User login
M. Alexander Otto began his reporting career early in 1999 covering the pharmaceutical industry for a national pharmacists' magazine and freelancing for the Washington Post and other newspapers. He then joined BNA, now part of Bloomberg News, covering health law and the protection of people and animals in medical research. Alex next worked for the McClatchy Company. Based on his work, Alex won a year-long Knight Science Journalism Fellowship to MIT in 2008-2009. He joined the company shortly thereafter. Alex has a newspaper journalism degree from Syracuse (N.Y.) University and a master's degree in medical science -- a physician assistant degree -- from George Washington University. Alex is based in Seattle.
Optimal MPE management requires early pulmonology referral
LOS ANGELES – About half of patients with symptomatic malignant pleural effusions at McGill University Health Centre in Montreal had unnecessary procedures and hospital admissions before definitive treatment with chemical pleurodesis or indwelling pleural catheters, according to researchers.
Instead of chest taps to relieve symptoms followed by referrals for definitive treatment, some patients got chest tubes – without pleurodesis – after presenting to the emergency department and being referred to radiology; they were then admitted to the hospital for a few days while the tubes were in place. In short, cancer patients were wasting what time they had left on medical care they didn’t need, and incurring unnecessary costs, said lead investigator Benjamin Shieh, MD, formerly at McGill but now an interventional pulmonology fellow at the University of Calgary. 
McGill is a tertiary care center able to perform both definitive procedures, so “we should be a center of excellence. I imagine there are similar situations” at other hospitals, especially those without the resources of McGill, Dr. Shieh said at the annual meeting of the American College of Chest Physicians.
McGill has taken several steps to address the problem, including early ED referral to the pulmonology service and discouraging radiology from placing chest tubes for malignant pleural effusions (MPE). “I think we can avoid a big proportion of hospitalizations for MPE, and certainly a proportion of repeat [ED] visits,” said senior author Anne Gonzalez, MD, an attending pulmonologist at McGill.
The investigators looked into the issue after noting that a lot of their MPE cases had been hospitalized with chest tubes. They reviewed 72 symptomatic MPE cases in 69 patients treated in 2014 and 2015. Management was ideal in 36 cases (50%), meaning that, prior to definitive treatment, patients had no more than two pleural taps for symptom relief, no more than one ED visit, no chest tubes without pleurodesis, and no hospitalizations. “We thought this would be reasonable to try to achieve for MPE,” since there’s no definition of ideal management, Dr. Shieh said.
Nonideal patients had a mean of 2.5 pleural procedures – almost twice the number in the ideal group – before definitive palliation, with no respiratory consult beforehand. Chest tubes were placed in 27 cases (38%) for an average of 3.7 days; 28 cases (39%) were hospitalized. Nonideal patients were far more likely to present first to the ED, and ED presentations were more likely to get chest tubes and be admitted. All the cases were eventually treated definitively, 68 with indwelling pleural catheters and 4 by thoracoscopic talc insufflation. Time from initial presentation to definitive palliation was about 1 month in both groups. The investigators didn’t consider rate of effusion recurrence, which might help explain why the ideal group wasn’t treated sooner; they might not have needed it. The higher number of ED visits in the nonideal group suggests that they may have had quicker recurrences, and should have been treated sooner, Dr. Gonzalez said.
The patients were 70 years old, on average, and about 60% were women. Lung and breast were the most common cancers.
There was no industry funding for the work, and the investigators had no disclosures.
LOS ANGELES – About half of patients with symptomatic malignant pleural effusions at McGill University Health Centre in Montreal had unnecessary procedures and hospital admissions before definitive treatment with chemical pleurodesis or indwelling pleural catheters, according to researchers.
Instead of chest taps to relieve symptoms followed by referrals for definitive treatment, some patients got chest tubes – without pleurodesis – after presenting to the emergency department and being referred to radiology; they were then admitted to the hospital for a few days while the tubes were in place. In short, cancer patients were wasting what time they had left on medical care they didn’t need, and incurring unnecessary costs, said lead investigator Benjamin Shieh, MD, formerly at McGill but now an interventional pulmonology fellow at the University of Calgary.
McGill is a tertiary care center able to perform both definitive procedures, so “we should be a center of excellence. I imagine there are similar situations” at other hospitals, especially those without the resources of McGill, Dr. Shieh said at the annual meeting of the American College of Chest Physicians.
McGill has taken several steps to address the problem, including early ED referral to the pulmonology service and discouraging radiology from placing chest tubes for malignant pleural effusions (MPE). “I think we can avoid a big proportion of hospitalizations for MPE, and certainly a proportion of repeat [ED] visits,” said senior author Anne Gonzalez, MD, an attending pulmonologist at McGill.
The investigators looked into the issue after noting that a lot of their MPE cases had been hospitalized with chest tubes. They reviewed 72 symptomatic MPE cases in 69 patients treated in 2014 and 2015. Management was ideal in 36 cases (50%), meaning that, prior to definitive treatment, patients had no more than two pleural taps for symptom relief, no more than one ED visit, no chest tubes without pleurodesis, and no hospitalizations. “We thought this would be reasonable to try to achieve for MPE,” since there’s no definition of ideal management, Dr. Shieh said.
Nonideal patients had a mean of 2.5 pleural procedures – almost twice the number in the ideal group – before definitive palliation, with no respiratory consult beforehand. Chest tubes were placed in 27 cases (38%) for an average of 3.7 days; 28 cases (39%) were hospitalized. Nonideal patients were far more likely to present first to the ED, and ED presentations were more likely to get chest tubes and be admitted. All the cases were eventually treated definitively, 68 with indwelling pleural catheters and 4 by thoracoscopic talc insufflation. Time from initial presentation to definitive palliation was about 1 month in both groups. The investigators didn’t consider rate of effusion recurrence, which might help explain why the ideal group wasn’t treated sooner; they might not have needed it. The higher number of ED visits in the nonideal group suggests that they may have had quicker recurrences, and should have been treated sooner, Dr. Gonzalez said.
The patients were 70 years old, on average, and about 60% were women. Lung and breast were the most common cancers.
There was no industry funding for the work, and the investigators had no disclosures.
LOS ANGELES – About half of patients with symptomatic malignant pleural effusions at McGill University Health Centre in Montreal had unnecessary procedures and hospital admissions before definitive treatment with chemical pleurodesis or indwelling pleural catheters, according to researchers.
Instead of chest taps to relieve symptoms followed by referrals for definitive treatment, some patients got chest tubes – without pleurodesis – after presenting to the emergency department and being referred to radiology; they were then admitted to the hospital for a few days while the tubes were in place. In short, cancer patients were wasting what time they had left on medical care they didn’t need, and incurring unnecessary costs, said lead investigator Benjamin Shieh, MD, formerly at McGill but now an interventional pulmonology fellow at the University of Calgary.
McGill is a tertiary care center able to perform both definitive procedures, so “we should be a center of excellence. I imagine there are similar situations” at other hospitals, especially those without the resources of McGill, Dr. Shieh said at the annual meeting of the American College of Chest Physicians.
McGill has taken several steps to address the problem, including early ED referral to the pulmonology service and discouraging radiology from placing chest tubes for malignant pleural effusions (MPE). “I think we can avoid a big proportion of hospitalizations for MPE, and certainly a proportion of repeat [ED] visits,” said senior author Anne Gonzalez, MD, an attending pulmonologist at McGill.
The investigators looked into the issue after noting that a lot of their MPE cases had been hospitalized with chest tubes. They reviewed 72 symptomatic MPE cases in 69 patients treated in 2014 and 2015. Management was ideal in 36 cases (50%), meaning that, prior to definitive treatment, patients had no more than two pleural taps for symptom relief, no more than one ED visit, no chest tubes without pleurodesis, and no hospitalizations. “We thought this would be reasonable to try to achieve for MPE,” since there’s no definition of ideal management, Dr. Shieh said.
Nonideal patients had a mean of 2.5 pleural procedures – almost twice the number in the ideal group – before definitive palliation, with no respiratory consult beforehand. Chest tubes were placed in 27 cases (38%) for an average of 3.7 days; 28 cases (39%) were hospitalized. Nonideal patients were far more likely to present first to the ED, and ED presentations were more likely to get chest tubes and be admitted. All the cases were eventually treated definitively, 68 with indwelling pleural catheters and 4 by thoracoscopic talc insufflation. Time from initial presentation to definitive palliation was about 1 month in both groups. The investigators didn’t consider rate of effusion recurrence, which might help explain why the ideal group wasn’t treated sooner; they might not have needed it. The higher number of ED visits in the nonideal group suggests that they may have had quicker recurrences, and should have been treated sooner, Dr. Gonzalez said.
The patients were 70 years old, on average, and about 60% were women. Lung and breast were the most common cancers.
There was no industry funding for the work, and the investigators had no disclosures.
AT CHEST 2016
Key clinical point:
Major finding: Those patients had a mean of 2.5 pleural procedures before definitive palliation, with no respiratory consult beforehand. Chest tubes were placed for an average of 3.7 days.
Data source: Review of 72 MPE cases in 69 patients.
Disclosures: There was no industry funding for the work, and the investigators had no disclosures.
Mitral valve disease often missed in pulmonary hypertension
LOS ANGELES – Dyspnea in pulmonary hypertension is caused by mitral valve disease until proven otherwise, according to Paul Forfia, MD, director of pulmonary hypertension, right heart failure, and pulmonary thromboendarterectomy at Temple University, Philadelphia.
Although mitral valve disease is a well-recognized cause of pulmonary hypertension, its significance is often underestimated in practice.
“Whether the valve is regurgitant or stenotic makes absolutely no difference. When you delay” repair or replacement, “the patient keeps getting sicker,” he said. In time, “everyone is standing around wringing their hands going, ‘Oh my god, what are we going to do? Are you serious? Fix the valve.’ We see this type of patient a couple times a month,” Dr. Forfia said at the American College of Chest Physicians annual meeting.
“I have seen lifesaving mitral valve surgery put off for many years in patients with pulmonary hypertension, when all they needed was to have their valve fixed,” he said.
Whatever the case, pulmonologists who want the valve fixed often end up playing patient ping pong with cardiologists who want the hypertension controlled beforehand, but “if I treat the pulmonary circulation first, all I am going to do is unmask the left heart failure. There will be no functional improvement whatsoever,” Dr. Forfia said.
Surgery is the best solution as long as patients are well enough to recover. “With pulmonary hypertension in the setting of severe mitral valve regurgitation or stenosis, whether the pulmonary hypertension is related to passive left heart congestion or associated with pulmonary arteriopathy, the only sensible option is to correct the underlying valvular abnormality,” he said. The surgery should be done at an institution capable of managing postop pulmonary arteriopathy, if present.
The ping pong solution is to send patients to an expert pulmonology center; the mitral valve problem will be spotted right away.
“There is no pulmonary pressure cutoff that should prohibit surgery” in patients able to recover. “There is no such thing as a pulmonary artery pressure too high to be explained by mitral valve disease. The pulmonary pressure can be as high as it wants to be. You will get nowhere by thinking the pressure is too high to address the valve,” Dr. Forfia said.
Often “you hear, ‘I’m afraid the person is going to die on the table.’ I always say ‘if the patient is not going to die on the table, they are going to die in their living room of progressive heart failure because you [didn’t] fix their valve. I have never had a patient with pulmonary hypertension not separate from cardiopulmonary bypass. It’s a myth,” he said.
When there’s a “question if the dyspnea is coming from the mitral valve, we routinely use exercise right heart catheterization to probe the situation. We have a recumbent bike in the cath lab. You’ll often provoke significant left heart congestion with a low workload. It’s very revealing to the significance of mitral valve disease,” he said.
Aortic valve disease is also missed in pulmonary hypertension. “It’s not [a] similar” problem; “it’s the same” problem, Dr. Forfia said.
Dr. Forfia is a consultant for Bayer, Actelion, and United Therapeutics.
LOS ANGELES – Dyspnea in pulmonary hypertension is caused by mitral valve disease until proven otherwise, according to Paul Forfia, MD, director of pulmonary hypertension, right heart failure, and pulmonary thromboendarterectomy at Temple University, Philadelphia.
Although mitral valve disease is a well-recognized cause of pulmonary hypertension, its significance is often underestimated in practice.
“Whether the valve is regurgitant or stenotic makes absolutely no difference. When you delay” repair or replacement, “the patient keeps getting sicker,” he said. In time, “everyone is standing around wringing their hands going, ‘Oh my god, what are we going to do? Are you serious? Fix the valve.’ We see this type of patient a couple times a month,” Dr. Forfia said at the American College of Chest Physicians annual meeting.
“I have seen lifesaving mitral valve surgery put off for many years in patients with pulmonary hypertension, when all they needed was to have their valve fixed,” he said.
Whatever the case, pulmonologists who want the valve fixed often end up playing patient ping pong with cardiologists who want the hypertension controlled beforehand, but “if I treat the pulmonary circulation first, all I am going to do is unmask the left heart failure. There will be no functional improvement whatsoever,” Dr. Forfia said.
Surgery is the best solution as long as patients are well enough to recover. “With pulmonary hypertension in the setting of severe mitral valve regurgitation or stenosis, whether the pulmonary hypertension is related to passive left heart congestion or associated with pulmonary arteriopathy, the only sensible option is to correct the underlying valvular abnormality,” he said. The surgery should be done at an institution capable of managing postop pulmonary arteriopathy, if present.
The ping pong solution is to send patients to an expert pulmonology center; the mitral valve problem will be spotted right away.
“There is no pulmonary pressure cutoff that should prohibit surgery” in patients able to recover. “There is no such thing as a pulmonary artery pressure too high to be explained by mitral valve disease. The pulmonary pressure can be as high as it wants to be. You will get nowhere by thinking the pressure is too high to address the valve,” Dr. Forfia said.
Often “you hear, ‘I’m afraid the person is going to die on the table.’ I always say ‘if the patient is not going to die on the table, they are going to die in their living room of progressive heart failure because you [didn’t] fix their valve. I have never had a patient with pulmonary hypertension not separate from cardiopulmonary bypass. It’s a myth,” he said.
When there’s a “question if the dyspnea is coming from the mitral valve, we routinely use exercise right heart catheterization to probe the situation. We have a recumbent bike in the cath lab. You’ll often provoke significant left heart congestion with a low workload. It’s very revealing to the significance of mitral valve disease,” he said.
Aortic valve disease is also missed in pulmonary hypertension. “It’s not [a] similar” problem; “it’s the same” problem, Dr. Forfia said.
Dr. Forfia is a consultant for Bayer, Actelion, and United Therapeutics.
LOS ANGELES – Dyspnea in pulmonary hypertension is caused by mitral valve disease until proven otherwise, according to Paul Forfia, MD, director of pulmonary hypertension, right heart failure, and pulmonary thromboendarterectomy at Temple University, Philadelphia.
Although mitral valve disease is a well-recognized cause of pulmonary hypertension, its significance is often underestimated in practice.
“Whether the valve is regurgitant or stenotic makes absolutely no difference. When you delay” repair or replacement, “the patient keeps getting sicker,” he said. In time, “everyone is standing around wringing their hands going, ‘Oh my god, what are we going to do? Are you serious? Fix the valve.’ We see this type of patient a couple times a month,” Dr. Forfia said at the American College of Chest Physicians annual meeting.
“I have seen lifesaving mitral valve surgery put off for many years in patients with pulmonary hypertension, when all they needed was to have their valve fixed,” he said.
Whatever the case, pulmonologists who want the valve fixed often end up playing patient ping pong with cardiologists who want the hypertension controlled beforehand, but “if I treat the pulmonary circulation first, all I am going to do is unmask the left heart failure. There will be no functional improvement whatsoever,” Dr. Forfia said.
Surgery is the best solution as long as patients are well enough to recover. “With pulmonary hypertension in the setting of severe mitral valve regurgitation or stenosis, whether the pulmonary hypertension is related to passive left heart congestion or associated with pulmonary arteriopathy, the only sensible option is to correct the underlying valvular abnormality,” he said. The surgery should be done at an institution capable of managing postop pulmonary arteriopathy, if present.
The ping pong solution is to send patients to an expert pulmonology center; the mitral valve problem will be spotted right away.
“There is no pulmonary pressure cutoff that should prohibit surgery” in patients able to recover. “There is no such thing as a pulmonary artery pressure too high to be explained by mitral valve disease. The pulmonary pressure can be as high as it wants to be. You will get nowhere by thinking the pressure is too high to address the valve,” Dr. Forfia said.
Often “you hear, ‘I’m afraid the person is going to die on the table.’ I always say ‘if the patient is not going to die on the table, they are going to die in their living room of progressive heart failure because you [didn’t] fix their valve. I have never had a patient with pulmonary hypertension not separate from cardiopulmonary bypass. It’s a myth,” he said.
When there’s a “question if the dyspnea is coming from the mitral valve, we routinely use exercise right heart catheterization to probe the situation. We have a recumbent bike in the cath lab. You’ll often provoke significant left heart congestion with a low workload. It’s very revealing to the significance of mitral valve disease,” he said.
Aortic valve disease is also missed in pulmonary hypertension. “It’s not [a] similar” problem; “it’s the same” problem, Dr. Forfia said.
Dr. Forfia is a consultant for Bayer, Actelion, and United Therapeutics.
EXPERT ANALYSIS FROM CHEST 2016
Blood assay rapidly identifies lung cancer mutations
LOS ANGELES – A newer blood test (GeneStrat from Biodesix) identified genetic mutations in lung tumors in about 24 hours, allowing for an early start of mutation-specific chemotherapy, in an investigation from Gundersen Health System in La Crosse, Wis.
Interventional pulmonologists drew blood samples when they performed biopsies on 84 patients with highly suspicious lung nodules and submitted both blood and tissue for mutation analysis. The blood was analyzed by Biodesix, the maker of GeneStrat, a commercially available digital droplet polymerase change reaction assay launched in 2015. The company sent the results back in an average of 24.1 hours, and all within 72 hours. The mutation results from tissue analysis took 2-3 weeks.
Fifteen patients (18%) had actionable epidermal growth factor receptor, anaplastic lymphoma kinase, or K-Ras protein gene mutations, and were candidates for targeted therapy. Compared with tissue testing, the blood assay had a sensitivity of 88% and a specificity of 99%. The tissue testing picked up two mutations missed by blood testing. One of the two mutations is rare and was not included in the blood assay. Meanwhile, the assay caught a mutation missed on tissue analysis.
She and her colleagues are now routinely using GeneStrat to guide initial lung cancer therapy. “The turnaround time is fantastic. It allows us to have [the mutation status] when oncologists meet with patients for the very first time,” she said.
It “definitely” makes a difference. “If you have an actionable mutation and there’s a targeted chemotherapy” – such as erlotinib (Tarceva) for epidermal growth factor receptor mutation patients – it can be started right out of the gate. “Time to treatment is very important,” not just psychologically for patients but also for them to have the best chance against the tumor. The sooner “we can start a targeted therapy,” the better outcomes are likely to be, Dr. Mattingley said.
When mutation status is delayed, patients might be started “on the wrong therapy upfront, and it’s really hard to back up and start over again,” she said.
“Once we give patients a diagnosis of lung cancer, the next thing they should hear right away is how we are going to attack it. We felt strongly [that there was a] need to look at this to see if we could truly expedite the time from diagnosis to treatment. We believe our patients should have no sleepless nights,” Dr. Mattingley said.
There’s also usually not much tissue left after genetic work-up to send into a clinical trial. Using blood to identify mutations “may allow us to conserve our tissue block for future trials, but still get the genetic information we need to start treatment plans for our patients,” she said.
There was no company funding for the work, but Dr. Mattingley is a speaker for GeneStrat’s maker, Biodesix.
The results of this study are very promising. The high concordance between liquid biopsies and tissue biopsies as well as the short turn-around time for the results of the liquid biopsies makes a big difference in terms of getting patients started on appropriate therapy sooner rather than later. We need additional studies to find out if liquid biopsies will be good for detection of other molecular alterations such as ROS-1 and EGFR acquired mutation T790M.
The results of this study are very promising. The high concordance between liquid biopsies and tissue biopsies as well as the short turn-around time for the results of the liquid biopsies makes a big difference in terms of getting patients started on appropriate therapy sooner rather than later. We need additional studies to find out if liquid biopsies will be good for detection of other molecular alterations such as ROS-1 and EGFR acquired mutation T790M.
The results of this study are very promising. The high concordance between liquid biopsies and tissue biopsies as well as the short turn-around time for the results of the liquid biopsies makes a big difference in terms of getting patients started on appropriate therapy sooner rather than later. We need additional studies to find out if liquid biopsies will be good for detection of other molecular alterations such as ROS-1 and EGFR acquired mutation T790M.
LOS ANGELES – A newer blood test (GeneStrat from Biodesix) identified genetic mutations in lung tumors in about 24 hours, allowing for an early start of mutation-specific chemotherapy, in an investigation from Gundersen Health System in La Crosse, Wis.
Interventional pulmonologists drew blood samples when they performed biopsies on 84 patients with highly suspicious lung nodules and submitted both blood and tissue for mutation analysis. The blood was analyzed by Biodesix, the maker of GeneStrat, a commercially available digital droplet polymerase change reaction assay launched in 2015. The company sent the results back in an average of 24.1 hours, and all within 72 hours. The mutation results from tissue analysis took 2-3 weeks.
Fifteen patients (18%) had actionable epidermal growth factor receptor, anaplastic lymphoma kinase, or K-Ras protein gene mutations, and were candidates for targeted therapy. Compared with tissue testing, the blood assay had a sensitivity of 88% and a specificity of 99%. The tissue testing picked up two mutations missed by blood testing. One of the two mutations is rare and was not included in the blood assay. Meanwhile, the assay caught a mutation missed on tissue analysis.
She and her colleagues are now routinely using GeneStrat to guide initial lung cancer therapy. “The turnaround time is fantastic. It allows us to have [the mutation status] when oncologists meet with patients for the very first time,” she said.
It “definitely” makes a difference. “If you have an actionable mutation and there’s a targeted chemotherapy” – such as erlotinib (Tarceva) for epidermal growth factor receptor mutation patients – it can be started right out of the gate. “Time to treatment is very important,” not just psychologically for patients but also for them to have the best chance against the tumor. The sooner “we can start a targeted therapy,” the better outcomes are likely to be, Dr. Mattingley said.
When mutation status is delayed, patients might be started “on the wrong therapy upfront, and it’s really hard to back up and start over again,” she said.
“Once we give patients a diagnosis of lung cancer, the next thing they should hear right away is how we are going to attack it. We felt strongly [that there was a] need to look at this to see if we could truly expedite the time from diagnosis to treatment. We believe our patients should have no sleepless nights,” Dr. Mattingley said.
There’s also usually not much tissue left after genetic work-up to send into a clinical trial. Using blood to identify mutations “may allow us to conserve our tissue block for future trials, but still get the genetic information we need to start treatment plans for our patients,” she said.
There was no company funding for the work, but Dr. Mattingley is a speaker for GeneStrat’s maker, Biodesix.
LOS ANGELES – A newer blood test (GeneStrat from Biodesix) identified genetic mutations in lung tumors in about 24 hours, allowing for an early start of mutation-specific chemotherapy, in an investigation from Gundersen Health System in La Crosse, Wis.
Interventional pulmonologists drew blood samples when they performed biopsies on 84 patients with highly suspicious lung nodules and submitted both blood and tissue for mutation analysis. The blood was analyzed by Biodesix, the maker of GeneStrat, a commercially available digital droplet polymerase change reaction assay launched in 2015. The company sent the results back in an average of 24.1 hours, and all within 72 hours. The mutation results from tissue analysis took 2-3 weeks.
Fifteen patients (18%) had actionable epidermal growth factor receptor, anaplastic lymphoma kinase, or K-Ras protein gene mutations, and were candidates for targeted therapy. Compared with tissue testing, the blood assay had a sensitivity of 88% and a specificity of 99%. The tissue testing picked up two mutations missed by blood testing. One of the two mutations is rare and was not included in the blood assay. Meanwhile, the assay caught a mutation missed on tissue analysis.
She and her colleagues are now routinely using GeneStrat to guide initial lung cancer therapy. “The turnaround time is fantastic. It allows us to have [the mutation status] when oncologists meet with patients for the very first time,” she said.
It “definitely” makes a difference. “If you have an actionable mutation and there’s a targeted chemotherapy” – such as erlotinib (Tarceva) for epidermal growth factor receptor mutation patients – it can be started right out of the gate. “Time to treatment is very important,” not just psychologically for patients but also for them to have the best chance against the tumor. The sooner “we can start a targeted therapy,” the better outcomes are likely to be, Dr. Mattingley said.
When mutation status is delayed, patients might be started “on the wrong therapy upfront, and it’s really hard to back up and start over again,” she said.
“Once we give patients a diagnosis of lung cancer, the next thing they should hear right away is how we are going to attack it. We felt strongly [that there was a] need to look at this to see if we could truly expedite the time from diagnosis to treatment. We believe our patients should have no sleepless nights,” Dr. Mattingley said.
There’s also usually not much tissue left after genetic work-up to send into a clinical trial. Using blood to identify mutations “may allow us to conserve our tissue block for future trials, but still get the genetic information we need to start treatment plans for our patients,” she said.
There was no company funding for the work, but Dr. Mattingley is a speaker for GeneStrat’s maker, Biodesix.
AT CHEST 2016
Key clinical point:
Major finding: Compared with tissue testing, the blood assay had a sensitivity of 88% and a specificity of 99%.
Data source: Eighty-four patients with highly suspicious lung nodules.
Disclosures: There was no company funding for the work, but the presenter is a paid speaker for GeneStrat’s maker, Biodesix.
AGA Clinical Practice Update: Refer early Barrett’s dysplasia to a specialist
Low-grade esophageal dysplasia must be confirmed by a GI pathologist with a special interest in Barrett’s esophagus, one who deals with the problem on a daily basis and whom peers recognize as an expert in the field, according to a new expert review from the American Gastroenterological Association (Gastroenterology. doi: http://dx.doi.org/10.1053/j.gastro.2016.09.040).
In the absence of reliable biomarkers, it’s the best guarantee that low-grade dysplasia (LGD) is truly present. Overdiagnosis of early dysplasia is common, and it leads to mistreatment and uncertainty about study results, the AGA said.
In the absence of reliable biomarkers, AGA turned to expertise to combat mistreatment. Although it’s clear that high-grade disease and esophageal adenocarcinoma need intervention, LGD sometimes seems to regress on its own, but it’s unclear if it’s due to natural history or diagnosis in patients who don’t really have it.
For now, expertise is the best solution. “Unfortunately, there is no database that clearly identifies experts in the field of Barrett’s esophagus,” but most practitioners can identify people to “refer these patients to within their state or region.” Meanwhile, “we are working tirelessly” to establish a referral and outcome database. “We owe it to” patients to let them know “how good the” people we are referring them to are, Dr. Wani said.
Given the diagnosis uncertainty, AGA side-stepped the biggest controversy in LGD: whether patients should be treated or watched. Among “patients with confirmed Barrett’s esophagus with LGD by expert GI pathology review that persists on a [second] endoscopy despite intensification of acid-suppressive therapy” at 8-12 weeks with proton pump inhibitors twice a day, “risks and benefits of management options of endoscopic eradication therapy (specifically adverse events associated with endoscopic resection and ablation) and ongoing surveillance should be discussed and documented,” the group said.
When patients opt for treatment, endoscopic eradication should proceed “with the goal of achieving complete eradication of intestinal metaplasia ... radiofrequency ablation should be used,” AGA said.
Meanwhile, “patients with LGD undergoing surveillance rather than endoscopic eradication therapy should undergo surveillance every 6 months times two, then annually unless there is reversion to nondysplastic Barrett’s esophagus. Biopsies should be obtained in 4-quadrants every 1-2 cm and of any visible lesions.”
AGA funded the work. Dr. Wani is a Medtronic and Boston Scientific consultant.
Low-grade esophageal dysplasia must be confirmed by a GI pathologist with a special interest in Barrett’s esophagus, one who deals with the problem on a daily basis and whom peers recognize as an expert in the field, according to a new expert review from the American Gastroenterological Association (Gastroenterology. doi: http://dx.doi.org/10.1053/j.gastro.2016.09.040).
In the absence of reliable biomarkers, it’s the best guarantee that low-grade dysplasia (LGD) is truly present. Overdiagnosis of early dysplasia is common, and it leads to mistreatment and uncertainty about study results, the AGA said.
In the absence of reliable biomarkers, AGA turned to expertise to combat mistreatment. Although it’s clear that high-grade disease and esophageal adenocarcinoma need intervention, LGD sometimes seems to regress on its own, but it’s unclear if it’s due to natural history or diagnosis in patients who don’t really have it.
For now, expertise is the best solution. “Unfortunately, there is no database that clearly identifies experts in the field of Barrett’s esophagus,” but most practitioners can identify people to “refer these patients to within their state or region.” Meanwhile, “we are working tirelessly” to establish a referral and outcome database. “We owe it to” patients to let them know “how good the” people we are referring them to are, Dr. Wani said.
Given the diagnosis uncertainty, AGA side-stepped the biggest controversy in LGD: whether patients should be treated or watched. Among “patients with confirmed Barrett’s esophagus with LGD by expert GI pathology review that persists on a [second] endoscopy despite intensification of acid-suppressive therapy” at 8-12 weeks with proton pump inhibitors twice a day, “risks and benefits of management options of endoscopic eradication therapy (specifically adverse events associated with endoscopic resection and ablation) and ongoing surveillance should be discussed and documented,” the group said.
When patients opt for treatment, endoscopic eradication should proceed “with the goal of achieving complete eradication of intestinal metaplasia ... radiofrequency ablation should be used,” AGA said.
Meanwhile, “patients with LGD undergoing surveillance rather than endoscopic eradication therapy should undergo surveillance every 6 months times two, then annually unless there is reversion to nondysplastic Barrett’s esophagus. Biopsies should be obtained in 4-quadrants every 1-2 cm and of any visible lesions.”
AGA funded the work. Dr. Wani is a Medtronic and Boston Scientific consultant.
Low-grade esophageal dysplasia must be confirmed by a GI pathologist with a special interest in Barrett’s esophagus, one who deals with the problem on a daily basis and whom peers recognize as an expert in the field, according to a new expert review from the American Gastroenterological Association (Gastroenterology. doi: http://dx.doi.org/10.1053/j.gastro.2016.09.040).
In the absence of reliable biomarkers, it’s the best guarantee that low-grade dysplasia (LGD) is truly present. Overdiagnosis of early dysplasia is common, and it leads to mistreatment and uncertainty about study results, the AGA said.
In the absence of reliable biomarkers, AGA turned to expertise to combat mistreatment. Although it’s clear that high-grade disease and esophageal adenocarcinoma need intervention, LGD sometimes seems to regress on its own, but it’s unclear if it’s due to natural history or diagnosis in patients who don’t really have it.
For now, expertise is the best solution. “Unfortunately, there is no database that clearly identifies experts in the field of Barrett’s esophagus,” but most practitioners can identify people to “refer these patients to within their state or region.” Meanwhile, “we are working tirelessly” to establish a referral and outcome database. “We owe it to” patients to let them know “how good the” people we are referring them to are, Dr. Wani said.
Given the diagnosis uncertainty, AGA side-stepped the biggest controversy in LGD: whether patients should be treated or watched. Among “patients with confirmed Barrett’s esophagus with LGD by expert GI pathology review that persists on a [second] endoscopy despite intensification of acid-suppressive therapy” at 8-12 weeks with proton pump inhibitors twice a day, “risks and benefits of management options of endoscopic eradication therapy (specifically adverse events associated with endoscopic resection and ablation) and ongoing surveillance should be discussed and documented,” the group said.
When patients opt for treatment, endoscopic eradication should proceed “with the goal of achieving complete eradication of intestinal metaplasia ... radiofrequency ablation should be used,” AGA said.
Meanwhile, “patients with LGD undergoing surveillance rather than endoscopic eradication therapy should undergo surveillance every 6 months times two, then annually unless there is reversion to nondysplastic Barrett’s esophagus. Biopsies should be obtained in 4-quadrants every 1-2 cm and of any visible lesions.”
AGA funded the work. Dr. Wani is a Medtronic and Boston Scientific consultant.
Fluid administration in sepsis did not increase need for dialysis
LOS ANGELES – Fluid administration of at least 1 L did not increase the incidence of acute respiratory or heart failure in severe sepsis, and actually seemed to decrease the need for dialysis in a review of 164 patients at Scott and White Memorial Hospital in Temple, Tex.
For every 1 mL of fluid administered per kilogram of body weight, the likelihood of dialysis decreased by 8.5% (odds ratio, 0.915; 95% confidence interval, 0.854-0.980; P = .0111), with no increase in heart or respiratory failure on univariate analysis. The 126 patients (77%) who received at least 1 L had a 68% reduction in the need for dialysis (OR, 0.32; CI, 0.117-0.890; P = .0288).
“The No. 1 reason we weren’t meeting benchmarks was fluid administration,” explained lead investigator Aruna Jahoor, MD, a pulmonary critical care and sleep medicine fellow at Texas Tech University Health Sciences Center.
Seventeen percent of patients received greater than or equal to 30 mL/kg of fluid resuscitation, while 28% received greater than or equal to 20 mL/kg of intravenous fluid resuscitation. It turned out that staff in the emergency department - where most of the patients were treated in the critical first 6 hours - were concerned about fluid overload and throwing patients into respiratory, heart, or renal failure, Dr. Jahoor said. The team didn’t find a difference in mortality when patients received 30 mL/kg - just over 2 L in a 70-kg patient - versus 20 mL/kg or 1 L. The patients’ in-hospital mortality rate and 28-day mortality rate were 27%, and 32%, respectively.
There also weren’t increased rates of heart failure, acute respiratory failure, or mechanical ventilation when patients received at least 1 L of fluid. “There were [also] lower rates of dialysis, which indicated that we weren’t overloading patients. Even when we looked at fluid as a continuous variable, we still didn’t see” complications, Dr. Jahoor said.
The findings should be reassuring to treating physicians. “When you have pushback against 30-mL/kg administration, you can say ‘well, at least let’s give a liter. You don’t have to worry as much about some of the complications you are citing,’ ” she said.
For very obese patients, “it can get a little uncomfortable to be given” enough fluid to meet the 30-mL/kg goal, “but you can give at least a liter” without having to worry too much, she said. The patients in the study were treated from 2010 to 2013; normal saline was the most common resuscitation fluid. The hospital has since added the 30-mL/kg fluid resuscitation to its sepsis admission orders, and compliance has increased significantly.
A multivariate analysis is in the works to control for confounders. “We will probably [still] see you are not having increased rates of congestive heart or respiratory failure, or needing dialysis,” Dr. Jahoor said. The protective effect against dialysis might drop out, “but I am hoping it doesn’t,” he said.
The investigators had no relevant financial disclosures.
LOS ANGELES – Fluid administration of at least 1 L did not increase the incidence of acute respiratory or heart failure in severe sepsis, and actually seemed to decrease the need for dialysis in a review of 164 patients at Scott and White Memorial Hospital in Temple, Tex.
For every 1 mL of fluid administered per kilogram of body weight, the likelihood of dialysis decreased by 8.5% (odds ratio, 0.915; 95% confidence interval, 0.854-0.980; P = .0111), with no increase in heart or respiratory failure on univariate analysis. The 126 patients (77%) who received at least 1 L had a 68% reduction in the need for dialysis (OR, 0.32; CI, 0.117-0.890; P = .0288).
“The No. 1 reason we weren’t meeting benchmarks was fluid administration,” explained lead investigator Aruna Jahoor, MD, a pulmonary critical care and sleep medicine fellow at Texas Tech University Health Sciences Center.
Seventeen percent of patients received greater than or equal to 30 mL/kg of fluid resuscitation, while 28% received greater than or equal to 20 mL/kg of intravenous fluid resuscitation. It turned out that staff in the emergency department - where most of the patients were treated in the critical first 6 hours - were concerned about fluid overload and throwing patients into respiratory, heart, or renal failure, Dr. Jahoor said. The team didn’t find a difference in mortality when patients received 30 mL/kg - just over 2 L in a 70-kg patient - versus 20 mL/kg or 1 L. The patients’ in-hospital mortality rate and 28-day mortality rate were 27%, and 32%, respectively.
There also weren’t increased rates of heart failure, acute respiratory failure, or mechanical ventilation when patients received at least 1 L of fluid. “There were [also] lower rates of dialysis, which indicated that we weren’t overloading patients. Even when we looked at fluid as a continuous variable, we still didn’t see” complications, Dr. Jahoor said.
The findings should be reassuring to treating physicians. “When you have pushback against 30-mL/kg administration, you can say ‘well, at least let’s give a liter. You don’t have to worry as much about some of the complications you are citing,’ ” she said.
For very obese patients, “it can get a little uncomfortable to be given” enough fluid to meet the 30-mL/kg goal, “but you can give at least a liter” without having to worry too much, she said. The patients in the study were treated from 2010 to 2013; normal saline was the most common resuscitation fluid. The hospital has since added the 30-mL/kg fluid resuscitation to its sepsis admission orders, and compliance has increased significantly.
A multivariate analysis is in the works to control for confounders. “We will probably [still] see you are not having increased rates of congestive heart or respiratory failure, or needing dialysis,” Dr. Jahoor said. The protective effect against dialysis might drop out, “but I am hoping it doesn’t,” he said.
The investigators had no relevant financial disclosures.
LOS ANGELES – Fluid administration of at least 1 L did not increase the incidence of acute respiratory or heart failure in severe sepsis, and actually seemed to decrease the need for dialysis in a review of 164 patients at Scott and White Memorial Hospital in Temple, Tex.
For every 1 mL of fluid administered per kilogram of body weight, the likelihood of dialysis decreased by 8.5% (odds ratio, 0.915; 95% confidence interval, 0.854-0.980; P = .0111), with no increase in heart or respiratory failure on univariate analysis. The 126 patients (77%) who received at least 1 L had a 68% reduction in the need for dialysis (OR, 0.32; CI, 0.117-0.890; P = .0288).
“The No. 1 reason we weren’t meeting benchmarks was fluid administration,” explained lead investigator Aruna Jahoor, MD, a pulmonary critical care and sleep medicine fellow at Texas Tech University Health Sciences Center.
Seventeen percent of patients received greater than or equal to 30 mL/kg of fluid resuscitation, while 28% received greater than or equal to 20 mL/kg of intravenous fluid resuscitation. It turned out that staff in the emergency department - where most of the patients were treated in the critical first 6 hours - were concerned about fluid overload and throwing patients into respiratory, heart, or renal failure, Dr. Jahoor said. The team didn’t find a difference in mortality when patients received 30 mL/kg - just over 2 L in a 70-kg patient - versus 20 mL/kg or 1 L. The patients’ in-hospital mortality rate and 28-day mortality rate were 27%, and 32%, respectively.
There also weren’t increased rates of heart failure, acute respiratory failure, or mechanical ventilation when patients received at least 1 L of fluid. “There were [also] lower rates of dialysis, which indicated that we weren’t overloading patients. Even when we looked at fluid as a continuous variable, we still didn’t see” complications, Dr. Jahoor said.
The findings should be reassuring to treating physicians. “When you have pushback against 30-mL/kg administration, you can say ‘well, at least let’s give a liter. You don’t have to worry as much about some of the complications you are citing,’ ” she said.
For very obese patients, “it can get a little uncomfortable to be given” enough fluid to meet the 30-mL/kg goal, “but you can give at least a liter” without having to worry too much, she said. The patients in the study were treated from 2010 to 2013; normal saline was the most common resuscitation fluid. The hospital has since added the 30-mL/kg fluid resuscitation to its sepsis admission orders, and compliance has increased significantly.
A multivariate analysis is in the works to control for confounders. “We will probably [still] see you are not having increased rates of congestive heart or respiratory failure, or needing dialysis,” Dr. Jahoor said. The protective effect against dialysis might drop out, “but I am hoping it doesn’t,” he said.
The investigators had no relevant financial disclosures.
AT CHEST 2016
Key clinical point:
Major finding: For every 1 mL/kg of fluid administered, the likelihood of dialysis decreased by 8.5% (OR, 0.915; 95% CI, 0.854-0.980; P = .0111), with no increase in heart or respiratory failure on univariate analysis.
Data source: A review of 164 septic patients.
Disclosures: The investigators had no relevant financial disclosures.
Riociguat shows benefit in PAH with poor response to PDE inhibitors
LOS ANGELES – Pulmonary artery hypertension patients who have an insufficient response to phosphodiesterase inhibitors may benefit from a switch to riociguat (Adempas), based on results from a 24-week, open-label investigation from the drug’s maker, Bayer.
The 61 patients – mean age 54 years, 74% of whom were women – had World Health Organization functional class 3 disease, with 6-minute walking distances of 165-440 meters, and cardiac indices below 3 L/min/m2 despite being on a phosphodiesterase inhibitor (PDEi) for 90 days or more, 40 (66%) on sildenafil (Viagra) and 21 (34%) on tadalafil (Cialis).
After PDEi washout, the researchers swapped them for riociguat titrated to a maximum oral dose of 2.5 mg t.i.d. The 50 patients (82%) on concomitant endothelin receptor antagonists (ERA) were allowed to stay on them. At week 24, 16 patients (34% of the 47 evaluable patients) achieved the combined endpoint of no clinical worsening, functional class 1 or 2, and 30 meters or more improvement on their walk test.
“The key point is that it was safe to switch people from a [PDEi] to riociguat, and it seemed to have improved efficacy, but we hesitate on these conclusions because it was an open-label trial, and the results need to be confirmed,” lead investigator James Klinger, MD, professor of medicine at Brown University, Providence, R.I., said at the annual meeting of the American College of Chest Physicians. A randomized, controlled trial is underway, he added.
The usual approach to PAH is to start patients on a PDEi, often with an ERA. If that doesn’t work, a prostacyclin is added. The cost can exceed $200,000 a year.
“This is a study that says, wait a minute, before you add a third drug to the first two, maybe it would be worthwhile to” switch out the PDEi. “You would save the person the addition of a third drug,” and the cost would be comparable or less than a three-drug regimen, Dr. Klinger said.
The researchers also found that after 24 weeks on riociguat, mean plasma cyclic guanosine monophosphate (cGMP) increased by 4.6 pmol/mL, urinary cGMP by 1,005 pmol/mL, and asymmetric dimethylarginine (ADMA) by 0.004 micromol/L.
The biomarkers were important because the team is trying to find a way to identify patients who would benefit most from riociguat. “As a field, we still don’t understand the disease well enough to know” how to best match patients and drugs. “We are trying to find a biomarker that would identify patients who are more likely to respond to one medication versus another,” Dr. Klinger said.
ADMA inhibits the production of nitric oxide, and is a bad player in PAH. The study results were reassuring because riociguat didn’t have much of an effect on ADMA levels, although the “slight difference was not enough to identify people who might do better with” it, Dr. Klinger said.
As for cGMP, “when we raise [levels] with riociguat, patients get better, so we think riociguat is raising cGMP in the right place, which we think is the lungs. Unfortunately, we don’t’ have a biomarker that can distinguish lung cGMP from total body cGMP,” he said.
The work was funded by Bayer, maker of riociguat. Dr. Klinger is an unpaid consultant, and also receives research support from the company.
LOS ANGELES – Pulmonary artery hypertension patients who have an insufficient response to phosphodiesterase inhibitors may benefit from a switch to riociguat (Adempas), based on results from a 24-week, open-label investigation from the drug’s maker, Bayer.
The 61 patients – mean age 54 years, 74% of whom were women – had World Health Organization functional class 3 disease, with 6-minute walking distances of 165-440 meters, and cardiac indices below 3 L/min/m2 despite being on a phosphodiesterase inhibitor (PDEi) for 90 days or more, 40 (66%) on sildenafil (Viagra) and 21 (34%) on tadalafil (Cialis).
After PDEi washout, the researchers swapped them for riociguat titrated to a maximum oral dose of 2.5 mg t.i.d. The 50 patients (82%) on concomitant endothelin receptor antagonists (ERA) were allowed to stay on them. At week 24, 16 patients (34% of the 47 evaluable patients) achieved the combined endpoint of no clinical worsening, functional class 1 or 2, and 30 meters or more improvement on their walk test.
“The key point is that it was safe to switch people from a [PDEi] to riociguat, and it seemed to have improved efficacy, but we hesitate on these conclusions because it was an open-label trial, and the results need to be confirmed,” lead investigator James Klinger, MD, professor of medicine at Brown University, Providence, R.I., said at the annual meeting of the American College of Chest Physicians. A randomized, controlled trial is underway, he added.
The usual approach to PAH is to start patients on a PDEi, often with an ERA. If that doesn’t work, a prostacyclin is added. The cost can exceed $200,000 a year.
“This is a study that says, wait a minute, before you add a third drug to the first two, maybe it would be worthwhile to” switch out the PDEi. “You would save the person the addition of a third drug,” and the cost would be comparable or less than a three-drug regimen, Dr. Klinger said.
The researchers also found that after 24 weeks on riociguat, mean plasma cyclic guanosine monophosphate (cGMP) increased by 4.6 pmol/mL, urinary cGMP by 1,005 pmol/mL, and asymmetric dimethylarginine (ADMA) by 0.004 micromol/L.
The biomarkers were important because the team is trying to find a way to identify patients who would benefit most from riociguat. “As a field, we still don’t understand the disease well enough to know” how to best match patients and drugs. “We are trying to find a biomarker that would identify patients who are more likely to respond to one medication versus another,” Dr. Klinger said.
ADMA inhibits the production of nitric oxide, and is a bad player in PAH. The study results were reassuring because riociguat didn’t have much of an effect on ADMA levels, although the “slight difference was not enough to identify people who might do better with” it, Dr. Klinger said.
As for cGMP, “when we raise [levels] with riociguat, patients get better, so we think riociguat is raising cGMP in the right place, which we think is the lungs. Unfortunately, we don’t’ have a biomarker that can distinguish lung cGMP from total body cGMP,” he said.
The work was funded by Bayer, maker of riociguat. Dr. Klinger is an unpaid consultant, and also receives research support from the company.
LOS ANGELES – Pulmonary artery hypertension patients who have an insufficient response to phosphodiesterase inhibitors may benefit from a switch to riociguat (Adempas), based on results from a 24-week, open-label investigation from the drug’s maker, Bayer.
The 61 patients – mean age 54 years, 74% of whom were women – had World Health Organization functional class 3 disease, with 6-minute walking distances of 165-440 meters, and cardiac indices below 3 L/min/m2 despite being on a phosphodiesterase inhibitor (PDEi) for 90 days or more, 40 (66%) on sildenafil (Viagra) and 21 (34%) on tadalafil (Cialis).
After PDEi washout, the researchers swapped them for riociguat titrated to a maximum oral dose of 2.5 mg t.i.d. The 50 patients (82%) on concomitant endothelin receptor antagonists (ERA) were allowed to stay on them. At week 24, 16 patients (34% of the 47 evaluable patients) achieved the combined endpoint of no clinical worsening, functional class 1 or 2, and 30 meters or more improvement on their walk test.
“The key point is that it was safe to switch people from a [PDEi] to riociguat, and it seemed to have improved efficacy, but we hesitate on these conclusions because it was an open-label trial, and the results need to be confirmed,” lead investigator James Klinger, MD, professor of medicine at Brown University, Providence, R.I., said at the annual meeting of the American College of Chest Physicians. A randomized, controlled trial is underway, he added.
The usual approach to PAH is to start patients on a PDEi, often with an ERA. If that doesn’t work, a prostacyclin is added. The cost can exceed $200,000 a year.
“This is a study that says, wait a minute, before you add a third drug to the first two, maybe it would be worthwhile to” switch out the PDEi. “You would save the person the addition of a third drug,” and the cost would be comparable or less than a three-drug regimen, Dr. Klinger said.
The researchers also found that after 24 weeks on riociguat, mean plasma cyclic guanosine monophosphate (cGMP) increased by 4.6 pmol/mL, urinary cGMP by 1,005 pmol/mL, and asymmetric dimethylarginine (ADMA) by 0.004 micromol/L.
The biomarkers were important because the team is trying to find a way to identify patients who would benefit most from riociguat. “As a field, we still don’t understand the disease well enough to know” how to best match patients and drugs. “We are trying to find a biomarker that would identify patients who are more likely to respond to one medication versus another,” Dr. Klinger said.
ADMA inhibits the production of nitric oxide, and is a bad player in PAH. The study results were reassuring because riociguat didn’t have much of an effect on ADMA levels, although the “slight difference was not enough to identify people who might do better with” it, Dr. Klinger said.
As for cGMP, “when we raise [levels] with riociguat, patients get better, so we think riociguat is raising cGMP in the right place, which we think is the lungs. Unfortunately, we don’t’ have a biomarker that can distinguish lung cGMP from total body cGMP,” he said.
The work was funded by Bayer, maker of riociguat. Dr. Klinger is an unpaid consultant, and also receives research support from the company.
AT CHEST 2016
Key clinical point:
Major finding: At week 24, 34% of 47 evaluable patients (16%) achieved the combined endpoint of no clinical worsening, functional class 1 or 2, and a 30-meter or more improvement on their walk test.
Data source: Open-label, nonrandomized 24-week study of 61 patients
Disclosures: The work was funded by Bayer, maker of riociguat. The lead investigator is an unpaid consultant, and also receives research support from the company.
COPD spirometry use suboptimal in primary care
LOS ANGELES – Spirometry is the standard for diagnosing chronic obstructive pulmonary disease, but it’s underused and misused in primary care, according to investigators from the Corpus Christi (Tex.) Medical Center.
The conclusion is based on a review of just 65 patients from internal medicine and family practice clinics near the medical center, but “I do think this [pattern] is representative of what we are seeing in every primary care office. This has been a problem [documented] in the literature for a decade, and it remains a problem,” said lead investigator Stephen Eikermann, DO, an internal medicine resident at the center.
Meanwhile, of those diagnosed by spirometry, 32% didn’t meet the gold-standard Global Initiative for Chronic Obstructive Lung Disease (GOLD) diagnostic criteria by having a postbronchodilator forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) of less than 70%. Clinicians might not have known that postbronchodilator values are the ones that matter. “People who have asthma are being tagged as having COPD,” and once that diagnosis is in the chart, it’s hard to remove, even when patients improve. “With the COPD readmission penalty in place, an erroneous diagnosis of COPD [has] significant financial risks,” Dr. Eikermann said.
“Misdiagnosis leads to significant financial consequences and puts patients at risk for osteoporotic fractures and malignant arrhythmias. It’s a problem of education.” Busy practitioners might not have had time to catch the latest 2015 GOLD standards, he said.
The guidelines state that COPD should be considered in any patient who has dyspnea, chronic cough, or sputum production, plus smoking or other risks. “Spirometry is required to make the diagnosis.”
To help, Dr. Eikermann and his colleagues plan lectures and a quick reference handout, and maybe a smartphone app. They also plan to remind practitioners that Medicare pays at a reasonable rate for spirometry.
The 65 patients in the study were about evenly split between men and women, and were 70 years old, on average. They had about 34 pack-years of smoking, and some were still smoking despite being on home oxygen.
Men were less likely to have spirometry than women; older subjects and current smokers – as opposed to former smokers – were, too. The risk of COPD increases with age and smoking, so the finding was puzzling. For unknown reasons, “there appears to be a bias against ordering spirometry” for some patients, Dr. Eikermann said.
There was no outside funding for the work, and the investigators had no disclosures.
LOS ANGELES – Spirometry is the standard for diagnosing chronic obstructive pulmonary disease, but it’s underused and misused in primary care, according to investigators from the Corpus Christi (Tex.) Medical Center.
The conclusion is based on a review of just 65 patients from internal medicine and family practice clinics near the medical center, but “I do think this [pattern] is representative of what we are seeing in every primary care office. This has been a problem [documented] in the literature for a decade, and it remains a problem,” said lead investigator Stephen Eikermann, DO, an internal medicine resident at the center.
Meanwhile, of those diagnosed by spirometry, 32% didn’t meet the gold-standard Global Initiative for Chronic Obstructive Lung Disease (GOLD) diagnostic criteria by having a postbronchodilator forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) of less than 70%. Clinicians might not have known that postbronchodilator values are the ones that matter. “People who have asthma are being tagged as having COPD,” and once that diagnosis is in the chart, it’s hard to remove, even when patients improve. “With the COPD readmission penalty in place, an erroneous diagnosis of COPD [has] significant financial risks,” Dr. Eikermann said.
“Misdiagnosis leads to significant financial consequences and puts patients at risk for osteoporotic fractures and malignant arrhythmias. It’s a problem of education.” Busy practitioners might not have had time to catch the latest 2015 GOLD standards, he said.
The guidelines state that COPD should be considered in any patient who has dyspnea, chronic cough, or sputum production, plus smoking or other risks. “Spirometry is required to make the diagnosis.”
To help, Dr. Eikermann and his colleagues plan lectures and a quick reference handout, and maybe a smartphone app. They also plan to remind practitioners that Medicare pays at a reasonable rate for spirometry.
The 65 patients in the study were about evenly split between men and women, and were 70 years old, on average. They had about 34 pack-years of smoking, and some were still smoking despite being on home oxygen.
Men were less likely to have spirometry than women; older subjects and current smokers – as opposed to former smokers – were, too. The risk of COPD increases with age and smoking, so the finding was puzzling. For unknown reasons, “there appears to be a bias against ordering spirometry” for some patients, Dr. Eikermann said.
There was no outside funding for the work, and the investigators had no disclosures.
LOS ANGELES – Spirometry is the standard for diagnosing chronic obstructive pulmonary disease, but it’s underused and misused in primary care, according to investigators from the Corpus Christi (Tex.) Medical Center.
The conclusion is based on a review of just 65 patients from internal medicine and family practice clinics near the medical center, but “I do think this [pattern] is representative of what we are seeing in every primary care office. This has been a problem [documented] in the literature for a decade, and it remains a problem,” said lead investigator Stephen Eikermann, DO, an internal medicine resident at the center.
Meanwhile, of those diagnosed by spirometry, 32% didn’t meet the gold-standard Global Initiative for Chronic Obstructive Lung Disease (GOLD) diagnostic criteria by having a postbronchodilator forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) of less than 70%. Clinicians might not have known that postbronchodilator values are the ones that matter. “People who have asthma are being tagged as having COPD,” and once that diagnosis is in the chart, it’s hard to remove, even when patients improve. “With the COPD readmission penalty in place, an erroneous diagnosis of COPD [has] significant financial risks,” Dr. Eikermann said.
“Misdiagnosis leads to significant financial consequences and puts patients at risk for osteoporotic fractures and malignant arrhythmias. It’s a problem of education.” Busy practitioners might not have had time to catch the latest 2015 GOLD standards, he said.
The guidelines state that COPD should be considered in any patient who has dyspnea, chronic cough, or sputum production, plus smoking or other risks. “Spirometry is required to make the diagnosis.”
To help, Dr. Eikermann and his colleagues plan lectures and a quick reference handout, and maybe a smartphone app. They also plan to remind practitioners that Medicare pays at a reasonable rate for spirometry.
The 65 patients in the study were about evenly split between men and women, and were 70 years old, on average. They had about 34 pack-years of smoking, and some were still smoking despite being on home oxygen.
Men were less likely to have spirometry than women; older subjects and current smokers – as opposed to former smokers – were, too. The risk of COPD increases with age and smoking, so the finding was puzzling. For unknown reasons, “there appears to be a bias against ordering spirometry” for some patients, Dr. Eikermann said.
There was no outside funding for the work, and the investigators had no disclosures.
Key clinical point:
Major finding: Only 29% of patients diagnosed with chronic obstructive pulmonary disease (COPD) at two clinics underwent spirometry. Of those diagnosed by spirometry, 32% didn’t meet the gold-standard Global Initiative for Chronic Obstructive Lung Disease (GOLD) diagnostic criteria by having a postbronchodilator FEV1/FVC of less than 70%.
Data source: Review of 65 COPD cases treated at two primary care clinics.
Disclosures: There was no outside funding for the work, and the investigators had no disclosures.
HIV hospitalizations continue to decline
The total number of HIV hospitalizations fell by a third during 2000-2013, even though the number of people living with HIV increased by more than 50%, according to an investigation by the Agency for Healthcare Research and Quality.
“To some extent, the considerable reduction in hospital utilization by persons with HIV disease may be attributed to the diffusion of new antiretroviral medications and the enhanced ability of clinicians to control viral replication,” wrote investigator Fred Hellinger, PhD, of AHRQ’s Center for Delivery, Organization, and Markets (Med Care. 2016 Jun;54[6]:639-44).
Dr. Hellinger used his agency’s State Inpatient Database to collect data on all HIV-related hospital admissions from California, Florida, New Jersey, New York, and South Carolina during 2000-2013. Overall, people with HIV were 64% less likely to be hospitalized in 2013 than they were in 2000; there was also a slight drop in length of stay.
Meanwhile, the average age of hospitalized HIV patients has risen from 41 to 49 years, and the average number of diagnoses from 6 to more than 12. That’s in part because HIV patients are living longer, and “older patients are generally sicker and have more chronic illnesses ... As HIV patients age, they are being hospitalized for conditions that are not closely related to HIV infection,” Dr. Hellinger said.
“Indeed, the principal diagnosis for almost two-thirds of the HIV patients hospitalized in 2013 in our sample was not HIV infection, and as time passes, the mix of diagnoses recorded for hospitalized patients with HIV is likely to resemble the mix of diagnoses found in the general population of hospitalized patients,” he wrote.
U.S. HIV spending continues to go up, but while the number of patients covered by Medicaid has fallen, the number treated by Medicare has risen 50%, reflecting the increase in average life span.
There has not been much demographic change among HIV inpatients. About half are black, a quarter white, and slightly less than one-fifth Hispanic. One-third are women. More than 1.1 million Americans are living with HIV, and 50,000 are newly infected each year.
Dr. Hellinger had no conflicts of interest.
The total number of HIV hospitalizations fell by a third during 2000-2013, even though the number of people living with HIV increased by more than 50%, according to an investigation by the Agency for Healthcare Research and Quality.
“To some extent, the considerable reduction in hospital utilization by persons with HIV disease may be attributed to the diffusion of new antiretroviral medications and the enhanced ability of clinicians to control viral replication,” wrote investigator Fred Hellinger, PhD, of AHRQ’s Center for Delivery, Organization, and Markets (Med Care. 2016 Jun;54[6]:639-44).
Dr. Hellinger used his agency’s State Inpatient Database to collect data on all HIV-related hospital admissions from California, Florida, New Jersey, New York, and South Carolina during 2000-2013. Overall, people with HIV were 64% less likely to be hospitalized in 2013 than they were in 2000; there was also a slight drop in length of stay.
Meanwhile, the average age of hospitalized HIV patients has risen from 41 to 49 years, and the average number of diagnoses from 6 to more than 12. That’s in part because HIV patients are living longer, and “older patients are generally sicker and have more chronic illnesses ... As HIV patients age, they are being hospitalized for conditions that are not closely related to HIV infection,” Dr. Hellinger said.
“Indeed, the principal diagnosis for almost two-thirds of the HIV patients hospitalized in 2013 in our sample was not HIV infection, and as time passes, the mix of diagnoses recorded for hospitalized patients with HIV is likely to resemble the mix of diagnoses found in the general population of hospitalized patients,” he wrote.
U.S. HIV spending continues to go up, but while the number of patients covered by Medicaid has fallen, the number treated by Medicare has risen 50%, reflecting the increase in average life span.
There has not been much demographic change among HIV inpatients. About half are black, a quarter white, and slightly less than one-fifth Hispanic. One-third are women. More than 1.1 million Americans are living with HIV, and 50,000 are newly infected each year.
Dr. Hellinger had no conflicts of interest.
The total number of HIV hospitalizations fell by a third during 2000-2013, even though the number of people living with HIV increased by more than 50%, according to an investigation by the Agency for Healthcare Research and Quality.
“To some extent, the considerable reduction in hospital utilization by persons with HIV disease may be attributed to the diffusion of new antiretroviral medications and the enhanced ability of clinicians to control viral replication,” wrote investigator Fred Hellinger, PhD, of AHRQ’s Center for Delivery, Organization, and Markets (Med Care. 2016 Jun;54[6]:639-44).
Dr. Hellinger used his agency’s State Inpatient Database to collect data on all HIV-related hospital admissions from California, Florida, New Jersey, New York, and South Carolina during 2000-2013. Overall, people with HIV were 64% less likely to be hospitalized in 2013 than they were in 2000; there was also a slight drop in length of stay.
Meanwhile, the average age of hospitalized HIV patients has risen from 41 to 49 years, and the average number of diagnoses from 6 to more than 12. That’s in part because HIV patients are living longer, and “older patients are generally sicker and have more chronic illnesses ... As HIV patients age, they are being hospitalized for conditions that are not closely related to HIV infection,” Dr. Hellinger said.
“Indeed, the principal diagnosis for almost two-thirds of the HIV patients hospitalized in 2013 in our sample was not HIV infection, and as time passes, the mix of diagnoses recorded for hospitalized patients with HIV is likely to resemble the mix of diagnoses found in the general population of hospitalized patients,” he wrote.
U.S. HIV spending continues to go up, but while the number of patients covered by Medicaid has fallen, the number treated by Medicare has risen 50%, reflecting the increase in average life span.
There has not been much demographic change among HIV inpatients. About half are black, a quarter white, and slightly less than one-fifth Hispanic. One-third are women. More than 1.1 million Americans are living with HIV, and 50,000 are newly infected each year.
Dr. Hellinger had no conflicts of interest.
FROM MEDICAL CARE
Key clinical point:
Major finding: People with HIV were 64% less likely to be hospitalized in 2013 than they were in 2000.
Data source: Review of HIV-related hospitalizations in five U.S. states.
Disclosures: The Agency for Healthcare Research and Quality funded the work. The investigator had no disclosures.
Psych issues adding to pediatric hospitalization costs
Although pediatric hospitalizations are driven mostly by medical costs, comorbid psychiatric problems are increasingly adding to the expense, according to a review of 3,114,099 hospitalizations at 33 children’s hospitals in the United States from 2005 to 2014.
For pediatric hospitalizations without a psychiatric diagnosis, costs rose from $3,696 to $4,150 per day over the past decade. For medical stays with a psychiatric diagnosis, the price rose from $2,694 to $3,393 per day, a higher percent change. Overall, the cost of hospitalizing sick children with comorbid psychiatric diagnoses increased from $671 million to $1.6 billion.
The “strategic planning to meet the rising demand for psychiatric care in tertiary care children’s hospitals should place high priority on the needs of children with a primary medical condition and co-occurring psychiatric disorders,” said investigators led by Bonnie Zima, MD, from the University of California, Los Angeles, Semel Institute for Neuroscience and Human Behavior (Pediatrics. 2016 Oct 21. doi: 10.1542/peds.2016-0909).
“From 2005 through 2014 ... there was significant cumulative percent increase in total number of hospitalizations, hospital days, and hospital costs for all patients. Of the total hospitalizations, 18.3% (568,449) were associated with a psychiatric disorder, either primary or secondary,” they noted.
Meanwhile, hospitalizations for psychiatric-only diagnoses were minimal, just 3.6% of the total with the most common problems again being depression, anxiety, and suicide and self-injury. “Hospital resource use for only psychiatric disorders declined, consistent with the national shift to managed care for behavioral health services,” the investigators said.
“Collectively, these data will further guide strategic planning by children’s hospitals as they strive to integrate mental health care into their health care systems. Together, these findings … underscore the need for quality improvement interventions that target improving linkage with community mental health care after pediatric hospitalization,” they said.
The National Institutes of Health funded the study. Dr. Zima was supported by the National Institute of Mental Health and Behavioral Health Centers of Excellence for California. Dr. Naomi S. Bardach and Dr. Tumaini R. Coker were supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development. Dr. Jay G. Berry was supported by the Agency for Healthcare Research and Quality. The authors had no conflicts of interest.
Although pediatric hospitalizations are driven mostly by medical costs, comorbid psychiatric problems are increasingly adding to the expense, according to a review of 3,114,099 hospitalizations at 33 children’s hospitals in the United States from 2005 to 2014.
For pediatric hospitalizations without a psychiatric diagnosis, costs rose from $3,696 to $4,150 per day over the past decade. For medical stays with a psychiatric diagnosis, the price rose from $2,694 to $3,393 per day, a higher percent change. Overall, the cost of hospitalizing sick children with comorbid psychiatric diagnoses increased from $671 million to $1.6 billion.
The “strategic planning to meet the rising demand for psychiatric care in tertiary care children’s hospitals should place high priority on the needs of children with a primary medical condition and co-occurring psychiatric disorders,” said investigators led by Bonnie Zima, MD, from the University of California, Los Angeles, Semel Institute for Neuroscience and Human Behavior (Pediatrics. 2016 Oct 21. doi: 10.1542/peds.2016-0909).
“From 2005 through 2014 ... there was significant cumulative percent increase in total number of hospitalizations, hospital days, and hospital costs for all patients. Of the total hospitalizations, 18.3% (568,449) were associated with a psychiatric disorder, either primary or secondary,” they noted.
Meanwhile, hospitalizations for psychiatric-only diagnoses were minimal, just 3.6% of the total with the most common problems again being depression, anxiety, and suicide and self-injury. “Hospital resource use for only psychiatric disorders declined, consistent with the national shift to managed care for behavioral health services,” the investigators said.
“Collectively, these data will further guide strategic planning by children’s hospitals as they strive to integrate mental health care into their health care systems. Together, these findings … underscore the need for quality improvement interventions that target improving linkage with community mental health care after pediatric hospitalization,” they said.
The National Institutes of Health funded the study. Dr. Zima was supported by the National Institute of Mental Health and Behavioral Health Centers of Excellence for California. Dr. Naomi S. Bardach and Dr. Tumaini R. Coker were supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development. Dr. Jay G. Berry was supported by the Agency for Healthcare Research and Quality. The authors had no conflicts of interest.
Although pediatric hospitalizations are driven mostly by medical costs, comorbid psychiatric problems are increasingly adding to the expense, according to a review of 3,114,099 hospitalizations at 33 children’s hospitals in the United States from 2005 to 2014.
For pediatric hospitalizations without a psychiatric diagnosis, costs rose from $3,696 to $4,150 per day over the past decade. For medical stays with a psychiatric diagnosis, the price rose from $2,694 to $3,393 per day, a higher percent change. Overall, the cost of hospitalizing sick children with comorbid psychiatric diagnoses increased from $671 million to $1.6 billion.
The “strategic planning to meet the rising demand for psychiatric care in tertiary care children’s hospitals should place high priority on the needs of children with a primary medical condition and co-occurring psychiatric disorders,” said investigators led by Bonnie Zima, MD, from the University of California, Los Angeles, Semel Institute for Neuroscience and Human Behavior (Pediatrics. 2016 Oct 21. doi: 10.1542/peds.2016-0909).
“From 2005 through 2014 ... there was significant cumulative percent increase in total number of hospitalizations, hospital days, and hospital costs for all patients. Of the total hospitalizations, 18.3% (568,449) were associated with a psychiatric disorder, either primary or secondary,” they noted.
Meanwhile, hospitalizations for psychiatric-only diagnoses were minimal, just 3.6% of the total with the most common problems again being depression, anxiety, and suicide and self-injury. “Hospital resource use for only psychiatric disorders declined, consistent with the national shift to managed care for behavioral health services,” the investigators said.
“Collectively, these data will further guide strategic planning by children’s hospitals as they strive to integrate mental health care into their health care systems. Together, these findings … underscore the need for quality improvement interventions that target improving linkage with community mental health care after pediatric hospitalization,” they said.
The National Institutes of Health funded the study. Dr. Zima was supported by the National Institute of Mental Health and Behavioral Health Centers of Excellence for California. Dr. Naomi S. Bardach and Dr. Tumaini R. Coker were supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development. Dr. Jay G. Berry was supported by the Agency for Healthcare Research and Quality. The authors had no conflicts of interest.
FROM PEDIATRICS
Key clinical point:
Major finding: For pediatric hospitalizations without a psychiatric diagnosis, costs rose during the past decade from $3,696 to $4,150 per day. For medical stays with a psychiatric diagnosis, the price rose from $2,694 to $3,393 per day.
Data source: Review of 3,114,099 hospitalizations at 33 children’s hospitals in the United States during 2005-2014
Disclosures: The National Institutes of Health funded the study. Dr. Zima was supported by the National Institute of Mental Health and Behavioral Health Centers of Excellence for California. Dr. Naomi S. Bardach and Dr. Tumaini R. Coker were supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development. Dr. Jay G. Berry was supported by the Agency for Healthcare Research and Quality. The authors had no conflicts of interest.
ACOS under-recognized, under-treated
Exacerbations in bronchodilator-responsive asthma–chronic obstructive pulmonary disease overlap syndrome (ACOS) were more frequent and severe than in COPD with emphysema, but only a minority of patients were treated to prevent them, in a review of 1,005 patients from the Annals of the American Thoracic Society.
All the subjects were current or former smokers culled from the COPDGene Study, a multicenter observational study looking for the genetic roots of COPD susceptibility; 385 patients met the investigators’ criteria for ACOS with bronchodilator response (ACOS-BDR), which included a history of asthma or hay fever, airway obstruction with significant bronchodilator responsiveness, and less then 15% emphysema on chest CT.
Another 620 subjects met criteria for COPD with emphysema, including airway obstruction without bronchodilator reversibility, and more than 15% emphysema on chest CT (Ann Am Thorac Soc. 2016 Sep;13(9):1483-9).
Although the ACOS patients had better lung function, they had similar severity and frequency of exacerbations, compared with the COPD group. After adjustment for forced expiratory volume in 1 second percent predicted and other factors, the patients with ACOS-BDR were actually more likely to have severe and frequent exacerbations. Possible explanations for this are that they were more likely to smoke and have gastroesophageal reflux disease and obstructive sleep apnea, all of which increase the risk of exacerbations.
Even so, ACOS-BDR patients were less likely to be on a long-acting beta-agonist (6.8% versus 13.9%); a long-acting muscarinic antagonist (20% versus 60.8%); or a combination long-acting beta-agonist/inhaled corticosteroid (29.9% versus 55.6%).
“Only a small percentage of them were being treated ... Early and aggressive treatment with combination therapy may help alleviate symptoms and decrease exacerbations,” said investigators led by James Cosentino, DO, of Temple University School of Medicine, Philadelphia. Patients with ACOS “are a particularly high-risk group.” They deserve “special attention, and practitioners need to be diligent in evaluation of them.”
ACOS is being increasingly recognized as a distinct clinical entity with perhaps a worse prognosis than either asthma or COPD alone. The goal of the study was to better characterize the disease.
To that end, the team found four features that seemed to distinguish ACOS-BDR from COPD with emphysema: ACOS-BDR patients were younger (60.6 versus 65.9 years old); heavier (body mass index 29.6 versus 25.1 kg/m2; more likely to be African American (26.8% versus 14.4%); and more likely to be current smokers (50.9% versus 20.7%).
It’s “likely that current smoking in subjects with ACOS, coupled with the long duration of asthma, leads to inflammation and small airway remodeling with development of symptoms earlier in the disease course than that seen in those with COPD with emphysema,” the investigators said.
“Early and aggressive treatment with combination therapy may help alleviate symptoms and decrease exacerbations. Recognition and treatment of comorbidities and aggressive smoking cessation may also play a key role in preventing exacerbations and alleviating the morbidity associated with ACOS; however, future studies on the treatment of ACOS are needed,” they said.
The majority of subjects with ACOS-BDR met criteria for Global Initiative for Chronic Obstructive Lung Disease grade B, indicating a high degree of symptoms despite less severe airflow obstruction.
The funding source wasn’t reported. Dr. Cosentino had no conflicts. Other authors disclosed personal fees from Concert Pharmaceuticals, CSA Medical, CSL Behring, Gala Therapeutics, and Novartis.
The importance of this study is that it used readily available metrics to define ACOS in a COPD population. Although diffusion capacity was not reported, quantification of emphysema on chest CT scans combined with history and spirometry provide a reasonable approach to distinguishing ACOS-BDR from COPD with emphysema.
Although subjects with COPD had smoked more heavily as measured by cigarette pack-years, subjects with ACOS were much more likely to be current smokers... Subjects with ACOS also had a higher prevalence of comorbidities such as sleep apnea, diabetes mellitus, hypertension, and hypercholesterolemia as compared with patients with COPD. Having a higher BMI, to near obesity, and a greater prevalence of gastroesophageal reflux disease raises questions related to diet, lifestyle, and nutrition as potential contributors to ACOS pathophysiology.
In the future, the use of diagnostic terms such as “asthma,” “COPD,” and “ACOS,” will likely give way to the more unifying diagnosis of obstructive airway disease (OAD)... OAD would be further delineated on the basis of molecular phenotyping, genomic, and systems biology approaches, in combination with more traditional clinical and physiological parameters... This new mindset can help us solve the problem of obstructive airway disease taxonomy and develop not only better treatments, but eventually invent lasting cures – if we are so lucky.
Amir Zeki, MD , is an assistant professor in the Division of Pulmonary, Critical Care, and Sleep Medicine at the University of California, Davis. Nizar Jarjour, MD , is a professor of medicine and head of the allergy, pulmonary, and critical care division at the University of Wisconsin, Madison. Dr. Zeki had no disclosures. Dr. Jarjour reported consulting fees from AstraZeneca, Daiichi Sankyo, and Teva. They made their comments in an editorial ( Ann Am Thorac Soc. 2016 Sep;13(9):1440-2 ).
The importance of this study is that it used readily available metrics to define ACOS in a COPD population. Although diffusion capacity was not reported, quantification of emphysema on chest CT scans combined with history and spirometry provide a reasonable approach to distinguishing ACOS-BDR from COPD with emphysema.
Although subjects with COPD had smoked more heavily as measured by cigarette pack-years, subjects with ACOS were much more likely to be current smokers... Subjects with ACOS also had a higher prevalence of comorbidities such as sleep apnea, diabetes mellitus, hypertension, and hypercholesterolemia as compared with patients with COPD. Having a higher BMI, to near obesity, and a greater prevalence of gastroesophageal reflux disease raises questions related to diet, lifestyle, and nutrition as potential contributors to ACOS pathophysiology.
In the future, the use of diagnostic terms such as “asthma,” “COPD,” and “ACOS,” will likely give way to the more unifying diagnosis of obstructive airway disease (OAD)... OAD would be further delineated on the basis of molecular phenotyping, genomic, and systems biology approaches, in combination with more traditional clinical and physiological parameters... This new mindset can help us solve the problem of obstructive airway disease taxonomy and develop not only better treatments, but eventually invent lasting cures – if we are so lucky.
Amir Zeki, MD , is an assistant professor in the Division of Pulmonary, Critical Care, and Sleep Medicine at the University of California, Davis. Nizar Jarjour, MD , is a professor of medicine and head of the allergy, pulmonary, and critical care division at the University of Wisconsin, Madison. Dr. Zeki had no disclosures. Dr. Jarjour reported consulting fees from AstraZeneca, Daiichi Sankyo, and Teva. They made their comments in an editorial ( Ann Am Thorac Soc. 2016 Sep;13(9):1440-2 ).
The importance of this study is that it used readily available metrics to define ACOS in a COPD population. Although diffusion capacity was not reported, quantification of emphysema on chest CT scans combined with history and spirometry provide a reasonable approach to distinguishing ACOS-BDR from COPD with emphysema.
Although subjects with COPD had smoked more heavily as measured by cigarette pack-years, subjects with ACOS were much more likely to be current smokers... Subjects with ACOS also had a higher prevalence of comorbidities such as sleep apnea, diabetes mellitus, hypertension, and hypercholesterolemia as compared with patients with COPD. Having a higher BMI, to near obesity, and a greater prevalence of gastroesophageal reflux disease raises questions related to diet, lifestyle, and nutrition as potential contributors to ACOS pathophysiology.
In the future, the use of diagnostic terms such as “asthma,” “COPD,” and “ACOS,” will likely give way to the more unifying diagnosis of obstructive airway disease (OAD)... OAD would be further delineated on the basis of molecular phenotyping, genomic, and systems biology approaches, in combination with more traditional clinical and physiological parameters... This new mindset can help us solve the problem of obstructive airway disease taxonomy and develop not only better treatments, but eventually invent lasting cures – if we are so lucky.
Amir Zeki, MD , is an assistant professor in the Division of Pulmonary, Critical Care, and Sleep Medicine at the University of California, Davis. Nizar Jarjour, MD , is a professor of medicine and head of the allergy, pulmonary, and critical care division at the University of Wisconsin, Madison. Dr. Zeki had no disclosures. Dr. Jarjour reported consulting fees from AstraZeneca, Daiichi Sankyo, and Teva. They made their comments in an editorial ( Ann Am Thorac Soc. 2016 Sep;13(9):1440-2 ).
Exacerbations in bronchodilator-responsive asthma–chronic obstructive pulmonary disease overlap syndrome (ACOS) were more frequent and severe than in COPD with emphysema, but only a minority of patients were treated to prevent them, in a review of 1,005 patients from the Annals of the American Thoracic Society.
All the subjects were current or former smokers culled from the COPDGene Study, a multicenter observational study looking for the genetic roots of COPD susceptibility; 385 patients met the investigators’ criteria for ACOS with bronchodilator response (ACOS-BDR), which included a history of asthma or hay fever, airway obstruction with significant bronchodilator responsiveness, and less then 15% emphysema on chest CT.
Another 620 subjects met criteria for COPD with emphysema, including airway obstruction without bronchodilator reversibility, and more than 15% emphysema on chest CT (Ann Am Thorac Soc. 2016 Sep;13(9):1483-9).
Although the ACOS patients had better lung function, they had similar severity and frequency of exacerbations, compared with the COPD group. After adjustment for forced expiratory volume in 1 second percent predicted and other factors, the patients with ACOS-BDR were actually more likely to have severe and frequent exacerbations. Possible explanations for this are that they were more likely to smoke and have gastroesophageal reflux disease and obstructive sleep apnea, all of which increase the risk of exacerbations.
Even so, ACOS-BDR patients were less likely to be on a long-acting beta-agonist (6.8% versus 13.9%); a long-acting muscarinic antagonist (20% versus 60.8%); or a combination long-acting beta-agonist/inhaled corticosteroid (29.9% versus 55.6%).
“Only a small percentage of them were being treated ... Early and aggressive treatment with combination therapy may help alleviate symptoms and decrease exacerbations,” said investigators led by James Cosentino, DO, of Temple University School of Medicine, Philadelphia. Patients with ACOS “are a particularly high-risk group.” They deserve “special attention, and practitioners need to be diligent in evaluation of them.”
ACOS is being increasingly recognized as a distinct clinical entity with perhaps a worse prognosis than either asthma or COPD alone. The goal of the study was to better characterize the disease.
To that end, the team found four features that seemed to distinguish ACOS-BDR from COPD with emphysema: ACOS-BDR patients were younger (60.6 versus 65.9 years old); heavier (body mass index 29.6 versus 25.1 kg/m2; more likely to be African American (26.8% versus 14.4%); and more likely to be current smokers (50.9% versus 20.7%).
It’s “likely that current smoking in subjects with ACOS, coupled with the long duration of asthma, leads to inflammation and small airway remodeling with development of symptoms earlier in the disease course than that seen in those with COPD with emphysema,” the investigators said.
“Early and aggressive treatment with combination therapy may help alleviate symptoms and decrease exacerbations. Recognition and treatment of comorbidities and aggressive smoking cessation may also play a key role in preventing exacerbations and alleviating the morbidity associated with ACOS; however, future studies on the treatment of ACOS are needed,” they said.
The majority of subjects with ACOS-BDR met criteria for Global Initiative for Chronic Obstructive Lung Disease grade B, indicating a high degree of symptoms despite less severe airflow obstruction.
The funding source wasn’t reported. Dr. Cosentino had no conflicts. Other authors disclosed personal fees from Concert Pharmaceuticals, CSA Medical, CSL Behring, Gala Therapeutics, and Novartis.
Exacerbations in bronchodilator-responsive asthma–chronic obstructive pulmonary disease overlap syndrome (ACOS) were more frequent and severe than in COPD with emphysema, but only a minority of patients were treated to prevent them, in a review of 1,005 patients from the Annals of the American Thoracic Society.
All the subjects were current or former smokers culled from the COPDGene Study, a multicenter observational study looking for the genetic roots of COPD susceptibility; 385 patients met the investigators’ criteria for ACOS with bronchodilator response (ACOS-BDR), which included a history of asthma or hay fever, airway obstruction with significant bronchodilator responsiveness, and less then 15% emphysema on chest CT.
Another 620 subjects met criteria for COPD with emphysema, including airway obstruction without bronchodilator reversibility, and more than 15% emphysema on chest CT (Ann Am Thorac Soc. 2016 Sep;13(9):1483-9).
Although the ACOS patients had better lung function, they had similar severity and frequency of exacerbations, compared with the COPD group. After adjustment for forced expiratory volume in 1 second percent predicted and other factors, the patients with ACOS-BDR were actually more likely to have severe and frequent exacerbations. Possible explanations for this are that they were more likely to smoke and have gastroesophageal reflux disease and obstructive sleep apnea, all of which increase the risk of exacerbations.
Even so, ACOS-BDR patients were less likely to be on a long-acting beta-agonist (6.8% versus 13.9%); a long-acting muscarinic antagonist (20% versus 60.8%); or a combination long-acting beta-agonist/inhaled corticosteroid (29.9% versus 55.6%).
“Only a small percentage of them were being treated ... Early and aggressive treatment with combination therapy may help alleviate symptoms and decrease exacerbations,” said investigators led by James Cosentino, DO, of Temple University School of Medicine, Philadelphia. Patients with ACOS “are a particularly high-risk group.” They deserve “special attention, and practitioners need to be diligent in evaluation of them.”
ACOS is being increasingly recognized as a distinct clinical entity with perhaps a worse prognosis than either asthma or COPD alone. The goal of the study was to better characterize the disease.
To that end, the team found four features that seemed to distinguish ACOS-BDR from COPD with emphysema: ACOS-BDR patients were younger (60.6 versus 65.9 years old); heavier (body mass index 29.6 versus 25.1 kg/m2; more likely to be African American (26.8% versus 14.4%); and more likely to be current smokers (50.9% versus 20.7%).
It’s “likely that current smoking in subjects with ACOS, coupled with the long duration of asthma, leads to inflammation and small airway remodeling with development of symptoms earlier in the disease course than that seen in those with COPD with emphysema,” the investigators said.
“Early and aggressive treatment with combination therapy may help alleviate symptoms and decrease exacerbations. Recognition and treatment of comorbidities and aggressive smoking cessation may also play a key role in preventing exacerbations and alleviating the morbidity associated with ACOS; however, future studies on the treatment of ACOS are needed,” they said.
The majority of subjects with ACOS-BDR met criteria for Global Initiative for Chronic Obstructive Lung Disease grade B, indicating a high degree of symptoms despite less severe airflow obstruction.
The funding source wasn’t reported. Dr. Cosentino had no conflicts. Other authors disclosed personal fees from Concert Pharmaceuticals, CSA Medical, CSL Behring, Gala Therapeutics, and Novartis.
FROM THE ANNALS OF THE AMERICAN THORACIC SOCIETY
Key clinical point:
Major finding: ACOS-BDR patients were less likely to be on a long-acting beta-agonist (6.8% versus 13.9%); a long-acting muscarinic antagonist (20% versus 60.8%); or a combination long-acting beta-agonist/inhaled corticosteroid (29.9% versus 55.6%).
Data source: 1,005 patients from the COPDGene study.
Disclosures: The funding source wasn’t reported. Authors disclosed personal fees from Concert Pharmaceuticals, CSA Medical, CSL Behring, Gala Therapeutics, and Novartis.