waves, thunderstorms, and floods, can worsen asthma and produce more pollen and mold, triggering debilitating respiratory problems.
According to the American Lung Association, ultrafine particles of air pollution can be inhaled and then travel throughout the bloodstream, wreaking havoc on organs and increasing risk of heart attack and stroke. Various types of air pollution also cause changes to the climate by trapping heat in the atmosphere, which leads to problems such as rising sea levels and extreme weather. Plus, in a new study published in Nature, scientists warn that warming climates are forcing animals to migrate to different areas, raising the risk that new infectious diseases will hop from animals – such as bats – to humans, a process called “zoonotic spillover” that many researchers believe is responsible for the COVID-19 pandemic.
The Philadelphia Regional Center for Children’s Environmental Health
One of the latest initiatives aimed at disseminating information about children’s health to health care providers is the Philadelphia Regional Center for Children’s Environmental Health, part of Children’s Hospital of Philadelphia and Penn Medicine. CHOP and Penn Medicine are jointly funding this center’s work, which will include educating health care providers on how to better screen for climate-caused health risks and treat related conditions, such as lead poisoning and asthma.
Outreach will focus on providers who treat patients with illnesses that researchers have linked to climate change, Dr. Howarth said. The center will offer clinicians access to seminars and webinars, along with online resources to help doctors treat environmental illnesses. For example, doctors at CHOP’s Poison Control Center are developing a toolkit for physicians to treat patients with elevated levels of lead in the blood. Scientists have linked extreme weather events related to climate change to flooding that pushes metals away from river banks where they were previously contained, allowing them to more easily contaminate homes, soils, and yards.
The initiative builds on CHOP’s Community Asthma Prevention Program (CAPP), which was launched in 1997 by Tyra Bryant-Stephens, MD, its current medical director. CAPP deploys community health workers into homes armed with supplies and tips for managing asthma. The new center will use similar tactics to provide education and resources to patients. The goal is to reach as many at-risk local children as possible.
Future generation of doctors fuel growth in climate change education
Lisa Doggett, MD, cofounder and president of the board of directors of Texas Physicians for Social Responsibility, announced in March that the University of Texas at Austin, Baylor College of Medicine, Houston, and the University of Texas Southwestern in Dallas have all decided to begin offering a course on environmental threats. Emory’s new curriculum has become more comprehensive every year since its start – thanks in part to the input of students like Ms. Manivannan. Faculty members tasked her with approving the new additions to the curriculum on how climate affects health, which in 2019 had consisted of a few slides about issues such as extreme heat exposure and air pollution and their effects on childbirth outcomes.
Material on climate change has now been woven into 13 courses. It is discussed at length in relation to pulmonology, cardiology, and gastropulmonology, for example, said Rebecca Philipsborn, MD, MPA, FAAP, faculty lead for the environmental and health curriculum at Emory.
The curriculum has only been incorporated into Emory’s program for the past 2 years. Dr. Philipsborn said the school plans to expand it to the clinical years to help trainees learn to treat conditions such as pediatric asthma.
“In the past few years, there has been so much momentum, and part of that is a testament to already seeing effects of climate change and how they affect delivery of health care,” she said.
At least one medical journal has recently ramped up its efforts to educate physicians on the links between health issues and climate change. Editors of Family Practice, from Oxford University Press, have announced that they plan to publish a special Climate Crisis and Primary Health Care issue in September.
Of course, not all climate initiatives in medicine are new. A select few have existed for decades.
But only now are physicians widely seeing the links between health and environment, according to Aaron Bernstein, MD, MPH, interim director of the Center for Climate, Health, and the Global Environment (C-CHANGE) at Harvard School of Public Health, Boston.
C-CHANGE, founded in 1996, was the first center in the world to focus on the health effects of environmental change.
“It’s taken 20 years, but what we’re seeing, I think, is the fruits of education,” Dr. Bernstein said. “There’s clearly a wave building here, and I think it really started with education and people younger than the people in charge calling them into account.”
Like the Philadelphia center, Harvard’s program conducts research on climate and health and educates people from high schoolers to health care veterans. Dr. Bernstein helps lead Climate MD, a program that aims to prepare health care workers for climate crises. The Climate MD team has published several articles in peer-reviewed journals on how to better treat patients struggling with environmental health problems. For example, an article on mapping patients in hurricane zones helped shed light on how systems can identify climate-vulnerable patients using public data.
They also developed a tool to help pediatricians provide “climate-informed primary care” – guidance on how to assess whether children are at risk of any harmful environmental exposures, a feature that is not part of standard pediatric visits.
Like the other programs, Climate MD uses community outreach to treat as many local patients as possible. Staff work with providers at more than 100 health clinics, particularly in areas where climate change disproportionately affects residents.
The next major step is to bring some of this into clinical practice, Dr. Bernstein said. In February 2020, C-CHANGE held its first symposium to address that issue.
“The key is to understand climate issues from a provider’s perspective,” he said. “Then those issues can really be brought to the bedside.”
A version of this article first appeared on Medscape.com.
COPD screening for asymptomatic adults? USPSTF weighs in, again
Screening for chronic obstructive pulmonary disease (COPD) in asymptomatic adults has no net benefit, according to a U.S. Preventive Services Task Force (USPSTF) reassessment of its 2016 screening recommendations. The new recommendation is in line with the previous one and is made with moderate certainty (grade D evidence).
The USPSTF recommendation applies to adults who do not recognize or report respiratory symptoms. It does not apply to people with symptoms such as chronic cough, sputum production, difficulty breathing, or wheezing, or those known to be at very high risk for COPD. These latter include people with alpha-1 antitrypsin deficiency or workers exposed to certain toxins at their jobs, according to the report published in JAMA.
“Considering that the outcomes of several other chronic conditions, including cardiovascular disease and cancer, have been improved over the years with early detection and intervention, it is logical to ask whether screening to achieve early detection of COPD might also lead to better outcomes,” Surya P. Bhatt, MD, of the University of Alabama at Birmingham, and George T. O’Connor, MD, of the Boston University, explained in an editorial.
Task force assessment
The task force examined relevant publications after the 2016 deliberations and found no new studies that directly assessed the effects of screening for COPD in asymptomatic adults on morbidity, mortality, or health-related quality of life.
Although, as in their previous review, serious harms from treatment trials were not consistently reported, more recent large observational studies in screen-relevant populations suggested possible harms from the initiation of long-acting beta-agonists (LABAs), long-acting muscarinic antagonists (LAMAs), and the use of inhaled corticosteroids.
“In addition to potential treatment harms, there are opportunity costs to screening that may include time spent on counseling and providing services and patient referrals for diagnostic testing,” the task force stated.
Because cigarette smoking is the leading cause of COPD, the USPSTF has reiterated its recommendations for physicians to address tobacco smoking cessation in adults, including pregnant persons, as well as tobacco use in children and adolescents.
Not the whole story?
“Truly asymptomatic individuals with airflow obstruction do not meet criteria for COPD therapy, but sensitive questionnaires may detect symptoms not previously reported by the patient. It may be more effective to redirect the focus from screening for asymptomatic COPD to case finding using sensitive and cost-effective tools,” Dr. Bhatt and Dr. O’Connor suggested in their editorial.
“Even though available data may not support screening asymptomatic adults for COPD, there is substantial rationale for further investigation of strategies to enhance earlier detection of this condition,” they concluded.
More research needed
Despite the recommendation, the USPSTF indicated that further studies are needed to fill in research gaps, including:
- The effectiveness of screening asymptomatic adults for COPD to reduce morbidity or mortality or improve health-related quality of life, with long-term follow-up.
- The effectiveness of early treatment for asymptomatic, minimally symptomatic, or screen-detected populations to slow disease progression and improve health outcomes, with long-term follow-up.
- The harms of screening in and treatment of persons with asymptomatic or minimally symptomatic COPD.
The USPSTF is an independent, voluntary body, and potential conflicts of interest of the members are on file with the organization. Dr. Bhatt reported serving on an advisory board for Boehringer Ingelheim and receiving consulting fees from Sanofi/Regeneron; and Dr. O’Connor reported receiving consulting fees from Grupo Menarini and Dicerna Pharmaceuticals.
Screening for chronic obstructive pulmonary disease (COPD) in asymptomatic adults has no net benefit, according to a U.S. Preventive Services Task Force (USPSTF) reassessment of its 2016 screening recommendations. The new recommendation is in line with the previous one and is made with moderate certainty (grade D evidence).
The USPSTF recommendation applies to adults who do not recognize or report respiratory symptoms. It does not apply to people with symptoms such as chronic cough, sputum production, difficulty breathing, or wheezing, or those known to be at very high risk for COPD. These latter include people with alpha-1 antitrypsin deficiency or workers exposed to certain toxins at their jobs, according to the report published in JAMA.
“Considering that the outcomes of several other chronic conditions, including cardiovascular disease and cancer, have been improved over the years with early detection and intervention, it is logical to ask whether screening to achieve early detection of COPD might also lead to better outcomes,” Surya P. Bhatt, MD, of the University of Alabama at Birmingham, and George T. O’Connor, MD, of the Boston University, explained in an editorial.
Task force assessment
The task force examined relevant publications after the 2016 deliberations and found no new studies that directly assessed the effects of screening for COPD in asymptomatic adults on morbidity, mortality, or health-related quality of life.
Although, as in their previous review, serious harms from treatment trials were not consistently reported, more recent large observational studies in screen-relevant populations suggested possible harms from the initiation of long-acting beta-agonists (LABAs), long-acting muscarinic antagonists (LAMAs), and the use of inhaled corticosteroids.
“In addition to potential treatment harms, there are opportunity costs to screening that may include time spent on counseling and providing services and patient referrals for diagnostic testing,” the task force stated.
Because cigarette smoking is the leading cause of COPD, the USPSTF has reiterated its recommendations for physicians to address tobacco smoking cessation in adults, including pregnant persons, as well as tobacco use in children and adolescents.
Not the whole story?
“Truly asymptomatic individuals with airflow obstruction do not meet criteria for COPD therapy, but sensitive questionnaires may detect symptoms not previously reported by the patient. It may be more effective to redirect the focus from screening for asymptomatic COPD to case finding using sensitive and cost-effective tools,” Dr. Bhatt and Dr. O’Connor suggested in their editorial.
“Even though available data may not support screening asymptomatic adults for COPD, there is substantial rationale for further investigation of strategies to enhance earlier detection of this condition,” they concluded.
More research needed
Despite the recommendation, the USPSTF indicated that further studies are needed to fill in research gaps, including:
- The effectiveness of screening asymptomatic adults for COPD to reduce morbidity or mortality or improve health-related quality of life, with long-term follow-up.
- The effectiveness of early treatment for asymptomatic, minimally symptomatic, or screen-detected populations to slow disease progression and improve health outcomes, with long-term follow-up.
- The harms of screening in and treatment of persons with asymptomatic or minimally symptomatic COPD.
The USPSTF is an independent, voluntary body, and potential conflicts of interest of the members are on file with the organization. Dr. Bhatt reported serving on an advisory board for Boehringer Ingelheim and receiving consulting fees from Sanofi/Regeneron; and Dr. O’Connor reported receiving consulting fees from Grupo Menarini and Dicerna Pharmaceuticals.
Screening for chronic obstructive pulmonary disease (COPD) in asymptomatic adults has no net benefit, according to a U.S. Preventive Services Task Force (USPSTF) reassessment of its 2016 screening recommendations. The new recommendation is in line with the previous one and is made with moderate certainty (grade D evidence).
The USPSTF recommendation applies to adults who do not recognize or report respiratory symptoms. It does not apply to people with symptoms such as chronic cough, sputum production, difficulty breathing, or wheezing, or those known to be at very high risk for COPD. These latter include people with alpha-1 antitrypsin deficiency or workers exposed to certain toxins at their jobs, according to the report published in JAMA.
“Considering that the outcomes of several other chronic conditions, including cardiovascular disease and cancer, have been improved over the years with early detection and intervention, it is logical to ask whether screening to achieve early detection of COPD might also lead to better outcomes,” Surya P. Bhatt, MD, of the University of Alabama at Birmingham, and George T. O’Connor, MD, of the Boston University, explained in an editorial.
Task force assessment
The task force examined relevant publications after the 2016 deliberations and found no new studies that directly assessed the effects of screening for COPD in asymptomatic adults on morbidity, mortality, or health-related quality of life.
Although, as in their previous review, serious harms from treatment trials were not consistently reported, more recent large observational studies in screen-relevant populations suggested possible harms from the initiation of long-acting beta-agonists (LABAs), long-acting muscarinic antagonists (LAMAs), and the use of inhaled corticosteroids.
“In addition to potential treatment harms, there are opportunity costs to screening that may include time spent on counseling and providing services and patient referrals for diagnostic testing,” the task force stated.
Because cigarette smoking is the leading cause of COPD, the USPSTF has reiterated its recommendations for physicians to address tobacco smoking cessation in adults, including pregnant persons, as well as tobacco use in children and adolescents.
Not the whole story?
“Truly asymptomatic individuals with airflow obstruction do not meet criteria for COPD therapy, but sensitive questionnaires may detect symptoms not previously reported by the patient. It may be more effective to redirect the focus from screening for asymptomatic COPD to case finding using sensitive and cost-effective tools,” Dr. Bhatt and Dr. O’Connor suggested in their editorial.
“Even though available data may not support screening asymptomatic adults for COPD, there is substantial rationale for further investigation of strategies to enhance earlier detection of this condition,” they concluded.
More research needed
Despite the recommendation, the USPSTF indicated that further studies are needed to fill in research gaps, including:
- The effectiveness of screening asymptomatic adults for COPD to reduce morbidity or mortality or improve health-related quality of life, with long-term follow-up.
- The effectiveness of early treatment for asymptomatic, minimally symptomatic, or screen-detected populations to slow disease progression and improve health outcomes, with long-term follow-up.
- The harms of screening in and treatment of persons with asymptomatic or minimally symptomatic COPD.
The USPSTF is an independent, voluntary body, and potential conflicts of interest of the members are on file with the organization. Dr. Bhatt reported serving on an advisory board for Boehringer Ingelheim and receiving consulting fees from Sanofi/Regeneron; and Dr. O’Connor reported receiving consulting fees from Grupo Menarini and Dicerna Pharmaceuticals.
FROM JAMA
Risk calculator may help predict death after COPD hospitalization
Researchers in Scotland have developed a risk calculator using a large electronic health records database that has shown a high reliability in predicting the risk of death for patients hospitalized for chronic occlusive pulmonary disease (COPD), providing another potential tool for improving postdischarge survival in these patients.
In a study published online in the journal Pharmacological Research, Pierpalo Pellicori, MD, and colleagues reported that a few variables, including prescriptions and laboratory data in routine EHRs, could help predict a patient’s risk of dying within 90 days after a hospital stay for COPD. Dr. Pellicori is a clinical cardiologist and research fellow at the Robertson Center for Biostatistics at the University of Glasgow.
“Identification of patients at high risk is valuable information for multidisciplinary teams,” Dr. Pellicori said in a written comment. “It allows the most vulnerable patients to be highlighted and prioritized for consideration of optimized value-based care, and for anticipatory care plan discussions.”
The retrospective cohort study analyzed EHR records of 17,973 patients who had an unplanned hospitalization for COPD in the Glasgow area from 2011 to 2017. The risk calculator model achieved a potential accuracy of 80%.
The study noted that, while a number of models have been developed to calculate the risk of exacerbations, inpatient death and prognosis in patients hospitalized for COPD, most of those models were based on cohorts of 1000 patients or less.
“Older age, male sex, and a longer hospital stay were important predictors of mortality in patients with COPD,” Dr. Pellicori said. “We also found that use of commonly prescribed medications such as digoxin identify patients with COPD more likely to die, perhaps because many have underlying heart failure, a highly prevalent but frequently missed diagnosis.”
He noted that heart failure and COPD share many risk factors, signs, and symptoms, such as smoking history, peripheral edema, and breathlessness. “Distinguishing between COPD and heart failure can be difficult, but is very important, as appropriate treatment for heart failure can improve a patient’s quality of life and survival substantially in many cases.”
The study also found that routinely collected and inexpensive blood markers – such as hemoglobin, neutrophil/lymphocyte ratio, serum chloride, urea, creatinine, and albumin – can also improve predictability of outcomes.
For example, the study found a linear increase in mortality of blood hemoglobin concentration less than 14 g/dL, but higher levels posed no greater risk. Higher white blood cell and neutrophil counts and lower lymphocyte and eosinophil counts were associated with a worse prognosis.
The study also found a linear increase in mortality with serum sodium less than 140 mmol/L or serum chloride less than 105 mmol/L – but that higher concentrations of each were associated with a worse outcome.
“Interestingly,” Pellicori added, “social deprivation was not associated with mortality in this cohort.”
The final predictive model included age, sex, length of stay, and just nine other variables. “The model can be applied easily in clinical practice, even if electronic records are not available, because there are only 12 variables,” Dr. Pellicori said. “These could easily be entered manually into the risk calculator that we provide.”
“What is notable about this risk calculator is that it uses some of the techniques of machine learning, although it’s not specifically machine learning,” Angel Coz, MD, a pulmonologist at the Cleveland Clinic Respiratory Institute, said in an interview. “But it’s a retrospective data analysis, and actually by doing that it may catch some factors that we may not have necessarily paid attention to on a regular basis.”
While he called it a “well-done study,” Dr. Coz cautioned that “we have to be conservative in how to interpret and apply this because it is retrospective,” adding that future research should also use a prospective cohort.
For future consideration, Dr. Pellicori said that, while EHRs provide a “rich source” of data for such risk calculators, systems differ greatly across hospitals and health care systems and don’t link easily.
Future research would focus on validating the model in other large national datasets and seeing if machine learning can improve its predictability, Dr. Pellicori said. “Whether such models can provide a real-time, refined risk assessment for all patients in both primary or secondary care settings and improve the efficacy, efficiency, and quality of health care is our long-term goal.”
Dr. Pellicori and Dr. Coz disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Researchers in Scotland have developed a risk calculator using a large electronic health records database that has shown a high reliability in predicting the risk of death for patients hospitalized for chronic occlusive pulmonary disease (COPD), providing another potential tool for improving postdischarge survival in these patients.
In a study published online in the journal Pharmacological Research, Pierpalo Pellicori, MD, and colleagues reported that a few variables, including prescriptions and laboratory data in routine EHRs, could help predict a patient’s risk of dying within 90 days after a hospital stay for COPD. Dr. Pellicori is a clinical cardiologist and research fellow at the Robertson Center for Biostatistics at the University of Glasgow.
“Identification of patients at high risk is valuable information for multidisciplinary teams,” Dr. Pellicori said in a written comment. “It allows the most vulnerable patients to be highlighted and prioritized for consideration of optimized value-based care, and for anticipatory care plan discussions.”
The retrospective cohort study analyzed EHR records of 17,973 patients who had an unplanned hospitalization for COPD in the Glasgow area from 2011 to 2017. The risk calculator model achieved a potential accuracy of 80%.
The study noted that, while a number of models have been developed to calculate the risk of exacerbations, inpatient death and prognosis in patients hospitalized for COPD, most of those models were based on cohorts of 1000 patients or less.
“Older age, male sex, and a longer hospital stay were important predictors of mortality in patients with COPD,” Dr. Pellicori said. “We also found that use of commonly prescribed medications such as digoxin identify patients with COPD more likely to die, perhaps because many have underlying heart failure, a highly prevalent but frequently missed diagnosis.”
He noted that heart failure and COPD share many risk factors, signs, and symptoms, such as smoking history, peripheral edema, and breathlessness. “Distinguishing between COPD and heart failure can be difficult, but is very important, as appropriate treatment for heart failure can improve a patient’s quality of life and survival substantially in many cases.”
The study also found that routinely collected and inexpensive blood markers – such as hemoglobin, neutrophil/lymphocyte ratio, serum chloride, urea, creatinine, and albumin – can also improve predictability of outcomes.
For example, the study found a linear increase in mortality of blood hemoglobin concentration less than 14 g/dL, but higher levels posed no greater risk. Higher white blood cell and neutrophil counts and lower lymphocyte and eosinophil counts were associated with a worse prognosis.
The study also found a linear increase in mortality with serum sodium less than 140 mmol/L or serum chloride less than 105 mmol/L – but that higher concentrations of each were associated with a worse outcome.
“Interestingly,” Pellicori added, “social deprivation was not associated with mortality in this cohort.”
The final predictive model included age, sex, length of stay, and just nine other variables. “The model can be applied easily in clinical practice, even if electronic records are not available, because there are only 12 variables,” Dr. Pellicori said. “These could easily be entered manually into the risk calculator that we provide.”
“What is notable about this risk calculator is that it uses some of the techniques of machine learning, although it’s not specifically machine learning,” Angel Coz, MD, a pulmonologist at the Cleveland Clinic Respiratory Institute, said in an interview. “But it’s a retrospective data analysis, and actually by doing that it may catch some factors that we may not have necessarily paid attention to on a regular basis.”
While he called it a “well-done study,” Dr. Coz cautioned that “we have to be conservative in how to interpret and apply this because it is retrospective,” adding that future research should also use a prospective cohort.
For future consideration, Dr. Pellicori said that, while EHRs provide a “rich source” of data for such risk calculators, systems differ greatly across hospitals and health care systems and don’t link easily.
Future research would focus on validating the model in other large national datasets and seeing if machine learning can improve its predictability, Dr. Pellicori said. “Whether such models can provide a real-time, refined risk assessment for all patients in both primary or secondary care settings and improve the efficacy, efficiency, and quality of health care is our long-term goal.”
Dr. Pellicori and Dr. Coz disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Researchers in Scotland have developed a risk calculator using a large electronic health records database that has shown a high reliability in predicting the risk of death for patients hospitalized for chronic occlusive pulmonary disease (COPD), providing another potential tool for improving postdischarge survival in these patients.
In a study published online in the journal Pharmacological Research, Pierpalo Pellicori, MD, and colleagues reported that a few variables, including prescriptions and laboratory data in routine EHRs, could help predict a patient’s risk of dying within 90 days after a hospital stay for COPD. Dr. Pellicori is a clinical cardiologist and research fellow at the Robertson Center for Biostatistics at the University of Glasgow.
“Identification of patients at high risk is valuable information for multidisciplinary teams,” Dr. Pellicori said in a written comment. “It allows the most vulnerable patients to be highlighted and prioritized for consideration of optimized value-based care, and for anticipatory care plan discussions.”
The retrospective cohort study analyzed EHR records of 17,973 patients who had an unplanned hospitalization for COPD in the Glasgow area from 2011 to 2017. The risk calculator model achieved a potential accuracy of 80%.
The study noted that, while a number of models have been developed to calculate the risk of exacerbations, inpatient death and prognosis in patients hospitalized for COPD, most of those models were based on cohorts of 1000 patients or less.
“Older age, male sex, and a longer hospital stay were important predictors of mortality in patients with COPD,” Dr. Pellicori said. “We also found that use of commonly prescribed medications such as digoxin identify patients with COPD more likely to die, perhaps because many have underlying heart failure, a highly prevalent but frequently missed diagnosis.”
He noted that heart failure and COPD share many risk factors, signs, and symptoms, such as smoking history, peripheral edema, and breathlessness. “Distinguishing between COPD and heart failure can be difficult, but is very important, as appropriate treatment for heart failure can improve a patient’s quality of life and survival substantially in many cases.”
The study also found that routinely collected and inexpensive blood markers – such as hemoglobin, neutrophil/lymphocyte ratio, serum chloride, urea, creatinine, and albumin – can also improve predictability of outcomes.
For example, the study found a linear increase in mortality of blood hemoglobin concentration less than 14 g/dL, but higher levels posed no greater risk. Higher white blood cell and neutrophil counts and lower lymphocyte and eosinophil counts were associated with a worse prognosis.
The study also found a linear increase in mortality with serum sodium less than 140 mmol/L or serum chloride less than 105 mmol/L – but that higher concentrations of each were associated with a worse outcome.
“Interestingly,” Pellicori added, “social deprivation was not associated with mortality in this cohort.”
The final predictive model included age, sex, length of stay, and just nine other variables. “The model can be applied easily in clinical practice, even if electronic records are not available, because there are only 12 variables,” Dr. Pellicori said. “These could easily be entered manually into the risk calculator that we provide.”
“What is notable about this risk calculator is that it uses some of the techniques of machine learning, although it’s not specifically machine learning,” Angel Coz, MD, a pulmonologist at the Cleveland Clinic Respiratory Institute, said in an interview. “But it’s a retrospective data analysis, and actually by doing that it may catch some factors that we may not have necessarily paid attention to on a regular basis.”
While he called it a “well-done study,” Dr. Coz cautioned that “we have to be conservative in how to interpret and apply this because it is retrospective,” adding that future research should also use a prospective cohort.
For future consideration, Dr. Pellicori said that, while EHRs provide a “rich source” of data for such risk calculators, systems differ greatly across hospitals and health care systems and don’t link easily.
Future research would focus on validating the model in other large national datasets and seeing if machine learning can improve its predictability, Dr. Pellicori said. “Whether such models can provide a real-time, refined risk assessment for all patients in both primary or secondary care settings and improve the efficacy, efficiency, and quality of health care is our long-term goal.”
Dr. Pellicori and Dr. Coz disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM PHARMACOLOGICAL RESEARCH