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Impact of climate change on mortality underlined by global study
Regardless of where people live in the world, air pollution is linked to increased rates of cardiovascular disease, respiratory problems, and all-cause mortality, according to one of the largest studies ever to assess the effects of inhalable particulate matter (PM), published Aug. 21 in the New England Journal of Medicine.
“These data reinforce the evidence of a link between mortality and PM concentration established in regional and local studies,” reported Cong Liu of the Huazhong University of Science and Technology in Wuhan, China, and an international team of researchers.
“Many people are experiencing worse allergy and asthma symptoms in the setting of increased heat and worse air quality,” Caren G. Solomon, MD, of Harvard Medical School, Boston, said in an interview. “It is often not appreciated that these are complications of climate change.”
Other such complications include heat-related illnesses and severe weather events, as well as the less visible manifestations, such as shifts in the epidemiology of vector-borne infectious disease, Dr. Solomon and colleagues wrote in an editorial accompanying Mr. Liu’s study.
“The stark reality is that high levels of greenhouse gases caused by the combustion of fossil fuels – and the resulting rise in temperature and sea levels and intensification of extreme weather – are having profound consequences for human health and health systems,” Dr. Solomon and colleagues wrote (N Engl J Med. 2019;381:773-4.).
In the new air pollution study, Mr. Liu and colleagues analyzed 59.6 million deaths from 652 cities across 24 countries, “thereby greatly increasing the generalizability of the association and decreasing the likelihood that the reported associations are subject to confounding bias,” wrote John R. Balmes, MD, of the University of California, San Francisco, and the University of California, Berkeley, in an editorial about the study (N Engl J Med. 2019;381:774-6).
The researchers compared air pollution data from 1986-2015 from the Multi-City Multi-Country (MCC) Collaborative Research Network to mortality data reported from individual countries. They assessed PM with an aerodynamic diameter of 10 mcg or less (PM10; n = 598 cities) and PM with an aerodynamic diameter of 2.5 mcg or less (PM2.5; n=499 cities).
Mr. Liu’s team used a time-series analysis – a standard upon which the majority of air pollution research relies. These studies “include daily measures of health events (e.g., daily mortality), regressed against concentrations of PM (e.g., 24-hour average PM2.5) and weather variables (e.g., daily average temperature) for a given geographic area,” Dr. Balmes wrote. “The population serves as its own control, and confounding by population characteristics is negligible because these are stable over short time frames.”
The researchers found a 0.44% increase in daily all-cause mortality for each 10-mcg/m3 increase in the 2-day moving average (current and previous day) of PM10. The same increase was linked to a 0.36% increase in daily cardiovascular mortality and a 0.47% increase in daily respiratory mortality. Similarly, a 10-mcg/m3 increase in the PM2.5 average was linked to 0.68% increase in all-cause mortality, a 0.55% increase in cardiovascular mortality, and 0.74% increase in respiratory mortality.
Locations with higher annual mean temperatures showed stronger associations, and all these associations remained statistically significant after the researchers adjusted for gaseous pollutants.
Although the majority of countries and cities included in the study came from the northern hemisphere, the researchers noted that the magnitude of effect they found, particularly for PM10 concentrations, matched up with that seen in previous studies of multiple cities or countries.
Still, they found “significant evidence of spatial heterogeneity in the associations between PM concentration and daily mortality across countries and regions.” Among the factors that could contribute to those variations are “different PM components, long-term air pollution levels, population susceptibility, and different lengths of study periods,” they speculated.
What makes this study remarkable – despite decades of previous similar studies – is its size and the implications of a curvilinear shape in its concentration-response relation, according to Dr. Balmes.
“The current study of PM data from many regions around the world provides the strongest evidence to date that higher levels of exposure may be associated with a lower per-unit risk,” Dr. Balmes wrote. “Regions that have lower exposures had a higher per-unit risk. This finding has profound policy implications, especially given that no threshold of effect was found. Even high-income countries, such as the United States, with relatively good air quality could still see public health benefits from further reduction of ambient PM concentrations.”
The policy implications, however, extend well beyond clean air regulations because the findings represent just one aspect of climate change’s negative effects on health, which are “frighteningly broad,” Dr. Solomon and colleagues wrote.
“As climate change continues to alter disease patterns and disrupt health systems, its effects on human health will become harder to ignore,” they wrote. “We, as a medical community, have the responsibility and the opportunity to mobilize the urgent, large-scale climate action required to protect health – as well as the ingenuity to develop novel and bold interventions to avert the most catastrophic outcomes.”
The new research and associated commentary marked the introduction of a new NEJM topic on climate change effects on health and health systems.
SOURCE: Liu C et al. N Engl J Med. 2019;381:705-15.
This article was updated 8/22/19.
The negative effects of climate change on global public health are already playing out around us, but scientific research shows that they will only get worse – unless we begin addressing the issue in earnest now.
At the macro level nationally, effective policy is actually being stripped away right now. “[While] scientists tell us we have little time to wait if we hope to avoid the most devastating effects of climate change, leaders in Washington, D.C., are attacking science and rolling back Obama-era rules from the Environmental Protection Agency,” such as working to weaken vehicle fuel-efficiency standards, relaxing methane emissions rules, ending mercury emissions regulation and taking other actions that will only increase air pollution.
“If these EPA rollbacks are successful, they will diminish our ability to mitigate health effects and diseases related to the burning of fossil fuels and the immense toll they take on our families. ... If we stop supporting and listening to the best available science, if we allow more pollution to be emitted, and if we start limiting the EPA’s ability to monitor and enforce pollution standards, then we put at risk everyone’s health – and especially the health and future of our children.”
Engaging in advocacy and communicating to our representatives that we want stronger regulations is one way people can personally take action, but we can take immediate actions in our everyday lives too. Rather than dwelling on the despair of helplessness and hopelessness that grips many people when it comes to climate change, this moment can be reframed as an opportunity for people to make decisions that immediately begin improving their health — and also happen to be good for the planet.
“To me, the most urgent challenge when it comes to health and climate change is the reality that, when climate change comes up, in the U.S. audience, the first thing that should come into people’s minds is that we need to do this now because we need to protect our children’s health. ... Too many people either don’t get that it matters to health at all, or they don’t get that the actions we need to take are exactly what we need to do to address the health problems that have been nearly impossible to deal with.”
For example, problems like rising child obesity and type 2 diabetes rates have plagued public health, yet people can make changes that reduce obesity and diabetes risk that also decrease their carbon footprints, he said. “One of the best ways to deal with obesity is to eat more plants, and it turns out that’s really good for the climate” Additionally, getting people out of cars and walking and cycling can reduce individuals’ risk of diabetes – while simultaneously decreasing air pollution. “We need to be doing these things regardless of climate change, and if parents and children understood that the pathway to a healthier future was through tackling climate change, we would see a transformation.”
The value of local policy actions should be emphasized, such as ones that call for a reduction in a city’s use of concrete – which increases localized heat – and constructing more efficient buildings. Healthcare providers have an opportunity – and responsibility – not only to recognize this reality but to help their patients recognize it too.
“We can also use our roles as trusted advisers to inform and motivate actions that are increasingly necessary to protect the health of the communities we serve.” They also need to be vigilant about conditions that will worsen as the planet heats up: For example, medications such as diuretics carry more risks in higher temperatures, and patients taking them need to know that.
The need to address climate change matters because we face the challenge of protecting the world’s most vulnerable people.
“One of the great things about climate change is if it causes us to rethink about what we need to do to protect the future, it’s going to help our health today. ... If we can use that as the motivator, then maybe we can stop arguing and start thinking about climate as a positive issue, as a more personal issue we can all participate in and be willing to invest in.”
Gina McCarthy, MS, was administrator of the Environmental Protection Agency during 2013-2017, and Aaron Bernstein, MD, MPH, is a pediatrician at Boston Children’s Hospital. Both are from the Center for Climate, Health, and the Global Environment (Harvard C-CHANGE) at the Harvard T.H. Chan School of Public Health in Boston. Their comments came from their perspective (N Engl J Med. 2019 Aug 22. doi: 10.1056/NEJMp1909643) published in NEJM along with this article and editorial and a phone interview. They reported not having any disclosures.
The negative effects of climate change on global public health are already playing out around us, but scientific research shows that they will only get worse – unless we begin addressing the issue in earnest now.
At the macro level nationally, effective policy is actually being stripped away right now. “[While] scientists tell us we have little time to wait if we hope to avoid the most devastating effects of climate change, leaders in Washington, D.C., are attacking science and rolling back Obama-era rules from the Environmental Protection Agency,” such as working to weaken vehicle fuel-efficiency standards, relaxing methane emissions rules, ending mercury emissions regulation and taking other actions that will only increase air pollution.
“If these EPA rollbacks are successful, they will diminish our ability to mitigate health effects and diseases related to the burning of fossil fuels and the immense toll they take on our families. ... If we stop supporting and listening to the best available science, if we allow more pollution to be emitted, and if we start limiting the EPA’s ability to monitor and enforce pollution standards, then we put at risk everyone’s health – and especially the health and future of our children.”
Engaging in advocacy and communicating to our representatives that we want stronger regulations is one way people can personally take action, but we can take immediate actions in our everyday lives too. Rather than dwelling on the despair of helplessness and hopelessness that grips many people when it comes to climate change, this moment can be reframed as an opportunity for people to make decisions that immediately begin improving their health — and also happen to be good for the planet.
“To me, the most urgent challenge when it comes to health and climate change is the reality that, when climate change comes up, in the U.S. audience, the first thing that should come into people’s minds is that we need to do this now because we need to protect our children’s health. ... Too many people either don’t get that it matters to health at all, or they don’t get that the actions we need to take are exactly what we need to do to address the health problems that have been nearly impossible to deal with.”
For example, problems like rising child obesity and type 2 diabetes rates have plagued public health, yet people can make changes that reduce obesity and diabetes risk that also decrease their carbon footprints, he said. “One of the best ways to deal with obesity is to eat more plants, and it turns out that’s really good for the climate” Additionally, getting people out of cars and walking and cycling can reduce individuals’ risk of diabetes – while simultaneously decreasing air pollution. “We need to be doing these things regardless of climate change, and if parents and children understood that the pathway to a healthier future was through tackling climate change, we would see a transformation.”
The value of local policy actions should be emphasized, such as ones that call for a reduction in a city’s use of concrete – which increases localized heat – and constructing more efficient buildings. Healthcare providers have an opportunity – and responsibility – not only to recognize this reality but to help their patients recognize it too.
“We can also use our roles as trusted advisers to inform and motivate actions that are increasingly necessary to protect the health of the communities we serve.” They also need to be vigilant about conditions that will worsen as the planet heats up: For example, medications such as diuretics carry more risks in higher temperatures, and patients taking them need to know that.
The need to address climate change matters because we face the challenge of protecting the world’s most vulnerable people.
“One of the great things about climate change is if it causes us to rethink about what we need to do to protect the future, it’s going to help our health today. ... If we can use that as the motivator, then maybe we can stop arguing and start thinking about climate as a positive issue, as a more personal issue we can all participate in and be willing to invest in.”
Gina McCarthy, MS, was administrator of the Environmental Protection Agency during 2013-2017, and Aaron Bernstein, MD, MPH, is a pediatrician at Boston Children’s Hospital. Both are from the Center for Climate, Health, and the Global Environment (Harvard C-CHANGE) at the Harvard T.H. Chan School of Public Health in Boston. Their comments came from their perspective (N Engl J Med. 2019 Aug 22. doi: 10.1056/NEJMp1909643) published in NEJM along with this article and editorial and a phone interview. They reported not having any disclosures.
The negative effects of climate change on global public health are already playing out around us, but scientific research shows that they will only get worse – unless we begin addressing the issue in earnest now.
At the macro level nationally, effective policy is actually being stripped away right now. “[While] scientists tell us we have little time to wait if we hope to avoid the most devastating effects of climate change, leaders in Washington, D.C., are attacking science and rolling back Obama-era rules from the Environmental Protection Agency,” such as working to weaken vehicle fuel-efficiency standards, relaxing methane emissions rules, ending mercury emissions regulation and taking other actions that will only increase air pollution.
“If these EPA rollbacks are successful, they will diminish our ability to mitigate health effects and diseases related to the burning of fossil fuels and the immense toll they take on our families. ... If we stop supporting and listening to the best available science, if we allow more pollution to be emitted, and if we start limiting the EPA’s ability to monitor and enforce pollution standards, then we put at risk everyone’s health – and especially the health and future of our children.”
Engaging in advocacy and communicating to our representatives that we want stronger regulations is one way people can personally take action, but we can take immediate actions in our everyday lives too. Rather than dwelling on the despair of helplessness and hopelessness that grips many people when it comes to climate change, this moment can be reframed as an opportunity for people to make decisions that immediately begin improving their health — and also happen to be good for the planet.
“To me, the most urgent challenge when it comes to health and climate change is the reality that, when climate change comes up, in the U.S. audience, the first thing that should come into people’s minds is that we need to do this now because we need to protect our children’s health. ... Too many people either don’t get that it matters to health at all, or they don’t get that the actions we need to take are exactly what we need to do to address the health problems that have been nearly impossible to deal with.”
For example, problems like rising child obesity and type 2 diabetes rates have plagued public health, yet people can make changes that reduce obesity and diabetes risk that also decrease their carbon footprints, he said. “One of the best ways to deal with obesity is to eat more plants, and it turns out that’s really good for the climate” Additionally, getting people out of cars and walking and cycling can reduce individuals’ risk of diabetes – while simultaneously decreasing air pollution. “We need to be doing these things regardless of climate change, and if parents and children understood that the pathway to a healthier future was through tackling climate change, we would see a transformation.”
The value of local policy actions should be emphasized, such as ones that call for a reduction in a city’s use of concrete – which increases localized heat – and constructing more efficient buildings. Healthcare providers have an opportunity – and responsibility – not only to recognize this reality but to help their patients recognize it too.
“We can also use our roles as trusted advisers to inform and motivate actions that are increasingly necessary to protect the health of the communities we serve.” They also need to be vigilant about conditions that will worsen as the planet heats up: For example, medications such as diuretics carry more risks in higher temperatures, and patients taking them need to know that.
The need to address climate change matters because we face the challenge of protecting the world’s most vulnerable people.
“One of the great things about climate change is if it causes us to rethink about what we need to do to protect the future, it’s going to help our health today. ... If we can use that as the motivator, then maybe we can stop arguing and start thinking about climate as a positive issue, as a more personal issue we can all participate in and be willing to invest in.”
Gina McCarthy, MS, was administrator of the Environmental Protection Agency during 2013-2017, and Aaron Bernstein, MD, MPH, is a pediatrician at Boston Children’s Hospital. Both are from the Center for Climate, Health, and the Global Environment (Harvard C-CHANGE) at the Harvard T.H. Chan School of Public Health in Boston. Their comments came from their perspective (N Engl J Med. 2019 Aug 22. doi: 10.1056/NEJMp1909643) published in NEJM along with this article and editorial and a phone interview. They reported not having any disclosures.
Regardless of where people live in the world, air pollution is linked to increased rates of cardiovascular disease, respiratory problems, and all-cause mortality, according to one of the largest studies ever to assess the effects of inhalable particulate matter (PM), published Aug. 21 in the New England Journal of Medicine.
“These data reinforce the evidence of a link between mortality and PM concentration established in regional and local studies,” reported Cong Liu of the Huazhong University of Science and Technology in Wuhan, China, and an international team of researchers.
“Many people are experiencing worse allergy and asthma symptoms in the setting of increased heat and worse air quality,” Caren G. Solomon, MD, of Harvard Medical School, Boston, said in an interview. “It is often not appreciated that these are complications of climate change.”
Other such complications include heat-related illnesses and severe weather events, as well as the less visible manifestations, such as shifts in the epidemiology of vector-borne infectious disease, Dr. Solomon and colleagues wrote in an editorial accompanying Mr. Liu’s study.
“The stark reality is that high levels of greenhouse gases caused by the combustion of fossil fuels – and the resulting rise in temperature and sea levels and intensification of extreme weather – are having profound consequences for human health and health systems,” Dr. Solomon and colleagues wrote (N Engl J Med. 2019;381:773-4.).
In the new air pollution study, Mr. Liu and colleagues analyzed 59.6 million deaths from 652 cities across 24 countries, “thereby greatly increasing the generalizability of the association and decreasing the likelihood that the reported associations are subject to confounding bias,” wrote John R. Balmes, MD, of the University of California, San Francisco, and the University of California, Berkeley, in an editorial about the study (N Engl J Med. 2019;381:774-6).
The researchers compared air pollution data from 1986-2015 from the Multi-City Multi-Country (MCC) Collaborative Research Network to mortality data reported from individual countries. They assessed PM with an aerodynamic diameter of 10 mcg or less (PM10; n = 598 cities) and PM with an aerodynamic diameter of 2.5 mcg or less (PM2.5; n=499 cities).
Mr. Liu’s team used a time-series analysis – a standard upon which the majority of air pollution research relies. These studies “include daily measures of health events (e.g., daily mortality), regressed against concentrations of PM (e.g., 24-hour average PM2.5) and weather variables (e.g., daily average temperature) for a given geographic area,” Dr. Balmes wrote. “The population serves as its own control, and confounding by population characteristics is negligible because these are stable over short time frames.”
The researchers found a 0.44% increase in daily all-cause mortality for each 10-mcg/m3 increase in the 2-day moving average (current and previous day) of PM10. The same increase was linked to a 0.36% increase in daily cardiovascular mortality and a 0.47% increase in daily respiratory mortality. Similarly, a 10-mcg/m3 increase in the PM2.5 average was linked to 0.68% increase in all-cause mortality, a 0.55% increase in cardiovascular mortality, and 0.74% increase in respiratory mortality.
Locations with higher annual mean temperatures showed stronger associations, and all these associations remained statistically significant after the researchers adjusted for gaseous pollutants.
Although the majority of countries and cities included in the study came from the northern hemisphere, the researchers noted that the magnitude of effect they found, particularly for PM10 concentrations, matched up with that seen in previous studies of multiple cities or countries.
Still, they found “significant evidence of spatial heterogeneity in the associations between PM concentration and daily mortality across countries and regions.” Among the factors that could contribute to those variations are “different PM components, long-term air pollution levels, population susceptibility, and different lengths of study periods,” they speculated.
What makes this study remarkable – despite decades of previous similar studies – is its size and the implications of a curvilinear shape in its concentration-response relation, according to Dr. Balmes.
“The current study of PM data from many regions around the world provides the strongest evidence to date that higher levels of exposure may be associated with a lower per-unit risk,” Dr. Balmes wrote. “Regions that have lower exposures had a higher per-unit risk. This finding has profound policy implications, especially given that no threshold of effect was found. Even high-income countries, such as the United States, with relatively good air quality could still see public health benefits from further reduction of ambient PM concentrations.”
The policy implications, however, extend well beyond clean air regulations because the findings represent just one aspect of climate change’s negative effects on health, which are “frighteningly broad,” Dr. Solomon and colleagues wrote.
“As climate change continues to alter disease patterns and disrupt health systems, its effects on human health will become harder to ignore,” they wrote. “We, as a medical community, have the responsibility and the opportunity to mobilize the urgent, large-scale climate action required to protect health – as well as the ingenuity to develop novel and bold interventions to avert the most catastrophic outcomes.”
The new research and associated commentary marked the introduction of a new NEJM topic on climate change effects on health and health systems.
SOURCE: Liu C et al. N Engl J Med. 2019;381:705-15.
This article was updated 8/22/19.
Regardless of where people live in the world, air pollution is linked to increased rates of cardiovascular disease, respiratory problems, and all-cause mortality, according to one of the largest studies ever to assess the effects of inhalable particulate matter (PM), published Aug. 21 in the New England Journal of Medicine.
“These data reinforce the evidence of a link between mortality and PM concentration established in regional and local studies,” reported Cong Liu of the Huazhong University of Science and Technology in Wuhan, China, and an international team of researchers.
“Many people are experiencing worse allergy and asthma symptoms in the setting of increased heat and worse air quality,” Caren G. Solomon, MD, of Harvard Medical School, Boston, said in an interview. “It is often not appreciated that these are complications of climate change.”
Other such complications include heat-related illnesses and severe weather events, as well as the less visible manifestations, such as shifts in the epidemiology of vector-borne infectious disease, Dr. Solomon and colleagues wrote in an editorial accompanying Mr. Liu’s study.
“The stark reality is that high levels of greenhouse gases caused by the combustion of fossil fuels – and the resulting rise in temperature and sea levels and intensification of extreme weather – are having profound consequences for human health and health systems,” Dr. Solomon and colleagues wrote (N Engl J Med. 2019;381:773-4.).
In the new air pollution study, Mr. Liu and colleagues analyzed 59.6 million deaths from 652 cities across 24 countries, “thereby greatly increasing the generalizability of the association and decreasing the likelihood that the reported associations are subject to confounding bias,” wrote John R. Balmes, MD, of the University of California, San Francisco, and the University of California, Berkeley, in an editorial about the study (N Engl J Med. 2019;381:774-6).
The researchers compared air pollution data from 1986-2015 from the Multi-City Multi-Country (MCC) Collaborative Research Network to mortality data reported from individual countries. They assessed PM with an aerodynamic diameter of 10 mcg or less (PM10; n = 598 cities) and PM with an aerodynamic diameter of 2.5 mcg or less (PM2.5; n=499 cities).
Mr. Liu’s team used a time-series analysis – a standard upon which the majority of air pollution research relies. These studies “include daily measures of health events (e.g., daily mortality), regressed against concentrations of PM (e.g., 24-hour average PM2.5) and weather variables (e.g., daily average temperature) for a given geographic area,” Dr. Balmes wrote. “The population serves as its own control, and confounding by population characteristics is negligible because these are stable over short time frames.”
The researchers found a 0.44% increase in daily all-cause mortality for each 10-mcg/m3 increase in the 2-day moving average (current and previous day) of PM10. The same increase was linked to a 0.36% increase in daily cardiovascular mortality and a 0.47% increase in daily respiratory mortality. Similarly, a 10-mcg/m3 increase in the PM2.5 average was linked to 0.68% increase in all-cause mortality, a 0.55% increase in cardiovascular mortality, and 0.74% increase in respiratory mortality.
Locations with higher annual mean temperatures showed stronger associations, and all these associations remained statistically significant after the researchers adjusted for gaseous pollutants.
Although the majority of countries and cities included in the study came from the northern hemisphere, the researchers noted that the magnitude of effect they found, particularly for PM10 concentrations, matched up with that seen in previous studies of multiple cities or countries.
Still, they found “significant evidence of spatial heterogeneity in the associations between PM concentration and daily mortality across countries and regions.” Among the factors that could contribute to those variations are “different PM components, long-term air pollution levels, population susceptibility, and different lengths of study periods,” they speculated.
What makes this study remarkable – despite decades of previous similar studies – is its size and the implications of a curvilinear shape in its concentration-response relation, according to Dr. Balmes.
“The current study of PM data from many regions around the world provides the strongest evidence to date that higher levels of exposure may be associated with a lower per-unit risk,” Dr. Balmes wrote. “Regions that have lower exposures had a higher per-unit risk. This finding has profound policy implications, especially given that no threshold of effect was found. Even high-income countries, such as the United States, with relatively good air quality could still see public health benefits from further reduction of ambient PM concentrations.”
The policy implications, however, extend well beyond clean air regulations because the findings represent just one aspect of climate change’s negative effects on health, which are “frighteningly broad,” Dr. Solomon and colleagues wrote.
“As climate change continues to alter disease patterns and disrupt health systems, its effects on human health will become harder to ignore,” they wrote. “We, as a medical community, have the responsibility and the opportunity to mobilize the urgent, large-scale climate action required to protect health – as well as the ingenuity to develop novel and bold interventions to avert the most catastrophic outcomes.”
The new research and associated commentary marked the introduction of a new NEJM topic on climate change effects on health and health systems.
SOURCE: Liu C et al. N Engl J Med. 2019;381:705-15.
This article was updated 8/22/19.
FROM NEJM
FDA approves lefamulin for community-acquired bacterial pneumonia treatment
The Food and Drug Administration has announced its approval of lefamulin (Xenleta) for the treatment of community-acquired bacterial pneumonia in adults.
Approval was based on results of two clinical trials assessing a total of 1,289 people with community-acquired bacterial pneumonia. In these trials, lefamulin was compared with moxifloxacin with and without linezolid. Patients who received lefamulin had similar rates of treatment success as those taking moxifloxacin alone or moxifloxacin plus linezolid.
The most common adverse reactions associated with lefamulin include diarrhea, nausea, reactions at the injection site, elevated liver enzymes, and vomiting. Patients with prolonged QT interval, patients with arrhythmias, patients receiving treatment with antiarrhythmic agents, and patients receiving other drugs that prolong the QT interval are contraindicated. In addition, because of evidence of fetal harm in animal studies, pregnant women should be advised of potential risks before receiving lefamulin.
“This new drug provides another option for the treatment of patients with community-acquired bacterial pneumonia, a serious disease. For managing this serious disease, it is important for physicians and patients to have treatment options,” Ed Cox, MD, MPH, director of the FDA’s Office of Antimicrobial Products, said in the press release.
The Food and Drug Administration has announced its approval of lefamulin (Xenleta) for the treatment of community-acquired bacterial pneumonia in adults.
Approval was based on results of two clinical trials assessing a total of 1,289 people with community-acquired bacterial pneumonia. In these trials, lefamulin was compared with moxifloxacin with and without linezolid. Patients who received lefamulin had similar rates of treatment success as those taking moxifloxacin alone or moxifloxacin plus linezolid.
The most common adverse reactions associated with lefamulin include diarrhea, nausea, reactions at the injection site, elevated liver enzymes, and vomiting. Patients with prolonged QT interval, patients with arrhythmias, patients receiving treatment with antiarrhythmic agents, and patients receiving other drugs that prolong the QT interval are contraindicated. In addition, because of evidence of fetal harm in animal studies, pregnant women should be advised of potential risks before receiving lefamulin.
“This new drug provides another option for the treatment of patients with community-acquired bacterial pneumonia, a serious disease. For managing this serious disease, it is important for physicians and patients to have treatment options,” Ed Cox, MD, MPH, director of the FDA’s Office of Antimicrobial Products, said in the press release.
The Food and Drug Administration has announced its approval of lefamulin (Xenleta) for the treatment of community-acquired bacterial pneumonia in adults.
Approval was based on results of two clinical trials assessing a total of 1,289 people with community-acquired bacterial pneumonia. In these trials, lefamulin was compared with moxifloxacin with and without linezolid. Patients who received lefamulin had similar rates of treatment success as those taking moxifloxacin alone or moxifloxacin plus linezolid.
The most common adverse reactions associated with lefamulin include diarrhea, nausea, reactions at the injection site, elevated liver enzymes, and vomiting. Patients with prolonged QT interval, patients with arrhythmias, patients receiving treatment with antiarrhythmic agents, and patients receiving other drugs that prolong the QT interval are contraindicated. In addition, because of evidence of fetal harm in animal studies, pregnant women should be advised of potential risks before receiving lefamulin.
“This new drug provides another option for the treatment of patients with community-acquired bacterial pneumonia, a serious disease. For managing this serious disease, it is important for physicians and patients to have treatment options,” Ed Cox, MD, MPH, director of the FDA’s Office of Antimicrobial Products, said in the press release.
Cardiovascular cost of smoking may last up to 25 years
Quitting smoking significantly reduces the risk of cardiovascular disease, but past smokers are still at elevated cardiovascular risk, compared with nonsmokers, for up to 25 years after smoking cessation, research in JAMA suggests.
A retrospective analysis of data from 8,770 individuals in the Framingham Heart Study compared the incidence of myocardial infarction, stroke, heart failure, or cardiovascular death in ever-smokers with that of never smokers.
Only 40% of the total cohort had never smoked. Of the 4,115 current smokers at baseline, 38.6% quit during the course of the study and did not relapse but 51.4% continued to smoke until they developed cardiovascular disease or dropped out of the study.
Current smokers had a significant 4.68-fold higher incidence of cardiovascular disease, compared with those who had never smoked, but those who stopped smoking showed a 39% decline in their risk of cardiovascular disease within 5 years of cessation.
However, individuals who were formerly heavy smokers – defined as at least 20 pack-years of smoking – retained a risk of cardiovascular disease 25% higher than that of never smokers until 10-15 years after quitting smoking. At 16 years, the 95% confidence interval for cardiovascular disease risk among former smokers versus that of never smokers finally and consistently included the null value of 1.
The study pooled two cohorts; the original cohort, who attended their fourth examination during 1954-1958 and an offspring cohort who attended their first examination during 1971-1975. The authors saw a difference between the two cohorts in the time course of cardiovascular disease risk in heavy smokers.
In the original cohort, former heavy smoking ceased to be significantly associated with increased cardiovascular disease risk within 5-10 years of cessation, but in the offspring cohort, it took 25 years after cessation for the incidence to decline to the same level of risk seen in never smokers.
“The upper estimate of this time course is a decade longer than that of the Nurses’ Health Study results for coronary heart disease and cardiovascular death and more than 20 years longer than in some prior reports for coronary heart disease and stroke,” wrote Meredith S. Duncan from the division of cardiovascular medicine at the Vanderbilt University Medical Center, Nashville, Tenn., and coauthors. “Although the exact amount of time after quitting at which former smokers’ CVD risk ceases to differ significantly from that of never smokers is unknown (and may further depend on cumulative exposure), these findings support a longer time course of risk reduction than was previously thought, yielding implications for CVD risk stratification of former smokers.”
However, they did note that the study could not account for environmental tobacco smoke exposure and that the participants were mostly of white European ancestry, which limited the generalizability of the findings to other populations.
The Framingham Health Study was supported by the National Heart, Lung, and Blood Institute. One author declared a consultancy with a pharmaceutical company on a proposed clinical trial. No other conflicts of interest were declared.
SOURCE: Duncan M et al. JAMA 2019. doi: 10.1001/jama.2019.10298.
Quitting smoking significantly reduces the risk of cardiovascular disease, but past smokers are still at elevated cardiovascular risk, compared with nonsmokers, for up to 25 years after smoking cessation, research in JAMA suggests.
A retrospective analysis of data from 8,770 individuals in the Framingham Heart Study compared the incidence of myocardial infarction, stroke, heart failure, or cardiovascular death in ever-smokers with that of never smokers.
Only 40% of the total cohort had never smoked. Of the 4,115 current smokers at baseline, 38.6% quit during the course of the study and did not relapse but 51.4% continued to smoke until they developed cardiovascular disease or dropped out of the study.
Current smokers had a significant 4.68-fold higher incidence of cardiovascular disease, compared with those who had never smoked, but those who stopped smoking showed a 39% decline in their risk of cardiovascular disease within 5 years of cessation.
However, individuals who were formerly heavy smokers – defined as at least 20 pack-years of smoking – retained a risk of cardiovascular disease 25% higher than that of never smokers until 10-15 years after quitting smoking. At 16 years, the 95% confidence interval for cardiovascular disease risk among former smokers versus that of never smokers finally and consistently included the null value of 1.
The study pooled two cohorts; the original cohort, who attended their fourth examination during 1954-1958 and an offspring cohort who attended their first examination during 1971-1975. The authors saw a difference between the two cohorts in the time course of cardiovascular disease risk in heavy smokers.
In the original cohort, former heavy smoking ceased to be significantly associated with increased cardiovascular disease risk within 5-10 years of cessation, but in the offspring cohort, it took 25 years after cessation for the incidence to decline to the same level of risk seen in never smokers.
“The upper estimate of this time course is a decade longer than that of the Nurses’ Health Study results for coronary heart disease and cardiovascular death and more than 20 years longer than in some prior reports for coronary heart disease and stroke,” wrote Meredith S. Duncan from the division of cardiovascular medicine at the Vanderbilt University Medical Center, Nashville, Tenn., and coauthors. “Although the exact amount of time after quitting at which former smokers’ CVD risk ceases to differ significantly from that of never smokers is unknown (and may further depend on cumulative exposure), these findings support a longer time course of risk reduction than was previously thought, yielding implications for CVD risk stratification of former smokers.”
However, they did note that the study could not account for environmental tobacco smoke exposure and that the participants were mostly of white European ancestry, which limited the generalizability of the findings to other populations.
The Framingham Health Study was supported by the National Heart, Lung, and Blood Institute. One author declared a consultancy with a pharmaceutical company on a proposed clinical trial. No other conflicts of interest were declared.
SOURCE: Duncan M et al. JAMA 2019. doi: 10.1001/jama.2019.10298.
Quitting smoking significantly reduces the risk of cardiovascular disease, but past smokers are still at elevated cardiovascular risk, compared with nonsmokers, for up to 25 years after smoking cessation, research in JAMA suggests.
A retrospective analysis of data from 8,770 individuals in the Framingham Heart Study compared the incidence of myocardial infarction, stroke, heart failure, or cardiovascular death in ever-smokers with that of never smokers.
Only 40% of the total cohort had never smoked. Of the 4,115 current smokers at baseline, 38.6% quit during the course of the study and did not relapse but 51.4% continued to smoke until they developed cardiovascular disease or dropped out of the study.
Current smokers had a significant 4.68-fold higher incidence of cardiovascular disease, compared with those who had never smoked, but those who stopped smoking showed a 39% decline in their risk of cardiovascular disease within 5 years of cessation.
However, individuals who were formerly heavy smokers – defined as at least 20 pack-years of smoking – retained a risk of cardiovascular disease 25% higher than that of never smokers until 10-15 years after quitting smoking. At 16 years, the 95% confidence interval for cardiovascular disease risk among former smokers versus that of never smokers finally and consistently included the null value of 1.
The study pooled two cohorts; the original cohort, who attended their fourth examination during 1954-1958 and an offspring cohort who attended their first examination during 1971-1975. The authors saw a difference between the two cohorts in the time course of cardiovascular disease risk in heavy smokers.
In the original cohort, former heavy smoking ceased to be significantly associated with increased cardiovascular disease risk within 5-10 years of cessation, but in the offspring cohort, it took 25 years after cessation for the incidence to decline to the same level of risk seen in never smokers.
“The upper estimate of this time course is a decade longer than that of the Nurses’ Health Study results for coronary heart disease and cardiovascular death and more than 20 years longer than in some prior reports for coronary heart disease and stroke,” wrote Meredith S. Duncan from the division of cardiovascular medicine at the Vanderbilt University Medical Center, Nashville, Tenn., and coauthors. “Although the exact amount of time after quitting at which former smokers’ CVD risk ceases to differ significantly from that of never smokers is unknown (and may further depend on cumulative exposure), these findings support a longer time course of risk reduction than was previously thought, yielding implications for CVD risk stratification of former smokers.”
However, they did note that the study could not account for environmental tobacco smoke exposure and that the participants were mostly of white European ancestry, which limited the generalizability of the findings to other populations.
The Framingham Health Study was supported by the National Heart, Lung, and Blood Institute. One author declared a consultancy with a pharmaceutical company on a proposed clinical trial. No other conflicts of interest were declared.
SOURCE: Duncan M et al. JAMA 2019. doi: 10.1001/jama.2019.10298.
FROM JAMA
Key clinical point:
Major finding: In the offspring cohort, heavy smokers showed elevated incidence of CVD for up to 25 years after quitting smoking.
Study details: A retrospective analysis of data from 8,770 individuals in the Framingham Heart Study.
Disclosures: The Framingham Health Study was supported by the National Heart, Lung, and Blood Institute. One author declared a consultancy with a pharmaceutical company on a proposed clinical trial. No other conflicts of interest were declared.
Source: Duncan M et al. JAMA. 2019. doi: 10.1001/jama.2019.10298.
FDA approves Xenleta for community-acquired bacterial pneumonia treatment
The Food and Drug Administration has announced its approval of lefamulin (Xenleta) for the treatment of community-acquired bacterial pneumonia in adults.
Approval was based on results of two clinical trials assessing a total of 1,289 people with community-acquired bacterial pneumonia. In these trials, lefamulin was compared with moxifloxacin with and without linezolid. Patients who received lefamulin had similar rates of treatment success as those taking moxifloxacin alone or moxifloxacin plus linezolid.
The most common adverse reactions associated with lefamulin include diarrhea, nausea, reactions at the injection site, elevated liver enzymes, and vomiting. Patients with prolonged QT interval, patients with arrhythmias, patients receiving treatment with antiarrhythmic agents, and patients receiving other drugs that prolong the QT interval are contraindicated. In addition, because of evidence of fetal harm in animal studies, pregnant women should be advised of potential risks before receiving lefamulin.
“This new drug provides another option for the treatment of patients with community-acquired bacterial pneumonia, a serious disease. For managing this serious disease, it is important for physicians and patients to have treatment options,” Ed Cox, MD, MPH, director of the FDA’s Office of Antimicrobial Products, said in the press release.
The Food and Drug Administration has announced its approval of lefamulin (Xenleta) for the treatment of community-acquired bacterial pneumonia in adults.
Approval was based on results of two clinical trials assessing a total of 1,289 people with community-acquired bacterial pneumonia. In these trials, lefamulin was compared with moxifloxacin with and without linezolid. Patients who received lefamulin had similar rates of treatment success as those taking moxifloxacin alone or moxifloxacin plus linezolid.
The most common adverse reactions associated with lefamulin include diarrhea, nausea, reactions at the injection site, elevated liver enzymes, and vomiting. Patients with prolonged QT interval, patients with arrhythmias, patients receiving treatment with antiarrhythmic agents, and patients receiving other drugs that prolong the QT interval are contraindicated. In addition, because of evidence of fetal harm in animal studies, pregnant women should be advised of potential risks before receiving lefamulin.
“This new drug provides another option for the treatment of patients with community-acquired bacterial pneumonia, a serious disease. For managing this serious disease, it is important for physicians and patients to have treatment options,” Ed Cox, MD, MPH, director of the FDA’s Office of Antimicrobial Products, said in the press release.
The Food and Drug Administration has announced its approval of lefamulin (Xenleta) for the treatment of community-acquired bacterial pneumonia in adults.
Approval was based on results of two clinical trials assessing a total of 1,289 people with community-acquired bacterial pneumonia. In these trials, lefamulin was compared with moxifloxacin with and without linezolid. Patients who received lefamulin had similar rates of treatment success as those taking moxifloxacin alone or moxifloxacin plus linezolid.
The most common adverse reactions associated with lefamulin include diarrhea, nausea, reactions at the injection site, elevated liver enzymes, and vomiting. Patients with prolonged QT interval, patients with arrhythmias, patients receiving treatment with antiarrhythmic agents, and patients receiving other drugs that prolong the QT interval are contraindicated. In addition, because of evidence of fetal harm in animal studies, pregnant women should be advised of potential risks before receiving lefamulin.
“This new drug provides another option for the treatment of patients with community-acquired bacterial pneumonia, a serious disease. For managing this serious disease, it is important for physicians and patients to have treatment options,” Ed Cox, MD, MPH, director of the FDA’s Office of Antimicrobial Products, said in the press release.
FDA takes another swing at updating cigarette pack warnings
illustrating the harms of smoking, but this could be subjected to legal challenge.
Several years ago, tobacco companies filed a lawsuit, which ultimately shut down a similar proposal.
The warnings focus on lesser-known complications – including diabetes, cataracts, gangrene, stroke, bladder cancer, erectile dysfunction, and obstructive pulmonary disease – and would take up the top half of the front and back of cigarette packs, and at least the top 20% of print advertisements. Each pack and ad would be required to carry 1 of the 13 proposed warnings, according to the announcement.
The approach would be similar to, but not as aggressive as Canada’s. For years, cigarettes packs sold in Canada have included disturbing photographs of diseased lungs, rotted teeth, and dying patients. The lasting impact of such imagery has been demonstrated in the literature (for example, Am J Prev Med. 2007 Mar;32[3]:202-9).
The new proposal is the FDA’s second attempt to enact something comparable in the United States, after being directed to do so by the Tobacco Control Act of 2009.
The first effort to add strong, illustrated warnings to cigarette packs was widely backed by medical groups, but challenged in the courts by R.J. Reynolds and other tobacco companies, and blocked on appeal in 2012 as an abridgment of commercial free speech. The federal government dropped the case in 2013.
The American Lung Association and other public health groups subsequently sued the FDA in 2016 to enact the Tobacco Act mandate. Subsequently, a federal judge ordered the agency to publish a new rule by August 2019, and issue a final rule in March 2020.
This time around, the FDA “took the necessary time to get these new proposed warnings right ... based on – and within the limits of – both science and the law,” the agency said. The new images, though graphic, are less disturbing than those used in Canada and the agency’s previous proposals, which included an apparent corpse with a sternotomy. The 1-800-Quit-Now cessation hotline number, which was a sticking point in the 2012 ruling, has also been dropped.
When asked about the new efforts, R.J. Reynolds spokesperson Kaelan Hollon said, “We are carefully reviewing FDA’s latest proposal for graphic warnings on cigarettes. We firmly support public awareness of the harms of smoking cigarettes, but the manner in which those messages are delivered to the public cannot run afoul of the First Amendment protections that apply to all speakers, including cigarette manufacturers.”
Warnings on U.S. cigarettes haven’t changed since 1984, when the risks of lung cancer, heart disease, emphysema, and pregnancy complications were added to the side of cigarette packs. With time, the FDA said the surgeon general’s warnings have become “virtually invisible” to consumers.
The American Lung Association, American Academy of Pediatrics, and other plaintiffs in the 2016 suit called the new proposal a “dramatic improvement” over the current situation and “long overdue” in a joint statement on Aug. 15.
Although rates have declined substantially in recent decades, about 34.3 million U.S. adults and almost 1.4 million teenagers still smoke. The habit kills about a half million Americans every year, at a health cost of more than $300 billion, the FDA said.
Comments on the proposed rule are being accepted through Oct. 15. The agency is open to suggestions for alternative text and images.
illustrating the harms of smoking, but this could be subjected to legal challenge.
Several years ago, tobacco companies filed a lawsuit, which ultimately shut down a similar proposal.
The warnings focus on lesser-known complications – including diabetes, cataracts, gangrene, stroke, bladder cancer, erectile dysfunction, and obstructive pulmonary disease – and would take up the top half of the front and back of cigarette packs, and at least the top 20% of print advertisements. Each pack and ad would be required to carry 1 of the 13 proposed warnings, according to the announcement.
The approach would be similar to, but not as aggressive as Canada’s. For years, cigarettes packs sold in Canada have included disturbing photographs of diseased lungs, rotted teeth, and dying patients. The lasting impact of such imagery has been demonstrated in the literature (for example, Am J Prev Med. 2007 Mar;32[3]:202-9).
The new proposal is the FDA’s second attempt to enact something comparable in the United States, after being directed to do so by the Tobacco Control Act of 2009.
The first effort to add strong, illustrated warnings to cigarette packs was widely backed by medical groups, but challenged in the courts by R.J. Reynolds and other tobacco companies, and blocked on appeal in 2012 as an abridgment of commercial free speech. The federal government dropped the case in 2013.
The American Lung Association and other public health groups subsequently sued the FDA in 2016 to enact the Tobacco Act mandate. Subsequently, a federal judge ordered the agency to publish a new rule by August 2019, and issue a final rule in March 2020.
This time around, the FDA “took the necessary time to get these new proposed warnings right ... based on – and within the limits of – both science and the law,” the agency said. The new images, though graphic, are less disturbing than those used in Canada and the agency’s previous proposals, which included an apparent corpse with a sternotomy. The 1-800-Quit-Now cessation hotline number, which was a sticking point in the 2012 ruling, has also been dropped.
When asked about the new efforts, R.J. Reynolds spokesperson Kaelan Hollon said, “We are carefully reviewing FDA’s latest proposal for graphic warnings on cigarettes. We firmly support public awareness of the harms of smoking cigarettes, but the manner in which those messages are delivered to the public cannot run afoul of the First Amendment protections that apply to all speakers, including cigarette manufacturers.”
Warnings on U.S. cigarettes haven’t changed since 1984, when the risks of lung cancer, heart disease, emphysema, and pregnancy complications were added to the side of cigarette packs. With time, the FDA said the surgeon general’s warnings have become “virtually invisible” to consumers.
The American Lung Association, American Academy of Pediatrics, and other plaintiffs in the 2016 suit called the new proposal a “dramatic improvement” over the current situation and “long overdue” in a joint statement on Aug. 15.
Although rates have declined substantially in recent decades, about 34.3 million U.S. adults and almost 1.4 million teenagers still smoke. The habit kills about a half million Americans every year, at a health cost of more than $300 billion, the FDA said.
Comments on the proposed rule are being accepted through Oct. 15. The agency is open to suggestions for alternative text and images.
illustrating the harms of smoking, but this could be subjected to legal challenge.
Several years ago, tobacco companies filed a lawsuit, which ultimately shut down a similar proposal.
The warnings focus on lesser-known complications – including diabetes, cataracts, gangrene, stroke, bladder cancer, erectile dysfunction, and obstructive pulmonary disease – and would take up the top half of the front and back of cigarette packs, and at least the top 20% of print advertisements. Each pack and ad would be required to carry 1 of the 13 proposed warnings, according to the announcement.
The approach would be similar to, but not as aggressive as Canada’s. For years, cigarettes packs sold in Canada have included disturbing photographs of diseased lungs, rotted teeth, and dying patients. The lasting impact of such imagery has been demonstrated in the literature (for example, Am J Prev Med. 2007 Mar;32[3]:202-9).
The new proposal is the FDA’s second attempt to enact something comparable in the United States, after being directed to do so by the Tobacco Control Act of 2009.
The first effort to add strong, illustrated warnings to cigarette packs was widely backed by medical groups, but challenged in the courts by R.J. Reynolds and other tobacco companies, and blocked on appeal in 2012 as an abridgment of commercial free speech. The federal government dropped the case in 2013.
The American Lung Association and other public health groups subsequently sued the FDA in 2016 to enact the Tobacco Act mandate. Subsequently, a federal judge ordered the agency to publish a new rule by August 2019, and issue a final rule in March 2020.
This time around, the FDA “took the necessary time to get these new proposed warnings right ... based on – and within the limits of – both science and the law,” the agency said. The new images, though graphic, are less disturbing than those used in Canada and the agency’s previous proposals, which included an apparent corpse with a sternotomy. The 1-800-Quit-Now cessation hotline number, which was a sticking point in the 2012 ruling, has also been dropped.
When asked about the new efforts, R.J. Reynolds spokesperson Kaelan Hollon said, “We are carefully reviewing FDA’s latest proposal for graphic warnings on cigarettes. We firmly support public awareness of the harms of smoking cigarettes, but the manner in which those messages are delivered to the public cannot run afoul of the First Amendment protections that apply to all speakers, including cigarette manufacturers.”
Warnings on U.S. cigarettes haven’t changed since 1984, when the risks of lung cancer, heart disease, emphysema, and pregnancy complications were added to the side of cigarette packs. With time, the FDA said the surgeon general’s warnings have become “virtually invisible” to consumers.
The American Lung Association, American Academy of Pediatrics, and other plaintiffs in the 2016 suit called the new proposal a “dramatic improvement” over the current situation and “long overdue” in a joint statement on Aug. 15.
Although rates have declined substantially in recent decades, about 34.3 million U.S. adults and almost 1.4 million teenagers still smoke. The habit kills about a half million Americans every year, at a health cost of more than $300 billion, the FDA said.
Comments on the proposed rule are being accepted through Oct. 15. The agency is open to suggestions for alternative text and images.
FDA approves drug combo to treat highly resistant TB
The U.S. Food and Drug Administration granted special approval to a new drug combo intended for the treatment of “a limited and specific population of adult patients with extensively drug resistant, treatment-intolerant or nonresponsive multidrug-resistant pulmonary” tuberculosis, according to an FDA news release.
The effectiveness of the combination treatment of pretomanid tablets with bedaquiline and linezolid was shown in a clinical study of patients with extensively drug-resistant, treatment-intolerant, or nonresponsive multidrug-resistant pulmonary tuberculosis of the lungs. Of 107 infected patients who were evaluated 6 months after the end of therapy, 95 (89%) were deemed successes, which significantly exceeded the historical success rates for treatment of extensively drug-resistant TB, the FDA reported. The trial is sponsored by the Global Alliance for TB Drug Development.
The most common adverse effects reported included peripheral neuropathy, anemia, nausea, vomiting, headache, increased liver enzymes, dyspepsia, rash, visual impairment, low blood sugar, and diarrhea, according to the release.
“Multidrug-resistant TB and extensively drug-resistant TB are public health threats due to limited treatment options. New treatments are important to meet patient national and global health needs,” stated FDA Principal Deputy Commissioner Amy Abernethy, MD, PhD, in the release. She also explained that the approval marked the second time a drug was approved under the “Limited Population Pathway for Antibacterial and Antifungal Drugs, a pathway advanced by Congress to spur development of drugs targeting infections that lack effective therapies.”
In 2016, the World Health Organization reported that there were an estimated 490,000 new cases of multidrug-resistant TB worldwide, with a smaller portion of cases of extensively drug-resistant TB, according to the release, demonstrating the need for new therapeutics.
SOURCE: U.S. Food and Drug Administration. Aug. 14, 2019. News release.
The U.S. Food and Drug Administration granted special approval to a new drug combo intended for the treatment of “a limited and specific population of adult patients with extensively drug resistant, treatment-intolerant or nonresponsive multidrug-resistant pulmonary” tuberculosis, according to an FDA news release.
The effectiveness of the combination treatment of pretomanid tablets with bedaquiline and linezolid was shown in a clinical study of patients with extensively drug-resistant, treatment-intolerant, or nonresponsive multidrug-resistant pulmonary tuberculosis of the lungs. Of 107 infected patients who were evaluated 6 months after the end of therapy, 95 (89%) were deemed successes, which significantly exceeded the historical success rates for treatment of extensively drug-resistant TB, the FDA reported. The trial is sponsored by the Global Alliance for TB Drug Development.
The most common adverse effects reported included peripheral neuropathy, anemia, nausea, vomiting, headache, increased liver enzymes, dyspepsia, rash, visual impairment, low blood sugar, and diarrhea, according to the release.
“Multidrug-resistant TB and extensively drug-resistant TB are public health threats due to limited treatment options. New treatments are important to meet patient national and global health needs,” stated FDA Principal Deputy Commissioner Amy Abernethy, MD, PhD, in the release. She also explained that the approval marked the second time a drug was approved under the “Limited Population Pathway for Antibacterial and Antifungal Drugs, a pathway advanced by Congress to spur development of drugs targeting infections that lack effective therapies.”
In 2016, the World Health Organization reported that there were an estimated 490,000 new cases of multidrug-resistant TB worldwide, with a smaller portion of cases of extensively drug-resistant TB, according to the release, demonstrating the need for new therapeutics.
SOURCE: U.S. Food and Drug Administration. Aug. 14, 2019. News release.
The U.S. Food and Drug Administration granted special approval to a new drug combo intended for the treatment of “a limited and specific population of adult patients with extensively drug resistant, treatment-intolerant or nonresponsive multidrug-resistant pulmonary” tuberculosis, according to an FDA news release.
The effectiveness of the combination treatment of pretomanid tablets with bedaquiline and linezolid was shown in a clinical study of patients with extensively drug-resistant, treatment-intolerant, or nonresponsive multidrug-resistant pulmonary tuberculosis of the lungs. Of 107 infected patients who were evaluated 6 months after the end of therapy, 95 (89%) were deemed successes, which significantly exceeded the historical success rates for treatment of extensively drug-resistant TB, the FDA reported. The trial is sponsored by the Global Alliance for TB Drug Development.
The most common adverse effects reported included peripheral neuropathy, anemia, nausea, vomiting, headache, increased liver enzymes, dyspepsia, rash, visual impairment, low blood sugar, and diarrhea, according to the release.
“Multidrug-resistant TB and extensively drug-resistant TB are public health threats due to limited treatment options. New treatments are important to meet patient national and global health needs,” stated FDA Principal Deputy Commissioner Amy Abernethy, MD, PhD, in the release. She also explained that the approval marked the second time a drug was approved under the “Limited Population Pathway for Antibacterial and Antifungal Drugs, a pathway advanced by Congress to spur development of drugs targeting infections that lack effective therapies.”
In 2016, the World Health Organization reported that there were an estimated 490,000 new cases of multidrug-resistant TB worldwide, with a smaller portion of cases of extensively drug-resistant TB, according to the release, demonstrating the need for new therapeutics.
SOURCE: U.S. Food and Drug Administration. Aug. 14, 2019. News release.
NEWS FROM THE FDA
Asthma hospitalization in kids linked with doubled migraine incidence
when compared with a similar pediatric population without asthma. The finding is based on an analysis of more than 11 million U.S. pediatric hospitalizations over the course of a decade.
Among children and adolescents aged 3-21 years who were hospitalized for asthma, migraine rates were significantly higher among girls, adolescents, and whites, compared with boys, children aged 12 years or younger, and nonwhites, respectively, in a trio of adjusted analyses, Riddhiben S. Patel, MD, and associates reported in a poster at the annual meeting of the American Headache Society.
“Our hope is that, by establishing an association between childhood asthma and migraine, [these children] may be more easily screened for, diagnosed, and treated early by providers,” wrote Dr. Patel, a pediatric neurologist and headache specialist at the University of Mississippi, Jackson, and associates.
Their analysis used administrative billing data collected by the Kids’ Inpatient Database, maintained by the U.S. Healthcare Cost and Utilization Project. The project includes a representative national sample of about 3 million pediatric hospital discharges every 3 years. The study used data from 11,483,103 hospitalizations of children and adolescents aged 3-21 years during 2003, 2006, 2009, and 2012, and found an overall hospitalization rate of 0.8% billed for migraine. For patients also hospitalized with a billing code for asthma, the rate jumped to 1.36%, a 120% statistically significant relative increase in migraine hospitalizations after adjustment for baseline demographic differences, the researchers said.
Among the children and adolescents hospitalized with an asthma billing code, the relative rate of also having a billing code for migraine after adjustment was a statistically significant 80% higher in girls, compared with boys, a statistically significant 7% higher in adolescents, compared with children 12 years or younger, and was significantly reduced by a relative 45% rate in nonwhites, compared with whites.
The mechanisms behind these associations are not known, but could involve mast-cell degranulation, autonomic dysfunction, or shared genetic or environmental etiologic factors, the authors said.
Dr. Patel reported no relevant disclosures.
SOURCE: Patel RS et al. Headache. 2019 June;59[S1]:1-208, Abstract P78.
when compared with a similar pediatric population without asthma. The finding is based on an analysis of more than 11 million U.S. pediatric hospitalizations over the course of a decade.
Among children and adolescents aged 3-21 years who were hospitalized for asthma, migraine rates were significantly higher among girls, adolescents, and whites, compared with boys, children aged 12 years or younger, and nonwhites, respectively, in a trio of adjusted analyses, Riddhiben S. Patel, MD, and associates reported in a poster at the annual meeting of the American Headache Society.
“Our hope is that, by establishing an association between childhood asthma and migraine, [these children] may be more easily screened for, diagnosed, and treated early by providers,” wrote Dr. Patel, a pediatric neurologist and headache specialist at the University of Mississippi, Jackson, and associates.
Their analysis used administrative billing data collected by the Kids’ Inpatient Database, maintained by the U.S. Healthcare Cost and Utilization Project. The project includes a representative national sample of about 3 million pediatric hospital discharges every 3 years. The study used data from 11,483,103 hospitalizations of children and adolescents aged 3-21 years during 2003, 2006, 2009, and 2012, and found an overall hospitalization rate of 0.8% billed for migraine. For patients also hospitalized with a billing code for asthma, the rate jumped to 1.36%, a 120% statistically significant relative increase in migraine hospitalizations after adjustment for baseline demographic differences, the researchers said.
Among the children and adolescents hospitalized with an asthma billing code, the relative rate of also having a billing code for migraine after adjustment was a statistically significant 80% higher in girls, compared with boys, a statistically significant 7% higher in adolescents, compared with children 12 years or younger, and was significantly reduced by a relative 45% rate in nonwhites, compared with whites.
The mechanisms behind these associations are not known, but could involve mast-cell degranulation, autonomic dysfunction, or shared genetic or environmental etiologic factors, the authors said.
Dr. Patel reported no relevant disclosures.
SOURCE: Patel RS et al. Headache. 2019 June;59[S1]:1-208, Abstract P78.
when compared with a similar pediatric population without asthma. The finding is based on an analysis of more than 11 million U.S. pediatric hospitalizations over the course of a decade.
Among children and adolescents aged 3-21 years who were hospitalized for asthma, migraine rates were significantly higher among girls, adolescents, and whites, compared with boys, children aged 12 years or younger, and nonwhites, respectively, in a trio of adjusted analyses, Riddhiben S. Patel, MD, and associates reported in a poster at the annual meeting of the American Headache Society.
“Our hope is that, by establishing an association between childhood asthma and migraine, [these children] may be more easily screened for, diagnosed, and treated early by providers,” wrote Dr. Patel, a pediatric neurologist and headache specialist at the University of Mississippi, Jackson, and associates.
Their analysis used administrative billing data collected by the Kids’ Inpatient Database, maintained by the U.S. Healthcare Cost and Utilization Project. The project includes a representative national sample of about 3 million pediatric hospital discharges every 3 years. The study used data from 11,483,103 hospitalizations of children and adolescents aged 3-21 years during 2003, 2006, 2009, and 2012, and found an overall hospitalization rate of 0.8% billed for migraine. For patients also hospitalized with a billing code for asthma, the rate jumped to 1.36%, a 120% statistically significant relative increase in migraine hospitalizations after adjustment for baseline demographic differences, the researchers said.
Among the children and adolescents hospitalized with an asthma billing code, the relative rate of also having a billing code for migraine after adjustment was a statistically significant 80% higher in girls, compared with boys, a statistically significant 7% higher in adolescents, compared with children 12 years or younger, and was significantly reduced by a relative 45% rate in nonwhites, compared with whites.
The mechanisms behind these associations are not known, but could involve mast-cell degranulation, autonomic dysfunction, or shared genetic or environmental etiologic factors, the authors said.
Dr. Patel reported no relevant disclosures.
SOURCE: Patel RS et al. Headache. 2019 June;59[S1]:1-208, Abstract P78.
REPORTING FROM AHS 2019
Study: Cardiac biomarkers predicted CV events in CAP
in a recently conducted study.
These biomarkers were also used to predict late cardiovascular events at day 30 of community-acquired pneumonia (CAP) in patients who did not have a history of cardiovascular disease, according to Rosario Menéndez, MD, from the Hospital Universitario y Politécnico La Fe and Instituto de Investigación Sanitaria La Fe in Valencia, Spain, and colleagues.
“Some patients have still high levels of inflammatory and cardiac biomarkers at 30 days, when they are usually referred to primary care without receiving any specific additional recommendations,” Dr. Menéndez and colleagues wrote in CHEST. “Our results suggest that a change in usual practice is needed to reduce current and further cardiovascular CAP complications.”
Dr. Menéndez and colleagues prospectively followed 730 patients for 1 year who were hospitalized for CAP, measuring the cardiac biomarkers proadrenomedullin (proADM), pro b-type natriuretic peptide (proBNP), proendothelin-1, and troponin T, and the inflammatory biomarkers interleukin 6 (IL-6), C-reactive protein (CRP), and procalcitonin (PCT). The researchers also collected data on age, gender, smoking status, and vaccination history, as well as whether patients had any cardiac, renal, pulmonary, neurological or diabetes-related comorbidities.
Overall, 95 patients experienced early cardiovascular events, 67 patients had long-term cardiovascular events, and 20 patients experienced both early and late events. In hospital, the mortality rate was 4.7%; the 30-day mortality rate was 5.3%, and the 1-year mortality rate was 9.9%.
With regard to biomarkers, patients who experienced both early and late cardiovascular events had significantly higher initial levels of proADM, proendothelin-1, troponin, proBNP, and IL-6. Patients who experienced later events had consistent levels of these biomarkers until day 30, except for a decrease at day 4 or day 5.
After adjustment for age, sepsis, previous cardiac disease, and a partial pressure of oxygen in the alveoli to fractional inspired oxygen ratio (PaO2/FiO2) of less than 250mm Hg, cardiac biomarkers proendothelin-1 (odds ratio, 2.25; 95% confidence interval, 1.34-3.79), proADM (OR, 2.53; 95% CI, 1.53-4.20), proBNP (OR, 2.67; 95% CI, 1.59-4.49), and troponin T (OR, 2.70; 95% CI, 1.62-4.49) significantly predicted early cardiovascular events, while proendothelin-1 (OR, 3.13; 95% CI, 1.41-7.80), proADM (2.29; 95% CI, 1.01-5.19) and proBNP (OR, 2.34; 95% CI, 1.01-5.56) significantly predicted late cardiovascular events. For day 30 results, when researchers added IL-6 levels to proendothelin-1, the odds ratio for late events increased to 3.53, and when they added IL-6 levels to proADM, the odds ratio increased to 2.80.
Researchers noted the limitations of the study included that they did not analyze cardiac biomarkers to predict specific cardiovascular events, did not identify the cause for mortality at 1 year in most patients, and did not include a control group.
This study was supported in part by funding from Instituto de Salud Carlos III, Sociedad Española de Neumología y Cirugía Torácica, and the Center for Biomedical Research Network in Respiratory Diseases. The authors reported no relevant conflicts of interest.
SOURCE: Menéndez R et al. Chest. 2019 Aug 2. doi: 10.1016/j.chest.2019.06.040.
in a recently conducted study.
These biomarkers were also used to predict late cardiovascular events at day 30 of community-acquired pneumonia (CAP) in patients who did not have a history of cardiovascular disease, according to Rosario Menéndez, MD, from the Hospital Universitario y Politécnico La Fe and Instituto de Investigación Sanitaria La Fe in Valencia, Spain, and colleagues.
“Some patients have still high levels of inflammatory and cardiac biomarkers at 30 days, when they are usually referred to primary care without receiving any specific additional recommendations,” Dr. Menéndez and colleagues wrote in CHEST. “Our results suggest that a change in usual practice is needed to reduce current and further cardiovascular CAP complications.”
Dr. Menéndez and colleagues prospectively followed 730 patients for 1 year who were hospitalized for CAP, measuring the cardiac biomarkers proadrenomedullin (proADM), pro b-type natriuretic peptide (proBNP), proendothelin-1, and troponin T, and the inflammatory biomarkers interleukin 6 (IL-6), C-reactive protein (CRP), and procalcitonin (PCT). The researchers also collected data on age, gender, smoking status, and vaccination history, as well as whether patients had any cardiac, renal, pulmonary, neurological or diabetes-related comorbidities.
Overall, 95 patients experienced early cardiovascular events, 67 patients had long-term cardiovascular events, and 20 patients experienced both early and late events. In hospital, the mortality rate was 4.7%; the 30-day mortality rate was 5.3%, and the 1-year mortality rate was 9.9%.
With regard to biomarkers, patients who experienced both early and late cardiovascular events had significantly higher initial levels of proADM, proendothelin-1, troponin, proBNP, and IL-6. Patients who experienced later events had consistent levels of these biomarkers until day 30, except for a decrease at day 4 or day 5.
After adjustment for age, sepsis, previous cardiac disease, and a partial pressure of oxygen in the alveoli to fractional inspired oxygen ratio (PaO2/FiO2) of less than 250mm Hg, cardiac biomarkers proendothelin-1 (odds ratio, 2.25; 95% confidence interval, 1.34-3.79), proADM (OR, 2.53; 95% CI, 1.53-4.20), proBNP (OR, 2.67; 95% CI, 1.59-4.49), and troponin T (OR, 2.70; 95% CI, 1.62-4.49) significantly predicted early cardiovascular events, while proendothelin-1 (OR, 3.13; 95% CI, 1.41-7.80), proADM (2.29; 95% CI, 1.01-5.19) and proBNP (OR, 2.34; 95% CI, 1.01-5.56) significantly predicted late cardiovascular events. For day 30 results, when researchers added IL-6 levels to proendothelin-1, the odds ratio for late events increased to 3.53, and when they added IL-6 levels to proADM, the odds ratio increased to 2.80.
Researchers noted the limitations of the study included that they did not analyze cardiac biomarkers to predict specific cardiovascular events, did not identify the cause for mortality at 1 year in most patients, and did not include a control group.
This study was supported in part by funding from Instituto de Salud Carlos III, Sociedad Española de Neumología y Cirugía Torácica, and the Center for Biomedical Research Network in Respiratory Diseases. The authors reported no relevant conflicts of interest.
SOURCE: Menéndez R et al. Chest. 2019 Aug 2. doi: 10.1016/j.chest.2019.06.040.
in a recently conducted study.
These biomarkers were also used to predict late cardiovascular events at day 30 of community-acquired pneumonia (CAP) in patients who did not have a history of cardiovascular disease, according to Rosario Menéndez, MD, from the Hospital Universitario y Politécnico La Fe and Instituto de Investigación Sanitaria La Fe in Valencia, Spain, and colleagues.
“Some patients have still high levels of inflammatory and cardiac biomarkers at 30 days, when they are usually referred to primary care without receiving any specific additional recommendations,” Dr. Menéndez and colleagues wrote in CHEST. “Our results suggest that a change in usual practice is needed to reduce current and further cardiovascular CAP complications.”
Dr. Menéndez and colleagues prospectively followed 730 patients for 1 year who were hospitalized for CAP, measuring the cardiac biomarkers proadrenomedullin (proADM), pro b-type natriuretic peptide (proBNP), proendothelin-1, and troponin T, and the inflammatory biomarkers interleukin 6 (IL-6), C-reactive protein (CRP), and procalcitonin (PCT). The researchers also collected data on age, gender, smoking status, and vaccination history, as well as whether patients had any cardiac, renal, pulmonary, neurological or diabetes-related comorbidities.
Overall, 95 patients experienced early cardiovascular events, 67 patients had long-term cardiovascular events, and 20 patients experienced both early and late events. In hospital, the mortality rate was 4.7%; the 30-day mortality rate was 5.3%, and the 1-year mortality rate was 9.9%.
With regard to biomarkers, patients who experienced both early and late cardiovascular events had significantly higher initial levels of proADM, proendothelin-1, troponin, proBNP, and IL-6. Patients who experienced later events had consistent levels of these biomarkers until day 30, except for a decrease at day 4 or day 5.
After adjustment for age, sepsis, previous cardiac disease, and a partial pressure of oxygen in the alveoli to fractional inspired oxygen ratio (PaO2/FiO2) of less than 250mm Hg, cardiac biomarkers proendothelin-1 (odds ratio, 2.25; 95% confidence interval, 1.34-3.79), proADM (OR, 2.53; 95% CI, 1.53-4.20), proBNP (OR, 2.67; 95% CI, 1.59-4.49), and troponin T (OR, 2.70; 95% CI, 1.62-4.49) significantly predicted early cardiovascular events, while proendothelin-1 (OR, 3.13; 95% CI, 1.41-7.80), proADM (2.29; 95% CI, 1.01-5.19) and proBNP (OR, 2.34; 95% CI, 1.01-5.56) significantly predicted late cardiovascular events. For day 30 results, when researchers added IL-6 levels to proendothelin-1, the odds ratio for late events increased to 3.53, and when they added IL-6 levels to proADM, the odds ratio increased to 2.80.
Researchers noted the limitations of the study included that they did not analyze cardiac biomarkers to predict specific cardiovascular events, did not identify the cause for mortality at 1 year in most patients, and did not include a control group.
This study was supported in part by funding from Instituto de Salud Carlos III, Sociedad Española de Neumología y Cirugía Torácica, and the Center for Biomedical Research Network in Respiratory Diseases. The authors reported no relevant conflicts of interest.
SOURCE: Menéndez R et al. Chest. 2019 Aug 2. doi: 10.1016/j.chest.2019.06.040.
FROM CHEST
Exposure to outdoor air pollutants linked to increased emphysema
Long-term exposure to ambient air pollutants was significantly associated with increases in emphysema and decreases in lung function, according to a diverse cohort study of six U.S. metropolitan areas.
“These associations in a community-based population demonstrate novel evidence that air pollution contributes to worsening lung health,” wrote Meng Wang, PhD, of the University of Washington, Seattle, and coauthors. The study was published in JAMA.
To determine whether exposure to outdoor air pollutants was associated with emphysema progression and change in lung function, the Multiethnic Study of Atherosclerosis (MESA) assessed 6,860 participants from six areas: Winston-Salem, N.C.; New York City; Baltimore; St. Paul, Minn.; Chicago; and Los Angeles. Percent emphysema was calculated based on all available CT scans; lung function was assessed via spirometry.
Spatiotemporal exposure models were developed for ozone, fine particulate matter less than 2.5 mcm in aerodynamic diameter, and oxides of nitrogen in each area based on Environmental Protection Agency measurements and the study’s cohort-specific monitoring. Annual mean concentrations of fine particulate matter and nitrogen decreased during follow-up, while ozone concentrations did not.
All participants underwent a cardiac CT scan at baseline, and 5,780 had at least one follow-up CT scan over a median period of 10 years. Ambient concentrations of ozone, fine particulate matter, nitrogen, and black carbon at baseline were significantly associated with greater increases in percent emphysema per 10 years, as were concentrations of zone and nitrogen during follow-up, reported Dr. Wang, formerly with the State University of New York at Buffalo.
Of the 3,636 participants who had at least one spirometric assessment, there was a mean decline in forced expiratory volume in 1 second (FEV1) of 309 mL (95% CI, 299-319 mL) and in forced vital capacity of 331 mL (95% CI, 317-345 mL) over 10 years. Ambient concentrations of ozone were significantly associated with a decline in FEV1, both at baseline and during follow-up.
The coauthors acknowledged their study’s limitations, including that general outdoor air pollution concentrations might not reflect individual exposure or concentrations indoors, where people spend most of their time. In addition, percent emphysema was only measured in the lower two-thirds of the lung, though they noted that “percent emphysema measured in the lower two-thirds of the lung correlates well with full-lung percent emphysema in this cohort and a cohort of smokers.”
This article was developed by the EPA and the University of Washington Center for Clean Air Research. MESA was funded by the National Institutes of Health and the National Heart, Lung, and Blood Institute, and supported by the National Institute of Environmental Health Sciences. The authors reported numerous conflicts of interest, including receiving grants and fees from the University of Washington, the EPA, the NIH, and various other pharmaceutical companies, foundations, and governmental entities.
SOURCE: Wang M et al. JAMA. 2019 Aug 13. doi: 10.1001/jama.2019.10255
Long-term exposure to ambient air pollutants was significantly associated with increases in emphysema and decreases in lung function, according to a diverse cohort study of six U.S. metropolitan areas.
“These associations in a community-based population demonstrate novel evidence that air pollution contributes to worsening lung health,” wrote Meng Wang, PhD, of the University of Washington, Seattle, and coauthors. The study was published in JAMA.
To determine whether exposure to outdoor air pollutants was associated with emphysema progression and change in lung function, the Multiethnic Study of Atherosclerosis (MESA) assessed 6,860 participants from six areas: Winston-Salem, N.C.; New York City; Baltimore; St. Paul, Minn.; Chicago; and Los Angeles. Percent emphysema was calculated based on all available CT scans; lung function was assessed via spirometry.
Spatiotemporal exposure models were developed for ozone, fine particulate matter less than 2.5 mcm in aerodynamic diameter, and oxides of nitrogen in each area based on Environmental Protection Agency measurements and the study’s cohort-specific monitoring. Annual mean concentrations of fine particulate matter and nitrogen decreased during follow-up, while ozone concentrations did not.
All participants underwent a cardiac CT scan at baseline, and 5,780 had at least one follow-up CT scan over a median period of 10 years. Ambient concentrations of ozone, fine particulate matter, nitrogen, and black carbon at baseline were significantly associated with greater increases in percent emphysema per 10 years, as were concentrations of zone and nitrogen during follow-up, reported Dr. Wang, formerly with the State University of New York at Buffalo.
Of the 3,636 participants who had at least one spirometric assessment, there was a mean decline in forced expiratory volume in 1 second (FEV1) of 309 mL (95% CI, 299-319 mL) and in forced vital capacity of 331 mL (95% CI, 317-345 mL) over 10 years. Ambient concentrations of ozone were significantly associated with a decline in FEV1, both at baseline and during follow-up.
The coauthors acknowledged their study’s limitations, including that general outdoor air pollution concentrations might not reflect individual exposure or concentrations indoors, where people spend most of their time. In addition, percent emphysema was only measured in the lower two-thirds of the lung, though they noted that “percent emphysema measured in the lower two-thirds of the lung correlates well with full-lung percent emphysema in this cohort and a cohort of smokers.”
This article was developed by the EPA and the University of Washington Center for Clean Air Research. MESA was funded by the National Institutes of Health and the National Heart, Lung, and Blood Institute, and supported by the National Institute of Environmental Health Sciences. The authors reported numerous conflicts of interest, including receiving grants and fees from the University of Washington, the EPA, the NIH, and various other pharmaceutical companies, foundations, and governmental entities.
SOURCE: Wang M et al. JAMA. 2019 Aug 13. doi: 10.1001/jama.2019.10255
Long-term exposure to ambient air pollutants was significantly associated with increases in emphysema and decreases in lung function, according to a diverse cohort study of six U.S. metropolitan areas.
“These associations in a community-based population demonstrate novel evidence that air pollution contributes to worsening lung health,” wrote Meng Wang, PhD, of the University of Washington, Seattle, and coauthors. The study was published in JAMA.
To determine whether exposure to outdoor air pollutants was associated with emphysema progression and change in lung function, the Multiethnic Study of Atherosclerosis (MESA) assessed 6,860 participants from six areas: Winston-Salem, N.C.; New York City; Baltimore; St. Paul, Minn.; Chicago; and Los Angeles. Percent emphysema was calculated based on all available CT scans; lung function was assessed via spirometry.
Spatiotemporal exposure models were developed for ozone, fine particulate matter less than 2.5 mcm in aerodynamic diameter, and oxides of nitrogen in each area based on Environmental Protection Agency measurements and the study’s cohort-specific monitoring. Annual mean concentrations of fine particulate matter and nitrogen decreased during follow-up, while ozone concentrations did not.
All participants underwent a cardiac CT scan at baseline, and 5,780 had at least one follow-up CT scan over a median period of 10 years. Ambient concentrations of ozone, fine particulate matter, nitrogen, and black carbon at baseline were significantly associated with greater increases in percent emphysema per 10 years, as were concentrations of zone and nitrogen during follow-up, reported Dr. Wang, formerly with the State University of New York at Buffalo.
Of the 3,636 participants who had at least one spirometric assessment, there was a mean decline in forced expiratory volume in 1 second (FEV1) of 309 mL (95% CI, 299-319 mL) and in forced vital capacity of 331 mL (95% CI, 317-345 mL) over 10 years. Ambient concentrations of ozone were significantly associated with a decline in FEV1, both at baseline and during follow-up.
The coauthors acknowledged their study’s limitations, including that general outdoor air pollution concentrations might not reflect individual exposure or concentrations indoors, where people spend most of their time. In addition, percent emphysema was only measured in the lower two-thirds of the lung, though they noted that “percent emphysema measured in the lower two-thirds of the lung correlates well with full-lung percent emphysema in this cohort and a cohort of smokers.”
This article was developed by the EPA and the University of Washington Center for Clean Air Research. MESA was funded by the National Institutes of Health and the National Heart, Lung, and Blood Institute, and supported by the National Institute of Environmental Health Sciences. The authors reported numerous conflicts of interest, including receiving grants and fees from the University of Washington, the EPA, the NIH, and various other pharmaceutical companies, foundations, and governmental entities.
SOURCE: Wang M et al. JAMA. 2019 Aug 13. doi: 10.1001/jama.2019.10255
FROM JAMA
Procalcitonin advocated to help rule out bacterial infections
SEATTLE – Procalcitonin, a marker of bacterial infection, rises and peaks sooner than C-reactive protein (CRP), and is especially useful to help rule out invasive bacterial infections in young infants and pediatric community acquired pneumonia due to typical bacteria, according to a presentation at the 2019 Pediatric Hospital Medicine Conference.
It’s “excellent for identifying low risk patients” and has the potential to decrease lumbar punctures and antibiotic exposure, but “the specificity isn’t great,” so there’s the potential for false positives, said Russell McCulloh, MD, a pediatric infectious disease specialist at the University of Nebraska Medical Center, Omaha.
There was great interest in procalcitonin at the meeting; the presentation room was packed, with a line out the door. It’s used mostly in Europe at this point. Testing is available in many U.S. hospitals, but a large majority of audience members, when polled, said they don’t currently use it in clinical practice, and that it’s not a part of diagnostic algorithms at their institutions.
Levels of procalcitonin, a calcitonin precursor normally produced by the thyroid, are low or undetectable in healthy people, but inflammation, be it from infectious or noninfectious causes, triggers production by parenchymal cells throughout the body.
Levels began to rise as early as 2.5 hours after healthy subjects in one study were injected with bacterial endotoxins, and peaked as early as 6 hours; CRP, in contrast, started to rise after 12 hours, and peaked at 30 hours. Procalcitonin levels also seem to correlate with bacterial load and severity of infection, said Nivedita Srinivas, MD, a pediatric infectious disease specialist at Stanford (Calif.) University (J Pediatr Intensive Care. 2016 Dec;5[4]:162-71).
Due to time, the presenters focused their talk on community acquired pneumonia (CAP) and invasive bacterial infections (IBI) in young infants, meaning essentially bacteremia and meningitis.
Different studies use different cutoffs, but a procalcitonin below, for instance, 0.5 ng/mL is “certainly more sensitive [for IBI] than any single biomarker we currently use,” including CRP, white blood cells, and absolute neutrophil count (ANC). “If it’s negative, you’re really confident it’s negative,” but “a positive test does not necessarily indicate the presence of IBI,” Dr. McCulloh said (Pediatrics. 2012 Nov;130[5]:815-22).
“Procalcitonin works really well as part of a validated step-wise rule” that includes, for instance, CRP and ANC; “I think that’s where its utility is. On its own, it is not a substitute for you examining the patient and doing your basic risk stratification, but it may enhance your decision making incrementally above what we currently have,” he said.
Meanwhile, in a study of 532 children a median age of 2.4 years with radiographically confirmed CAP, procalcitonin levels were a median of 6.1 ng/mL in children whose pneumonia was caused by Streptococcus pneumoniae or other typical bacteria, and no child infected with typical bacteria had a level under 0.1 ng/mL. Below that level, “you can be very sure you do not have typical bacteria pneumonia,” said Marie Wang, MD, also a pediatric infectious disease specialist at Stanford (J Pediatric Infect Dis Soc. 2018 Feb 19;7[1]:46-53).
As procalcitonin levels went up, the likelihood of having bacterial pneumonia increased; at 2 ng/mL, 26% of subjects were infected with typical bacteria, “but even in that group, 58% still had viral infection, so you are still detecting a lot of viral” disease, she said.
Prolcalcitonin-guided therapy – antibiotics until patients fall below a level of 0.25 ng/ml, for instance – has also been associated with decreased antibiotic exposure (Respir Med. 2011 Dec;105[12]:1939-45).
The speakers had no disclosures. The meeting was sponsored by the Society of Hospital Medicine, the American Academy of Pediatrics, and the Academic Pediatric Association.
SEATTLE – Procalcitonin, a marker of bacterial infection, rises and peaks sooner than C-reactive protein (CRP), and is especially useful to help rule out invasive bacterial infections in young infants and pediatric community acquired pneumonia due to typical bacteria, according to a presentation at the 2019 Pediatric Hospital Medicine Conference.
It’s “excellent for identifying low risk patients” and has the potential to decrease lumbar punctures and antibiotic exposure, but “the specificity isn’t great,” so there’s the potential for false positives, said Russell McCulloh, MD, a pediatric infectious disease specialist at the University of Nebraska Medical Center, Omaha.
There was great interest in procalcitonin at the meeting; the presentation room was packed, with a line out the door. It’s used mostly in Europe at this point. Testing is available in many U.S. hospitals, but a large majority of audience members, when polled, said they don’t currently use it in clinical practice, and that it’s not a part of diagnostic algorithms at their institutions.
Levels of procalcitonin, a calcitonin precursor normally produced by the thyroid, are low or undetectable in healthy people, but inflammation, be it from infectious or noninfectious causes, triggers production by parenchymal cells throughout the body.
Levels began to rise as early as 2.5 hours after healthy subjects in one study were injected with bacterial endotoxins, and peaked as early as 6 hours; CRP, in contrast, started to rise after 12 hours, and peaked at 30 hours. Procalcitonin levels also seem to correlate with bacterial load and severity of infection, said Nivedita Srinivas, MD, a pediatric infectious disease specialist at Stanford (Calif.) University (J Pediatr Intensive Care. 2016 Dec;5[4]:162-71).
Due to time, the presenters focused their talk on community acquired pneumonia (CAP) and invasive bacterial infections (IBI) in young infants, meaning essentially bacteremia and meningitis.
Different studies use different cutoffs, but a procalcitonin below, for instance, 0.5 ng/mL is “certainly more sensitive [for IBI] than any single biomarker we currently use,” including CRP, white blood cells, and absolute neutrophil count (ANC). “If it’s negative, you’re really confident it’s negative,” but “a positive test does not necessarily indicate the presence of IBI,” Dr. McCulloh said (Pediatrics. 2012 Nov;130[5]:815-22).
“Procalcitonin works really well as part of a validated step-wise rule” that includes, for instance, CRP and ANC; “I think that’s where its utility is. On its own, it is not a substitute for you examining the patient and doing your basic risk stratification, but it may enhance your decision making incrementally above what we currently have,” he said.
Meanwhile, in a study of 532 children a median age of 2.4 years with radiographically confirmed CAP, procalcitonin levels were a median of 6.1 ng/mL in children whose pneumonia was caused by Streptococcus pneumoniae or other typical bacteria, and no child infected with typical bacteria had a level under 0.1 ng/mL. Below that level, “you can be very sure you do not have typical bacteria pneumonia,” said Marie Wang, MD, also a pediatric infectious disease specialist at Stanford (J Pediatric Infect Dis Soc. 2018 Feb 19;7[1]:46-53).
As procalcitonin levels went up, the likelihood of having bacterial pneumonia increased; at 2 ng/mL, 26% of subjects were infected with typical bacteria, “but even in that group, 58% still had viral infection, so you are still detecting a lot of viral” disease, she said.
Prolcalcitonin-guided therapy – antibiotics until patients fall below a level of 0.25 ng/ml, for instance – has also been associated with decreased antibiotic exposure (Respir Med. 2011 Dec;105[12]:1939-45).
The speakers had no disclosures. The meeting was sponsored by the Society of Hospital Medicine, the American Academy of Pediatrics, and the Academic Pediatric Association.
SEATTLE – Procalcitonin, a marker of bacterial infection, rises and peaks sooner than C-reactive protein (CRP), and is especially useful to help rule out invasive bacterial infections in young infants and pediatric community acquired pneumonia due to typical bacteria, according to a presentation at the 2019 Pediatric Hospital Medicine Conference.
It’s “excellent for identifying low risk patients” and has the potential to decrease lumbar punctures and antibiotic exposure, but “the specificity isn’t great,” so there’s the potential for false positives, said Russell McCulloh, MD, a pediatric infectious disease specialist at the University of Nebraska Medical Center, Omaha.
There was great interest in procalcitonin at the meeting; the presentation room was packed, with a line out the door. It’s used mostly in Europe at this point. Testing is available in many U.S. hospitals, but a large majority of audience members, when polled, said they don’t currently use it in clinical practice, and that it’s not a part of diagnostic algorithms at their institutions.
Levels of procalcitonin, a calcitonin precursor normally produced by the thyroid, are low or undetectable in healthy people, but inflammation, be it from infectious or noninfectious causes, triggers production by parenchymal cells throughout the body.
Levels began to rise as early as 2.5 hours after healthy subjects in one study were injected with bacterial endotoxins, and peaked as early as 6 hours; CRP, in contrast, started to rise after 12 hours, and peaked at 30 hours. Procalcitonin levels also seem to correlate with bacterial load and severity of infection, said Nivedita Srinivas, MD, a pediatric infectious disease specialist at Stanford (Calif.) University (J Pediatr Intensive Care. 2016 Dec;5[4]:162-71).
Due to time, the presenters focused their talk on community acquired pneumonia (CAP) and invasive bacterial infections (IBI) in young infants, meaning essentially bacteremia and meningitis.
Different studies use different cutoffs, but a procalcitonin below, for instance, 0.5 ng/mL is “certainly more sensitive [for IBI] than any single biomarker we currently use,” including CRP, white blood cells, and absolute neutrophil count (ANC). “If it’s negative, you’re really confident it’s negative,” but “a positive test does not necessarily indicate the presence of IBI,” Dr. McCulloh said (Pediatrics. 2012 Nov;130[5]:815-22).
“Procalcitonin works really well as part of a validated step-wise rule” that includes, for instance, CRP and ANC; “I think that’s where its utility is. On its own, it is not a substitute for you examining the patient and doing your basic risk stratification, but it may enhance your decision making incrementally above what we currently have,” he said.
Meanwhile, in a study of 532 children a median age of 2.4 years with radiographically confirmed CAP, procalcitonin levels were a median of 6.1 ng/mL in children whose pneumonia was caused by Streptococcus pneumoniae or other typical bacteria, and no child infected with typical bacteria had a level under 0.1 ng/mL. Below that level, “you can be very sure you do not have typical bacteria pneumonia,” said Marie Wang, MD, also a pediatric infectious disease specialist at Stanford (J Pediatric Infect Dis Soc. 2018 Feb 19;7[1]:46-53).
As procalcitonin levels went up, the likelihood of having bacterial pneumonia increased; at 2 ng/mL, 26% of subjects were infected with typical bacteria, “but even in that group, 58% still had viral infection, so you are still detecting a lot of viral” disease, she said.
Prolcalcitonin-guided therapy – antibiotics until patients fall below a level of 0.25 ng/ml, for instance – has also been associated with decreased antibiotic exposure (Respir Med. 2011 Dec;105[12]:1939-45).
The speakers had no disclosures. The meeting was sponsored by the Society of Hospital Medicine, the American Academy of Pediatrics, and the Academic Pediatric Association.
EXPERT ANALYSIS FROM PHM 2019