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More evidence the flu vaccine may guard against Alzheimer’s
In a large propensity-matched cohort of older adults, those who had received at least one influenza inoculation were 40% less likely than unvaccinated peers to develop AD over the course of 4 years.
“Influenza infection can cause serious health complications, particularly in adults 65 and older. Our study’s findings – that vaccination against the flu virus may also reduce the risk of Alzheimer’s dementia for at least a few years – adds to the already compelling reasons get the flu vaccine annually,” Avram Bukhbinder, MD, of the University of Texas, Houston, said in an interview.
The new findings support earlier work by the same researchers that also suggested a protective effect of flu vaccination on dementia risk.
The latest study was published online in the Journal of Alzheimer’s Disease.
40% lower risk
Prior studies have found a lower risk of dementia of any etiology following influenza vaccination in selected populations, including veterans and patients with serious chronic health conditions.
However, the effect of influenza vaccination on AD risk in a general cohort of older U.S. adults has not been characterized.
Dr. Bukhbinder and colleagues used claims data to create a propensity-matched cohort of 935,887 influenza-vaccinated adults and a like number of unvaccinated adults aged 65 and older.
The median age of the persons in the matched sample was 73.7 years, and 57% were women. All were free of dementia during the 6-year look-back study period.
During median follow-up of 46 months, 47,889 (5.1%) flu-vaccinated adults and 79,630 (8.5%) unvaccinated adults developed AD.
The risk of AD was 40% lower in the vaccinated group (relative risk, 0.60; 95% confidence interval, 0.59-0.61). The absolute risk reduction was 0.034 (95% CI, 0.033-0.035), corresponding to a number needed to treat of 29.4.
Mechanism unclear
“Our study does not address the mechanism(s) underlying the apparent effect of influenza vaccination on Alzheimer’s risk, but we look forward to future research investigating this important question,” Dr. Bukhbinder said.
“One possible mechanism is that, by helping to prevent or mitigate infection with the flu virus and the systemic inflammation that follows such an infection, the flu vaccine helps to decrease the systemic inflammation that may have otherwise occurred,” he explained.
It’s also possible that influenza vaccination may trigger non–influenza-specific changes in the immune system that help to reduce the damage caused by AD pathology, including amyloid plaques and neurofibrillary tangles, he said.
“For example, the influenza vaccine may alter the brain’s immune cells such that they are better at clearing Alzheimer’s pathologies, an effect that has been seen in mice, or it may reprogram these immune cells to respond to Alzheimer’s pathologies in ways that are less likely to damage nearby healthy brain cells, or it may do both,” Dr. Bukhbinder noted.
Alzheimer’s expert weighs in
Heather M. Snyder, PhD, vice president of medical and scientific relations for the Alzheimer’s Association, said this study “suggests that flu vaccination may be valuable for maintaining cognition and memory as we age. This is even more relevant today in the COVID-19 environment.
“It is too early to tell if getting flu vaccine, on its own, can reduce risk of Alzheimer’s. More research is needed to understand the biological mechanisms behind the results in this study,” Dr. Snyder said in an interview.
“For example, it is possible that people who are getting vaccinated also take better care of their health in other ways, and these things add up to lower risk of Alzheimer’s and other dementias,” she noted.
“It is also possible that there are issues related to unequal access and/or vaccine hesitancy and how this may influence the study population and the research results,” Dr. Snyder said.
The study had no specific funding. Dr. Bukhbinder and Dr. Snyder disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
In a large propensity-matched cohort of older adults, those who had received at least one influenza inoculation were 40% less likely than unvaccinated peers to develop AD over the course of 4 years.
“Influenza infection can cause serious health complications, particularly in adults 65 and older. Our study’s findings – that vaccination against the flu virus may also reduce the risk of Alzheimer’s dementia for at least a few years – adds to the already compelling reasons get the flu vaccine annually,” Avram Bukhbinder, MD, of the University of Texas, Houston, said in an interview.
The new findings support earlier work by the same researchers that also suggested a protective effect of flu vaccination on dementia risk.
The latest study was published online in the Journal of Alzheimer’s Disease.
40% lower risk
Prior studies have found a lower risk of dementia of any etiology following influenza vaccination in selected populations, including veterans and patients with serious chronic health conditions.
However, the effect of influenza vaccination on AD risk in a general cohort of older U.S. adults has not been characterized.
Dr. Bukhbinder and colleagues used claims data to create a propensity-matched cohort of 935,887 influenza-vaccinated adults and a like number of unvaccinated adults aged 65 and older.
The median age of the persons in the matched sample was 73.7 years, and 57% were women. All were free of dementia during the 6-year look-back study period.
During median follow-up of 46 months, 47,889 (5.1%) flu-vaccinated adults and 79,630 (8.5%) unvaccinated adults developed AD.
The risk of AD was 40% lower in the vaccinated group (relative risk, 0.60; 95% confidence interval, 0.59-0.61). The absolute risk reduction was 0.034 (95% CI, 0.033-0.035), corresponding to a number needed to treat of 29.4.
Mechanism unclear
“Our study does not address the mechanism(s) underlying the apparent effect of influenza vaccination on Alzheimer’s risk, but we look forward to future research investigating this important question,” Dr. Bukhbinder said.
“One possible mechanism is that, by helping to prevent or mitigate infection with the flu virus and the systemic inflammation that follows such an infection, the flu vaccine helps to decrease the systemic inflammation that may have otherwise occurred,” he explained.
It’s also possible that influenza vaccination may trigger non–influenza-specific changes in the immune system that help to reduce the damage caused by AD pathology, including amyloid plaques and neurofibrillary tangles, he said.
“For example, the influenza vaccine may alter the brain’s immune cells such that they are better at clearing Alzheimer’s pathologies, an effect that has been seen in mice, or it may reprogram these immune cells to respond to Alzheimer’s pathologies in ways that are less likely to damage nearby healthy brain cells, or it may do both,” Dr. Bukhbinder noted.
Alzheimer’s expert weighs in
Heather M. Snyder, PhD, vice president of medical and scientific relations for the Alzheimer’s Association, said this study “suggests that flu vaccination may be valuable for maintaining cognition and memory as we age. This is even more relevant today in the COVID-19 environment.
“It is too early to tell if getting flu vaccine, on its own, can reduce risk of Alzheimer’s. More research is needed to understand the biological mechanisms behind the results in this study,” Dr. Snyder said in an interview.
“For example, it is possible that people who are getting vaccinated also take better care of their health in other ways, and these things add up to lower risk of Alzheimer’s and other dementias,” she noted.
“It is also possible that there are issues related to unequal access and/or vaccine hesitancy and how this may influence the study population and the research results,” Dr. Snyder said.
The study had no specific funding. Dr. Bukhbinder and Dr. Snyder disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
In a large propensity-matched cohort of older adults, those who had received at least one influenza inoculation were 40% less likely than unvaccinated peers to develop AD over the course of 4 years.
“Influenza infection can cause serious health complications, particularly in adults 65 and older. Our study’s findings – that vaccination against the flu virus may also reduce the risk of Alzheimer’s dementia for at least a few years – adds to the already compelling reasons get the flu vaccine annually,” Avram Bukhbinder, MD, of the University of Texas, Houston, said in an interview.
The new findings support earlier work by the same researchers that also suggested a protective effect of flu vaccination on dementia risk.
The latest study was published online in the Journal of Alzheimer’s Disease.
40% lower risk
Prior studies have found a lower risk of dementia of any etiology following influenza vaccination in selected populations, including veterans and patients with serious chronic health conditions.
However, the effect of influenza vaccination on AD risk in a general cohort of older U.S. adults has not been characterized.
Dr. Bukhbinder and colleagues used claims data to create a propensity-matched cohort of 935,887 influenza-vaccinated adults and a like number of unvaccinated adults aged 65 and older.
The median age of the persons in the matched sample was 73.7 years, and 57% were women. All were free of dementia during the 6-year look-back study period.
During median follow-up of 46 months, 47,889 (5.1%) flu-vaccinated adults and 79,630 (8.5%) unvaccinated adults developed AD.
The risk of AD was 40% lower in the vaccinated group (relative risk, 0.60; 95% confidence interval, 0.59-0.61). The absolute risk reduction was 0.034 (95% CI, 0.033-0.035), corresponding to a number needed to treat of 29.4.
Mechanism unclear
“Our study does not address the mechanism(s) underlying the apparent effect of influenza vaccination on Alzheimer’s risk, but we look forward to future research investigating this important question,” Dr. Bukhbinder said.
“One possible mechanism is that, by helping to prevent or mitigate infection with the flu virus and the systemic inflammation that follows such an infection, the flu vaccine helps to decrease the systemic inflammation that may have otherwise occurred,” he explained.
It’s also possible that influenza vaccination may trigger non–influenza-specific changes in the immune system that help to reduce the damage caused by AD pathology, including amyloid plaques and neurofibrillary tangles, he said.
“For example, the influenza vaccine may alter the brain’s immune cells such that they are better at clearing Alzheimer’s pathologies, an effect that has been seen in mice, or it may reprogram these immune cells to respond to Alzheimer’s pathologies in ways that are less likely to damage nearby healthy brain cells, or it may do both,” Dr. Bukhbinder noted.
Alzheimer’s expert weighs in
Heather M. Snyder, PhD, vice president of medical and scientific relations for the Alzheimer’s Association, said this study “suggests that flu vaccination may be valuable for maintaining cognition and memory as we age. This is even more relevant today in the COVID-19 environment.
“It is too early to tell if getting flu vaccine, on its own, can reduce risk of Alzheimer’s. More research is needed to understand the biological mechanisms behind the results in this study,” Dr. Snyder said in an interview.
“For example, it is possible that people who are getting vaccinated also take better care of their health in other ways, and these things add up to lower risk of Alzheimer’s and other dementias,” she noted.
“It is also possible that there are issues related to unequal access and/or vaccine hesitancy and how this may influence the study population and the research results,” Dr. Snyder said.
The study had no specific funding. Dr. Bukhbinder and Dr. Snyder disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF ALZHEIMER’S DISEASE
Anorexia linked to notable shrinkage of key brain structures
, a new brain imaging study shows.
The reductions of cortical thickness, subcortical volumes, and cortical surface area were “very pronounced in acutely underweight anorexia,” Stefan Ehrlich, MD, PhD, head of the Eating Disorder Treatment and Research Center, Technical University, Dresden, Germany, told this news organization.
Yet even a “partial weight gain brings some normalization of these shrinkages. From this it can be deduced that a fast/early normalization of weight is also very important for brain health,” said Dr. Ehrlich.
The study was published online in Biological Psychiatry.
‘A wake-up call’
Researchers with the international ENIGMA Eating Disorders Working Group analyzed T1-weighted structural magnetic resonance imaging scans for nearly 2,000 people with AN (including those in recovery) and healthy controls across 22 sites worldwide.
In the AN sample, reductions in cortical thickness, subcortical volumes, and, to a lesser extent, cortical surface area, were “sizable (Cohen’s d up to 0.95), widespread, and co-localized with hub regions,” they report.
These reductions were two and four times larger than the abnormalities in brain size and shape seen in patients with other mental illnesses, the researchers note.
Noting the harmful impact of anorexia-related undernutrition on the brain, these deficits were associated with lower body mass index in the AN sample and were less severe in partially weight-restored patients – implying that, with appropriate early treatment and support, the brain might be able to repair itself, the investigators note.
“This really is a wake-up call, showing the need for early interventions for people with eating disorders,” Paul Thompson, PhD, author and lead scientist for the ENIGMA Consortium, said in a news release.
“The international scale of this work is extraordinary. Scientists from 22 centers worldwide pooled their brain scans to create the most detailed picture to date of how anorexia affects the brain,” Dr. Thompson added.
“The brain changes in anorexia were more severe than in other any psychiatric condition we have studied. Effects of treatments and interventions can now be evaluated, using these new brain maps as a reference,” he noted.
Immediate clinical implications
Reached for comment, Allison Eliscu, MD, chief of the division of adolescent medicine, department of pediatrics, at Stony Brook (N.Y.) University, said the findings have immediate implications for clinical care.
“When we talk to our patients and the parents, a lot of them focus on things that they can see, such as the way they look. It adds a lot to the conversation to be able to say: You’re obviously not seeing these changes in the brain, but they’re happening and could be potentially long term if you don’t start weight restoring, or if you weight restore and then continue to drop again,” Dr. Eliscu said in an interview.
The findings, she said, really do highlight what anorexia can do to the brain.
“Adolescents need to know, anorexia can absolutely decrease the size of your brain in different areas; you’re not just losing weight in your belly and your thighs, you’re losing weight in the brain as well and that’s really concerning,” said Dr. Eliscu.
The study had no commercial funding. The authors and Dr. Eliscu report no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
, a new brain imaging study shows.
The reductions of cortical thickness, subcortical volumes, and cortical surface area were “very pronounced in acutely underweight anorexia,” Stefan Ehrlich, MD, PhD, head of the Eating Disorder Treatment and Research Center, Technical University, Dresden, Germany, told this news organization.
Yet even a “partial weight gain brings some normalization of these shrinkages. From this it can be deduced that a fast/early normalization of weight is also very important for brain health,” said Dr. Ehrlich.
The study was published online in Biological Psychiatry.
‘A wake-up call’
Researchers with the international ENIGMA Eating Disorders Working Group analyzed T1-weighted structural magnetic resonance imaging scans for nearly 2,000 people with AN (including those in recovery) and healthy controls across 22 sites worldwide.
In the AN sample, reductions in cortical thickness, subcortical volumes, and, to a lesser extent, cortical surface area, were “sizable (Cohen’s d up to 0.95), widespread, and co-localized with hub regions,” they report.
These reductions were two and four times larger than the abnormalities in brain size and shape seen in patients with other mental illnesses, the researchers note.
Noting the harmful impact of anorexia-related undernutrition on the brain, these deficits were associated with lower body mass index in the AN sample and were less severe in partially weight-restored patients – implying that, with appropriate early treatment and support, the brain might be able to repair itself, the investigators note.
“This really is a wake-up call, showing the need for early interventions for people with eating disorders,” Paul Thompson, PhD, author and lead scientist for the ENIGMA Consortium, said in a news release.
“The international scale of this work is extraordinary. Scientists from 22 centers worldwide pooled their brain scans to create the most detailed picture to date of how anorexia affects the brain,” Dr. Thompson added.
“The brain changes in anorexia were more severe than in other any psychiatric condition we have studied. Effects of treatments and interventions can now be evaluated, using these new brain maps as a reference,” he noted.
Immediate clinical implications
Reached for comment, Allison Eliscu, MD, chief of the division of adolescent medicine, department of pediatrics, at Stony Brook (N.Y.) University, said the findings have immediate implications for clinical care.
“When we talk to our patients and the parents, a lot of them focus on things that they can see, such as the way they look. It adds a lot to the conversation to be able to say: You’re obviously not seeing these changes in the brain, but they’re happening and could be potentially long term if you don’t start weight restoring, or if you weight restore and then continue to drop again,” Dr. Eliscu said in an interview.
The findings, she said, really do highlight what anorexia can do to the brain.
“Adolescents need to know, anorexia can absolutely decrease the size of your brain in different areas; you’re not just losing weight in your belly and your thighs, you’re losing weight in the brain as well and that’s really concerning,” said Dr. Eliscu.
The study had no commercial funding. The authors and Dr. Eliscu report no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
, a new brain imaging study shows.
The reductions of cortical thickness, subcortical volumes, and cortical surface area were “very pronounced in acutely underweight anorexia,” Stefan Ehrlich, MD, PhD, head of the Eating Disorder Treatment and Research Center, Technical University, Dresden, Germany, told this news organization.
Yet even a “partial weight gain brings some normalization of these shrinkages. From this it can be deduced that a fast/early normalization of weight is also very important for brain health,” said Dr. Ehrlich.
The study was published online in Biological Psychiatry.
‘A wake-up call’
Researchers with the international ENIGMA Eating Disorders Working Group analyzed T1-weighted structural magnetic resonance imaging scans for nearly 2,000 people with AN (including those in recovery) and healthy controls across 22 sites worldwide.
In the AN sample, reductions in cortical thickness, subcortical volumes, and, to a lesser extent, cortical surface area, were “sizable (Cohen’s d up to 0.95), widespread, and co-localized with hub regions,” they report.
These reductions were two and four times larger than the abnormalities in brain size and shape seen in patients with other mental illnesses, the researchers note.
Noting the harmful impact of anorexia-related undernutrition on the brain, these deficits were associated with lower body mass index in the AN sample and were less severe in partially weight-restored patients – implying that, with appropriate early treatment and support, the brain might be able to repair itself, the investigators note.
“This really is a wake-up call, showing the need for early interventions for people with eating disorders,” Paul Thompson, PhD, author and lead scientist for the ENIGMA Consortium, said in a news release.
“The international scale of this work is extraordinary. Scientists from 22 centers worldwide pooled their brain scans to create the most detailed picture to date of how anorexia affects the brain,” Dr. Thompson added.
“The brain changes in anorexia were more severe than in other any psychiatric condition we have studied. Effects of treatments and interventions can now be evaluated, using these new brain maps as a reference,” he noted.
Immediate clinical implications
Reached for comment, Allison Eliscu, MD, chief of the division of adolescent medicine, department of pediatrics, at Stony Brook (N.Y.) University, said the findings have immediate implications for clinical care.
“When we talk to our patients and the parents, a lot of them focus on things that they can see, such as the way they look. It adds a lot to the conversation to be able to say: You’re obviously not seeing these changes in the brain, but they’re happening and could be potentially long term if you don’t start weight restoring, or if you weight restore and then continue to drop again,” Dr. Eliscu said in an interview.
The findings, she said, really do highlight what anorexia can do to the brain.
“Adolescents need to know, anorexia can absolutely decrease the size of your brain in different areas; you’re not just losing weight in your belly and your thighs, you’re losing weight in the brain as well and that’s really concerning,” said Dr. Eliscu.
The study had no commercial funding. The authors and Dr. Eliscu report no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
FROM BIOLOGICAL PSYCHIATRY
FDA unveils 5-year plan for ALS and other neurodegenerative diseases
The agency’s Action Plan for Rare Neurodegenerative Diseases including Amyotrophic Lateral Sclerosis (ALS) aims to advance the development of safe and effective medical products and facilitate patient access to novel treatments.
“The effects of rare neurodegenerative diseases are devastating, with very few effective therapeutic options available to patients. We recognize the urgent need for new treatments that can both improve and extend the lives of people diagnosed with these diseases,” FDA Commissioner Robert M. Califf, MD, said in a news release.
“To face that challenge and to accelerate drug development, we need innovative approaches to better understand these diseases while also building on current scientific and research capabilities,” Dr. Califf acknowledged.
“This action plan, especially including the use of public-private partnerships and direct involvement of patients, will ensure the FDA is working toward meeting the task set forth by Congress to enhance the quality of life for those suffering by facilitating access to new therapies,” Dr. Califf added.
Blueprint to ‘aggressively’ move forward
The action plan represents a “blueprint” for how the agency will “aggressively” move forward to address challenges in drug development for rare neurodegenerative diseases to improve patient health, the FDA said.
The plan was created in accordance with provisions in the Accelerating Access to Critical Therapies for ALS Act (ACT for ALS) that President Biden signed into law in late 2021.
Targeted activities include establishing the FDA Rare Neurodegenerative Diseases Task Force and the public-private partnership for rare neurodegenerative diseases, developing disease-specific science strategies over the next 5 years, and leveraging ongoing FDA regulatory science efforts.
The ALS Science Strategy is part of the plan focused specifically on ALS. It provides a “forward-leaning” framework for FDA activities, which include efforts to improve characterization of disease pathogenesis and natural history, boost clinical trial infrastructure and agility to enable early selection of promising therapeutic candidates for further development, optimize clinical trial design, improve access to the trials, streamline clinical trial operations, and reduce the time and cost of drug development.
The FDA says patient engagement, public workshops, research projects, coordination across FDA centers and offices, and collaboration with the National Institutes of Health will be key to the success of implementation of the ALS Science Strategy.
A version of this article first appeared on Medscape.com.
The agency’s Action Plan for Rare Neurodegenerative Diseases including Amyotrophic Lateral Sclerosis (ALS) aims to advance the development of safe and effective medical products and facilitate patient access to novel treatments.
“The effects of rare neurodegenerative diseases are devastating, with very few effective therapeutic options available to patients. We recognize the urgent need for new treatments that can both improve and extend the lives of people diagnosed with these diseases,” FDA Commissioner Robert M. Califf, MD, said in a news release.
“To face that challenge and to accelerate drug development, we need innovative approaches to better understand these diseases while also building on current scientific and research capabilities,” Dr. Califf acknowledged.
“This action plan, especially including the use of public-private partnerships and direct involvement of patients, will ensure the FDA is working toward meeting the task set forth by Congress to enhance the quality of life for those suffering by facilitating access to new therapies,” Dr. Califf added.
Blueprint to ‘aggressively’ move forward
The action plan represents a “blueprint” for how the agency will “aggressively” move forward to address challenges in drug development for rare neurodegenerative diseases to improve patient health, the FDA said.
The plan was created in accordance with provisions in the Accelerating Access to Critical Therapies for ALS Act (ACT for ALS) that President Biden signed into law in late 2021.
Targeted activities include establishing the FDA Rare Neurodegenerative Diseases Task Force and the public-private partnership for rare neurodegenerative diseases, developing disease-specific science strategies over the next 5 years, and leveraging ongoing FDA regulatory science efforts.
The ALS Science Strategy is part of the plan focused specifically on ALS. It provides a “forward-leaning” framework for FDA activities, which include efforts to improve characterization of disease pathogenesis and natural history, boost clinical trial infrastructure and agility to enable early selection of promising therapeutic candidates for further development, optimize clinical trial design, improve access to the trials, streamline clinical trial operations, and reduce the time and cost of drug development.
The FDA says patient engagement, public workshops, research projects, coordination across FDA centers and offices, and collaboration with the National Institutes of Health will be key to the success of implementation of the ALS Science Strategy.
A version of this article first appeared on Medscape.com.
The agency’s Action Plan for Rare Neurodegenerative Diseases including Amyotrophic Lateral Sclerosis (ALS) aims to advance the development of safe and effective medical products and facilitate patient access to novel treatments.
“The effects of rare neurodegenerative diseases are devastating, with very few effective therapeutic options available to patients. We recognize the urgent need for new treatments that can both improve and extend the lives of people diagnosed with these diseases,” FDA Commissioner Robert M. Califf, MD, said in a news release.
“To face that challenge and to accelerate drug development, we need innovative approaches to better understand these diseases while also building on current scientific and research capabilities,” Dr. Califf acknowledged.
“This action plan, especially including the use of public-private partnerships and direct involvement of patients, will ensure the FDA is working toward meeting the task set forth by Congress to enhance the quality of life for those suffering by facilitating access to new therapies,” Dr. Califf added.
Blueprint to ‘aggressively’ move forward
The action plan represents a “blueprint” for how the agency will “aggressively” move forward to address challenges in drug development for rare neurodegenerative diseases to improve patient health, the FDA said.
The plan was created in accordance with provisions in the Accelerating Access to Critical Therapies for ALS Act (ACT for ALS) that President Biden signed into law in late 2021.
Targeted activities include establishing the FDA Rare Neurodegenerative Diseases Task Force and the public-private partnership for rare neurodegenerative diseases, developing disease-specific science strategies over the next 5 years, and leveraging ongoing FDA regulatory science efforts.
The ALS Science Strategy is part of the plan focused specifically on ALS. It provides a “forward-leaning” framework for FDA activities, which include efforts to improve characterization of disease pathogenesis and natural history, boost clinical trial infrastructure and agility to enable early selection of promising therapeutic candidates for further development, optimize clinical trial design, improve access to the trials, streamline clinical trial operations, and reduce the time and cost of drug development.
The FDA says patient engagement, public workshops, research projects, coordination across FDA centers and offices, and collaboration with the National Institutes of Health will be key to the success of implementation of the ALS Science Strategy.
A version of this article first appeared on Medscape.com.
‘Unexpected’: Breast cancer spreads most during sleep
a discovery the investigators called “striking and unexpected.”
“This has not been shown before [and] we were surprised, indeed,” Nicola Aceto, PhD, professor of molecular oncology, Swiss Federal Institute of Technology Zürich, said in an interview.
The findings carry potential implications for the timing of biopsy and treatment of metastasis-prone cancers, the authors said.
The study was published online in Nature.
Circulating tumor cells (CTCs) are generally believed to shed constantly or following particular events such as surgery or physical activity; however, the processes that regulate tumor cell metastasis and how circadian rhythms may play into tumorigenesis remain unclear.
To better understand these processes, Dr. Aceto and colleagues collected blood samples from 30 women with breast cancer at 4:00 a.m. and 10:00 a.m. – times representing the body’s resting and active phases, respectively.
The researchers observed that more than 78% of all CTCs obtained were from samples taken during the resting phase.
This finding is astounding, Harrison Ball, a PhD candidate, and Sunitha Nagrath, PhD, with the University of Michigan, Ann Arbor, wrote in Nature News & Views .
Dr. Aceto and colleagues also found that CTCs generated at night divide more quickly and therefore have a higher potential to metastasize, compared with those generated during the day, which “are devoid of metastatic ability,” according to the authors, who obtained similar results in a series of mouse models.
The team also observed that key circadian rhythm hormones (such as melatonin, testosterone, and glucocorticoids) regulate CTC generation, and insulin promotes tumor cell proliferation in a time-dependent manner, suggesting a “need for time-controlled approaches for the characterization and treatment of breast cancer,” the authors wrote.
Practice changing?
Dr. Ball and Dr. Nagrath said the time-dependent nature of CTC dynamics could very well transform how cancer patients are assessed and treated.
“The data pointing to CTC proliferation and release during the rest phase suggest that doctors might need to become more conscious of when to administer specific treatments,” they wrote.
Both cautioned, however, that large clinical trials would be needed before any consideration of circadian rhythms is incorporated into standard practice. It’s also unclear whether these results in breast cancer hold true for other tumor types.
Mariana G. Figueiro, PhD, who was not involved in the research, agreed that, if studies confirm more metastatic spread at night, “there is an opportunity to treat patients at strategic times.”
Dr. Figueiro, of the Icahn School of Medicine at Mount Sinai, New York, also saw a potential impact on the timing of blood draws. “I think tightening up on how people do biopsies and bloodwork based on circadian time is important.”
Marleen Meyers, MD, agreed that these findings could have many clinical implications.
“The most obvious is that the time of day [that] treatment is administered may influence efficacy,” said Dr. Meyers, clinical professor of medicine at New York University Langone’s Perlmutter Cancer Center.
But, Dr. Meyers noted, the benefits of treating someone at night would need to be weighed against the downsides of interrupting a person’s normal sleep-wake cycle. “If this finding is clinically important it will be a challenge incorporating this into clinical care,” she said.
The study had no funding reported. Dr. Aceto is a cofounder and member of the board of PAGE Therapeutics, listed as an inventor in patent applications related to circulating tumor cells, a paid consultant for several companies, and a Novartis shareholder. One coauthor is a cofounder of PAGE Therapeutics. All other authors declare no competing interests. Dr. Meyers and Dr. Figueiro reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
a discovery the investigators called “striking and unexpected.”
“This has not been shown before [and] we were surprised, indeed,” Nicola Aceto, PhD, professor of molecular oncology, Swiss Federal Institute of Technology Zürich, said in an interview.
The findings carry potential implications for the timing of biopsy and treatment of metastasis-prone cancers, the authors said.
The study was published online in Nature.
Circulating tumor cells (CTCs) are generally believed to shed constantly or following particular events such as surgery or physical activity; however, the processes that regulate tumor cell metastasis and how circadian rhythms may play into tumorigenesis remain unclear.
To better understand these processes, Dr. Aceto and colleagues collected blood samples from 30 women with breast cancer at 4:00 a.m. and 10:00 a.m. – times representing the body’s resting and active phases, respectively.
The researchers observed that more than 78% of all CTCs obtained were from samples taken during the resting phase.
This finding is astounding, Harrison Ball, a PhD candidate, and Sunitha Nagrath, PhD, with the University of Michigan, Ann Arbor, wrote in Nature News & Views .
Dr. Aceto and colleagues also found that CTCs generated at night divide more quickly and therefore have a higher potential to metastasize, compared with those generated during the day, which “are devoid of metastatic ability,” according to the authors, who obtained similar results in a series of mouse models.
The team also observed that key circadian rhythm hormones (such as melatonin, testosterone, and glucocorticoids) regulate CTC generation, and insulin promotes tumor cell proliferation in a time-dependent manner, suggesting a “need for time-controlled approaches for the characterization and treatment of breast cancer,” the authors wrote.
Practice changing?
Dr. Ball and Dr. Nagrath said the time-dependent nature of CTC dynamics could very well transform how cancer patients are assessed and treated.
“The data pointing to CTC proliferation and release during the rest phase suggest that doctors might need to become more conscious of when to administer specific treatments,” they wrote.
Both cautioned, however, that large clinical trials would be needed before any consideration of circadian rhythms is incorporated into standard practice. It’s also unclear whether these results in breast cancer hold true for other tumor types.
Mariana G. Figueiro, PhD, who was not involved in the research, agreed that, if studies confirm more metastatic spread at night, “there is an opportunity to treat patients at strategic times.”
Dr. Figueiro, of the Icahn School of Medicine at Mount Sinai, New York, also saw a potential impact on the timing of blood draws. “I think tightening up on how people do biopsies and bloodwork based on circadian time is important.”
Marleen Meyers, MD, agreed that these findings could have many clinical implications.
“The most obvious is that the time of day [that] treatment is administered may influence efficacy,” said Dr. Meyers, clinical professor of medicine at New York University Langone’s Perlmutter Cancer Center.
But, Dr. Meyers noted, the benefits of treating someone at night would need to be weighed against the downsides of interrupting a person’s normal sleep-wake cycle. “If this finding is clinically important it will be a challenge incorporating this into clinical care,” she said.
The study had no funding reported. Dr. Aceto is a cofounder and member of the board of PAGE Therapeutics, listed as an inventor in patent applications related to circulating tumor cells, a paid consultant for several companies, and a Novartis shareholder. One coauthor is a cofounder of PAGE Therapeutics. All other authors declare no competing interests. Dr. Meyers and Dr. Figueiro reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
a discovery the investigators called “striking and unexpected.”
“This has not been shown before [and] we were surprised, indeed,” Nicola Aceto, PhD, professor of molecular oncology, Swiss Federal Institute of Technology Zürich, said in an interview.
The findings carry potential implications for the timing of biopsy and treatment of metastasis-prone cancers, the authors said.
The study was published online in Nature.
Circulating tumor cells (CTCs) are generally believed to shed constantly or following particular events such as surgery or physical activity; however, the processes that regulate tumor cell metastasis and how circadian rhythms may play into tumorigenesis remain unclear.
To better understand these processes, Dr. Aceto and colleagues collected blood samples from 30 women with breast cancer at 4:00 a.m. and 10:00 a.m. – times representing the body’s resting and active phases, respectively.
The researchers observed that more than 78% of all CTCs obtained were from samples taken during the resting phase.
This finding is astounding, Harrison Ball, a PhD candidate, and Sunitha Nagrath, PhD, with the University of Michigan, Ann Arbor, wrote in Nature News & Views .
Dr. Aceto and colleagues also found that CTCs generated at night divide more quickly and therefore have a higher potential to metastasize, compared with those generated during the day, which “are devoid of metastatic ability,” according to the authors, who obtained similar results in a series of mouse models.
The team also observed that key circadian rhythm hormones (such as melatonin, testosterone, and glucocorticoids) regulate CTC generation, and insulin promotes tumor cell proliferation in a time-dependent manner, suggesting a “need for time-controlled approaches for the characterization and treatment of breast cancer,” the authors wrote.
Practice changing?
Dr. Ball and Dr. Nagrath said the time-dependent nature of CTC dynamics could very well transform how cancer patients are assessed and treated.
“The data pointing to CTC proliferation and release during the rest phase suggest that doctors might need to become more conscious of when to administer specific treatments,” they wrote.
Both cautioned, however, that large clinical trials would be needed before any consideration of circadian rhythms is incorporated into standard practice. It’s also unclear whether these results in breast cancer hold true for other tumor types.
Mariana G. Figueiro, PhD, who was not involved in the research, agreed that, if studies confirm more metastatic spread at night, “there is an opportunity to treat patients at strategic times.”
Dr. Figueiro, of the Icahn School of Medicine at Mount Sinai, New York, also saw a potential impact on the timing of blood draws. “I think tightening up on how people do biopsies and bloodwork based on circadian time is important.”
Marleen Meyers, MD, agreed that these findings could have many clinical implications.
“The most obvious is that the time of day [that] treatment is administered may influence efficacy,” said Dr. Meyers, clinical professor of medicine at New York University Langone’s Perlmutter Cancer Center.
But, Dr. Meyers noted, the benefits of treating someone at night would need to be weighed against the downsides of interrupting a person’s normal sleep-wake cycle. “If this finding is clinically important it will be a challenge incorporating this into clinical care,” she said.
The study had no funding reported. Dr. Aceto is a cofounder and member of the board of PAGE Therapeutics, listed as an inventor in patent applications related to circulating tumor cells, a paid consultant for several companies, and a Novartis shareholder. One coauthor is a cofounder of PAGE Therapeutics. All other authors declare no competing interests. Dr. Meyers and Dr. Figueiro reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM NATURE
Jury out on low-FODMAP diet for kids
There is scarce evidence to support the use of a FODMAP-lowering diet for children with irritable bowel syndrome (IBS), and there is no evidence to recommend its use for other gastrointestinal (GI) diseases and complaints in children, according to a position paper from the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN).
A low-FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) diet is increasingly being used to treat children with various GI complaints and disorders.
“Awareness of how and when to use the diet is crucial, as a restrictive diet may impact nutritional adequacy and/or promote distorted eating in vulnerable subjects,” the authors note.
Rut Anne Thomassen, department of pediatric medicine, Oslo University Hospital, and an international team of experts conducted a systematic literature review of the evidence on the safety and efficacy of the low-FODMAP diet in children.
The low-FODMAP diet has not been well studied in children, they report.
From 53 publications and registers that they screened, only seven studies (four randomized clinical trials and three interventions without control group or observational studies) were included in their assessment.
In the seven studies, only 111 children received the low-FODMAP diet, while 85 followed a control diet for comparison (a diet described as healthy, usual, or typical American diet for children).
All of the pediatric studies focused on functional abdominal pain disorders. None addressed nonceliac gluten sensitivity, small-intestinal bacterial overgrowth, or inflammatory bowel disease.
From their review, the authors conclude that, at present, there is “insufficient evidence” to routinely recommend the low-FODMAP diet for the treatment of functional GI disorders, nonceliac gluten sensitivity, inflammatory bowel diseases, or small-intestinal bacterial overgrowth in children.
When the low-FODMAP diet is considered for children, the authors recommend a thorough clinical history, physical examination, and assessment of nutritional status and GI symptoms by a multidisciplinary team.
“Ideally, a standardized questionnaire should be used before and following the start of the diet to assess objectively the effect of the low-FODMAP diet,” the authors advise.
A dietitian should assess the child’s diet to highlight any potential deficiencies, which could be exacerbated by the restrictions of the low-FODMAP diet.
To promote adherence to the diet, potential difficulties, such as how to provide a suitable lunch at school or what to do when the child is staying at a friend’s house, should be addressed.
The authors suggest providing parents with written information about sources of FODMAPs and suitable replacement foods. Offering meal plans can reduce the risk of diet mistakes as well as the risk of offering a diet insufficient in essential nutrients, they say.
‘Useful paper’
“This is a useful paper primarily to outline the paucity of data regarding dietary therapies in children and the importance of doing studies in this population,” Ashwin Ananthakrishnan, MD, MPH, a gastroenterologist with Massachusetts General Hospital and Harvard Medical School, both in Boston, who wasn’t involved in the research, told this news organization.
Samuel Nurko, MD, MPH, director of the Center for Motility and Functional Gastrointestinal Disorders at Boston Children’s Hospital, Massachusetts, noted that some studies have shown that a low-FODMAP diet can be effective in controlling symptoms for both adults and kids.
“The problem in kids is that the trials are very small, and there’s not a lot of them, so the evidence is limited,” said Dr. Nurko, who wasn’t involved in writing the position paper.
That’s not to say that it should not be tried in appropriate cases. “There’s no question that in some patients, taking away the FODMAPs gives them a big improvement in GI symptoms,” Dr. Nurko told this news organization.
“The problem with the low-FODMAP diet is, if you don’t do it right, then you get into trouble with nutritional deficiencies,” he cautioned.
“If you are going to try the low-FODMAP diet, it has to be short, no more than 4-6 weeks, and you need to do a top-down approach. Take FODMAPs out, and then start to reintroduce them. Either kids will respond to the diet, or they won’t. If they don’t, there is no reason to keep them on the diet. It’s a very hard diet to take,” Dr. Nurko said.
No source of funding for the study was disclosed. The authors, Dr. Ananthakrishnan, and Dr. Nurko have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
There is scarce evidence to support the use of a FODMAP-lowering diet for children with irritable bowel syndrome (IBS), and there is no evidence to recommend its use for other gastrointestinal (GI) diseases and complaints in children, according to a position paper from the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN).
A low-FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) diet is increasingly being used to treat children with various GI complaints and disorders.
“Awareness of how and when to use the diet is crucial, as a restrictive diet may impact nutritional adequacy and/or promote distorted eating in vulnerable subjects,” the authors note.
Rut Anne Thomassen, department of pediatric medicine, Oslo University Hospital, and an international team of experts conducted a systematic literature review of the evidence on the safety and efficacy of the low-FODMAP diet in children.
The low-FODMAP diet has not been well studied in children, they report.
From 53 publications and registers that they screened, only seven studies (four randomized clinical trials and three interventions without control group or observational studies) were included in their assessment.
In the seven studies, only 111 children received the low-FODMAP diet, while 85 followed a control diet for comparison (a diet described as healthy, usual, or typical American diet for children).
All of the pediatric studies focused on functional abdominal pain disorders. None addressed nonceliac gluten sensitivity, small-intestinal bacterial overgrowth, or inflammatory bowel disease.
From their review, the authors conclude that, at present, there is “insufficient evidence” to routinely recommend the low-FODMAP diet for the treatment of functional GI disorders, nonceliac gluten sensitivity, inflammatory bowel diseases, or small-intestinal bacterial overgrowth in children.
When the low-FODMAP diet is considered for children, the authors recommend a thorough clinical history, physical examination, and assessment of nutritional status and GI symptoms by a multidisciplinary team.
“Ideally, a standardized questionnaire should be used before and following the start of the diet to assess objectively the effect of the low-FODMAP diet,” the authors advise.
A dietitian should assess the child’s diet to highlight any potential deficiencies, which could be exacerbated by the restrictions of the low-FODMAP diet.
To promote adherence to the diet, potential difficulties, such as how to provide a suitable lunch at school or what to do when the child is staying at a friend’s house, should be addressed.
The authors suggest providing parents with written information about sources of FODMAPs and suitable replacement foods. Offering meal plans can reduce the risk of diet mistakes as well as the risk of offering a diet insufficient in essential nutrients, they say.
‘Useful paper’
“This is a useful paper primarily to outline the paucity of data regarding dietary therapies in children and the importance of doing studies in this population,” Ashwin Ananthakrishnan, MD, MPH, a gastroenterologist with Massachusetts General Hospital and Harvard Medical School, both in Boston, who wasn’t involved in the research, told this news organization.
Samuel Nurko, MD, MPH, director of the Center for Motility and Functional Gastrointestinal Disorders at Boston Children’s Hospital, Massachusetts, noted that some studies have shown that a low-FODMAP diet can be effective in controlling symptoms for both adults and kids.
“The problem in kids is that the trials are very small, and there’s not a lot of them, so the evidence is limited,” said Dr. Nurko, who wasn’t involved in writing the position paper.
That’s not to say that it should not be tried in appropriate cases. “There’s no question that in some patients, taking away the FODMAPs gives them a big improvement in GI symptoms,” Dr. Nurko told this news organization.
“The problem with the low-FODMAP diet is, if you don’t do it right, then you get into trouble with nutritional deficiencies,” he cautioned.
“If you are going to try the low-FODMAP diet, it has to be short, no more than 4-6 weeks, and you need to do a top-down approach. Take FODMAPs out, and then start to reintroduce them. Either kids will respond to the diet, or they won’t. If they don’t, there is no reason to keep them on the diet. It’s a very hard diet to take,” Dr. Nurko said.
No source of funding for the study was disclosed. The authors, Dr. Ananthakrishnan, and Dr. Nurko have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
There is scarce evidence to support the use of a FODMAP-lowering diet for children with irritable bowel syndrome (IBS), and there is no evidence to recommend its use for other gastrointestinal (GI) diseases and complaints in children, according to a position paper from the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN).
A low-FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) diet is increasingly being used to treat children with various GI complaints and disorders.
“Awareness of how and when to use the diet is crucial, as a restrictive diet may impact nutritional adequacy and/or promote distorted eating in vulnerable subjects,” the authors note.
Rut Anne Thomassen, department of pediatric medicine, Oslo University Hospital, and an international team of experts conducted a systematic literature review of the evidence on the safety and efficacy of the low-FODMAP diet in children.
The low-FODMAP diet has not been well studied in children, they report.
From 53 publications and registers that they screened, only seven studies (four randomized clinical trials and three interventions without control group or observational studies) were included in their assessment.
In the seven studies, only 111 children received the low-FODMAP diet, while 85 followed a control diet for comparison (a diet described as healthy, usual, or typical American diet for children).
All of the pediatric studies focused on functional abdominal pain disorders. None addressed nonceliac gluten sensitivity, small-intestinal bacterial overgrowth, or inflammatory bowel disease.
From their review, the authors conclude that, at present, there is “insufficient evidence” to routinely recommend the low-FODMAP diet for the treatment of functional GI disorders, nonceliac gluten sensitivity, inflammatory bowel diseases, or small-intestinal bacterial overgrowth in children.
When the low-FODMAP diet is considered for children, the authors recommend a thorough clinical history, physical examination, and assessment of nutritional status and GI symptoms by a multidisciplinary team.
“Ideally, a standardized questionnaire should be used before and following the start of the diet to assess objectively the effect of the low-FODMAP diet,” the authors advise.
A dietitian should assess the child’s diet to highlight any potential deficiencies, which could be exacerbated by the restrictions of the low-FODMAP diet.
To promote adherence to the diet, potential difficulties, such as how to provide a suitable lunch at school or what to do when the child is staying at a friend’s house, should be addressed.
The authors suggest providing parents with written information about sources of FODMAPs and suitable replacement foods. Offering meal plans can reduce the risk of diet mistakes as well as the risk of offering a diet insufficient in essential nutrients, they say.
‘Useful paper’
“This is a useful paper primarily to outline the paucity of data regarding dietary therapies in children and the importance of doing studies in this population,” Ashwin Ananthakrishnan, MD, MPH, a gastroenterologist with Massachusetts General Hospital and Harvard Medical School, both in Boston, who wasn’t involved in the research, told this news organization.
Samuel Nurko, MD, MPH, director of the Center for Motility and Functional Gastrointestinal Disorders at Boston Children’s Hospital, Massachusetts, noted that some studies have shown that a low-FODMAP diet can be effective in controlling symptoms for both adults and kids.
“The problem in kids is that the trials are very small, and there’s not a lot of them, so the evidence is limited,” said Dr. Nurko, who wasn’t involved in writing the position paper.
That’s not to say that it should not be tried in appropriate cases. “There’s no question that in some patients, taking away the FODMAPs gives them a big improvement in GI symptoms,” Dr. Nurko told this news organization.
“The problem with the low-FODMAP diet is, if you don’t do it right, then you get into trouble with nutritional deficiencies,” he cautioned.
“If you are going to try the low-FODMAP diet, it has to be short, no more than 4-6 weeks, and you need to do a top-down approach. Take FODMAPs out, and then start to reintroduce them. Either kids will respond to the diet, or they won’t. If they don’t, there is no reason to keep them on the diet. It’s a very hard diet to take,” Dr. Nurko said.
No source of funding for the study was disclosed. The authors, Dr. Ananthakrishnan, and Dr. Nurko have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
$150K: Average industry payment to top 1% of oncologists
A small number of U.S. medical oncologists make more than $100,000 a year in general payments from drug companies, a new study shows.
These high-payment physicians represent just 1% of all U.S. medical oncologists, yet they account for 37% of industry payments. These oncologists often hold important leadership positions, draft treatment guidelines, and sit on journal editorial boards.
The findings highlight a risk for “perceived and real conflict of interest,” corresponding author Christopher Booth, MD, of Queen’s University Cancer Research Center, Kingston, Ont., said in an interview. “Because of the leadership positions they hold, the potential impact of this small group of physicians on oncology practice and policy may be substantial.”
The study was published online in JCO Oncology Practice.
‘We have a problem’
It’s no secret that many oncologists have financial relationships with pharmaceutical companies. They receive payments for research initiatives, but they also receive more general, personal payments in the form of honoraria, consultant fees, gifts, and reimbursement for travel and meals.
Prior studies have shown that these payments are typically modest, but a small subset of medical oncologists receive more than $100,000 annually. Dr. Booth and colleagues wanted to know more about the characteristics of these “high-payment” oncologists.
Using the national Open Payments database, the researchers identified a total of 139 medical oncologists who practice in the United States and who received $100,000 or more in general payments linked to cancer medications in 2018.
In U.S. dollars, the median payment was $154,613, and the total was $24.2 million.
The majority (95%) of high-payment oncologists were active in clinical work, 56% worked in an academic setting, 31% worked at National Cancer Institute–designated cancer centers, and 23% worked at National Comprehensive Cancer Network (NCCN) centers.
Many were based in California (17%), Texas (12%), Florida (10%), and New York (8%).
Most currently hold or have held hospital leadership positions (60%) or faculty appointments (72%) and 21% have held leadership positions in specialty associations in the past 5 years. Nearly one-quarter (24%) have served on journal editorial boards, and 10% have authored clinical practice guidelines in the past 5 years.
More specifically, three physicians authored NCCN guidelines, and two authored American Society of Clinical Oncology guidelines during 2016-2021; one guideline was published in 2018 when payments were made.
“Oncology specialty associations, guideline panels, and journal editorial boards should reconsider if it is appropriate for physicians with such large payments to hold these high-profile positions,” Dr. Booth said.
Following publication of the study, some oncologists took to Twitter with reactions, including Manni Mohyuddin, MD (@ManniMD1), from the Huntsman Cancer Institute, University of Utah, Salt Lake City, who wrote: “I recognize that some conflict of interest ‘may’ be unavoidable in order to run trials. But when greater than TWICE the average American household annual salary is taken in payments from industry by those in leadership/editorial roles, we have a problem.”
Weighing in on the results, ASCO CEO Clifford A. Hudis, MD, told this news organization that the “limitations of the study make it difficult to draw conclusions about the scope or potential impact of these payments on care.”
For example, he explained, some payments attributed to individuals may have been made directly to the physicians’ institutions or employers for sponsored research expenses.
Dr. Hudis also noted that the payments examined in the study were made in 2018, whereas the potentially relevant leadership positions could have been attained at a different time.
Furthermore, in 2020, an editorial appeared in Cancer, showing that errors in Open Payments are “fairly common,” Dr. Hudis said. It’s also unclear whether the reported financial relationships were appropriately disclosed and were managed at the time under relevant conflict of interest policies, he said.
“The question left unanswered by this study is whether or not these relationships influence patient care,” said Dr. Hudis. He noted that decisions about care should come from physicians and patients who are informed of the best available, unbiased, peer-reviewed, scientific evidence.
“The potential impact of financial conflicts of interest on this effort is an issue of concern, even if this study does not directly address it,” Dr. Hudis said.
The study had no specific funding. Dr. Booth has disclosed no relevant financial relationships. A complete list of author disclosures is available with the original article. Dr. Hudis has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A small number of U.S. medical oncologists make more than $100,000 a year in general payments from drug companies, a new study shows.
These high-payment physicians represent just 1% of all U.S. medical oncologists, yet they account for 37% of industry payments. These oncologists often hold important leadership positions, draft treatment guidelines, and sit on journal editorial boards.
The findings highlight a risk for “perceived and real conflict of interest,” corresponding author Christopher Booth, MD, of Queen’s University Cancer Research Center, Kingston, Ont., said in an interview. “Because of the leadership positions they hold, the potential impact of this small group of physicians on oncology practice and policy may be substantial.”
The study was published online in JCO Oncology Practice.
‘We have a problem’
It’s no secret that many oncologists have financial relationships with pharmaceutical companies. They receive payments for research initiatives, but they also receive more general, personal payments in the form of honoraria, consultant fees, gifts, and reimbursement for travel and meals.
Prior studies have shown that these payments are typically modest, but a small subset of medical oncologists receive more than $100,000 annually. Dr. Booth and colleagues wanted to know more about the characteristics of these “high-payment” oncologists.
Using the national Open Payments database, the researchers identified a total of 139 medical oncologists who practice in the United States and who received $100,000 or more in general payments linked to cancer medications in 2018.
In U.S. dollars, the median payment was $154,613, and the total was $24.2 million.
The majority (95%) of high-payment oncologists were active in clinical work, 56% worked in an academic setting, 31% worked at National Cancer Institute–designated cancer centers, and 23% worked at National Comprehensive Cancer Network (NCCN) centers.
Many were based in California (17%), Texas (12%), Florida (10%), and New York (8%).
Most currently hold or have held hospital leadership positions (60%) or faculty appointments (72%) and 21% have held leadership positions in specialty associations in the past 5 years. Nearly one-quarter (24%) have served on journal editorial boards, and 10% have authored clinical practice guidelines in the past 5 years.
More specifically, three physicians authored NCCN guidelines, and two authored American Society of Clinical Oncology guidelines during 2016-2021; one guideline was published in 2018 when payments were made.
“Oncology specialty associations, guideline panels, and journal editorial boards should reconsider if it is appropriate for physicians with such large payments to hold these high-profile positions,” Dr. Booth said.
Following publication of the study, some oncologists took to Twitter with reactions, including Manni Mohyuddin, MD (@ManniMD1), from the Huntsman Cancer Institute, University of Utah, Salt Lake City, who wrote: “I recognize that some conflict of interest ‘may’ be unavoidable in order to run trials. But when greater than TWICE the average American household annual salary is taken in payments from industry by those in leadership/editorial roles, we have a problem.”
Weighing in on the results, ASCO CEO Clifford A. Hudis, MD, told this news organization that the “limitations of the study make it difficult to draw conclusions about the scope or potential impact of these payments on care.”
For example, he explained, some payments attributed to individuals may have been made directly to the physicians’ institutions or employers for sponsored research expenses.
Dr. Hudis also noted that the payments examined in the study were made in 2018, whereas the potentially relevant leadership positions could have been attained at a different time.
Furthermore, in 2020, an editorial appeared in Cancer, showing that errors in Open Payments are “fairly common,” Dr. Hudis said. It’s also unclear whether the reported financial relationships were appropriately disclosed and were managed at the time under relevant conflict of interest policies, he said.
“The question left unanswered by this study is whether or not these relationships influence patient care,” said Dr. Hudis. He noted that decisions about care should come from physicians and patients who are informed of the best available, unbiased, peer-reviewed, scientific evidence.
“The potential impact of financial conflicts of interest on this effort is an issue of concern, even if this study does not directly address it,” Dr. Hudis said.
The study had no specific funding. Dr. Booth has disclosed no relevant financial relationships. A complete list of author disclosures is available with the original article. Dr. Hudis has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A small number of U.S. medical oncologists make more than $100,000 a year in general payments from drug companies, a new study shows.
These high-payment physicians represent just 1% of all U.S. medical oncologists, yet they account for 37% of industry payments. These oncologists often hold important leadership positions, draft treatment guidelines, and sit on journal editorial boards.
The findings highlight a risk for “perceived and real conflict of interest,” corresponding author Christopher Booth, MD, of Queen’s University Cancer Research Center, Kingston, Ont., said in an interview. “Because of the leadership positions they hold, the potential impact of this small group of physicians on oncology practice and policy may be substantial.”
The study was published online in JCO Oncology Practice.
‘We have a problem’
It’s no secret that many oncologists have financial relationships with pharmaceutical companies. They receive payments for research initiatives, but they also receive more general, personal payments in the form of honoraria, consultant fees, gifts, and reimbursement for travel and meals.
Prior studies have shown that these payments are typically modest, but a small subset of medical oncologists receive more than $100,000 annually. Dr. Booth and colleagues wanted to know more about the characteristics of these “high-payment” oncologists.
Using the national Open Payments database, the researchers identified a total of 139 medical oncologists who practice in the United States and who received $100,000 or more in general payments linked to cancer medications in 2018.
In U.S. dollars, the median payment was $154,613, and the total was $24.2 million.
The majority (95%) of high-payment oncologists were active in clinical work, 56% worked in an academic setting, 31% worked at National Cancer Institute–designated cancer centers, and 23% worked at National Comprehensive Cancer Network (NCCN) centers.
Many were based in California (17%), Texas (12%), Florida (10%), and New York (8%).
Most currently hold or have held hospital leadership positions (60%) or faculty appointments (72%) and 21% have held leadership positions in specialty associations in the past 5 years. Nearly one-quarter (24%) have served on journal editorial boards, and 10% have authored clinical practice guidelines in the past 5 years.
More specifically, three physicians authored NCCN guidelines, and two authored American Society of Clinical Oncology guidelines during 2016-2021; one guideline was published in 2018 when payments were made.
“Oncology specialty associations, guideline panels, and journal editorial boards should reconsider if it is appropriate for physicians with such large payments to hold these high-profile positions,” Dr. Booth said.
Following publication of the study, some oncologists took to Twitter with reactions, including Manni Mohyuddin, MD (@ManniMD1), from the Huntsman Cancer Institute, University of Utah, Salt Lake City, who wrote: “I recognize that some conflict of interest ‘may’ be unavoidable in order to run trials. But when greater than TWICE the average American household annual salary is taken in payments from industry by those in leadership/editorial roles, we have a problem.”
Weighing in on the results, ASCO CEO Clifford A. Hudis, MD, told this news organization that the “limitations of the study make it difficult to draw conclusions about the scope or potential impact of these payments on care.”
For example, he explained, some payments attributed to individuals may have been made directly to the physicians’ institutions or employers for sponsored research expenses.
Dr. Hudis also noted that the payments examined in the study were made in 2018, whereas the potentially relevant leadership positions could have been attained at a different time.
Furthermore, in 2020, an editorial appeared in Cancer, showing that errors in Open Payments are “fairly common,” Dr. Hudis said. It’s also unclear whether the reported financial relationships were appropriately disclosed and were managed at the time under relevant conflict of interest policies, he said.
“The question left unanswered by this study is whether or not these relationships influence patient care,” said Dr. Hudis. He noted that decisions about care should come from physicians and patients who are informed of the best available, unbiased, peer-reviewed, scientific evidence.
“The potential impact of financial conflicts of interest on this effort is an issue of concern, even if this study does not directly address it,” Dr. Hudis said.
The study had no specific funding. Dr. Booth has disclosed no relevant financial relationships. A complete list of author disclosures is available with the original article. Dr. Hudis has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JCO ONCOLOGY PRACTICE
Class I recall for Medtronic’s HeartWare HVAD batteries
Medtronic is recalling a single lot of HeartWare Ventricular Assist Device (HVAD) System batteries because of welding defects that may cause separation of the two cell battery packs used to power the system, according to an alert on the Food and Drug Administration website.
“The welding defect may cause the battery to malfunction and no longer provide power or prevent the battery from holding a full charge or properly recharging,” the FDA said.
The agency has identified this as a class I recall, the most serious type because of the potential for serious injury or death.
Medtronic reports one death associated with this recall and two complaints in the affected lot.
Back in April, as reported by this news organization, Medtronic alerted providers that patients implanted with the Medtronic HVAD System who develop pump thrombosis could have a welding defect in the internal pump that causes the pump to malfunction.
The batteries from the recalled lot have a model number of 1650DE, were manufactured from April 13 to 19, 2021 and distributed from April 20 to July 19, 2021. The recall affects a total of 429 devices.
On May 5, 2022, Medtronic sent an urgent medical device correction notice to customers asking them to identify and quarantine all affected batteries and notify affected patients. The notice includes a patient template to help communicate directly with patients.
It also includes a customer confirmation form to initiate an exchange. The completed form should be returned to [email protected].
Medtronic is replacing the affected batteries with new product and has implemented actions to improve control of the welding process.
The Medtronic HVAD System was approved as a bridge to heart transplantation in 2012. Since then, it’s been fraught with problems.
Earlier in June, the company announced it was stopping all sales of the device and advised physicians to stop implanting it, as reported by this news organization.
Problems related to the Medtronic HVAD System should be reported to the FDA’s MedWatch program.
A version of this article first appeared on Medscape.com.
Medtronic is recalling a single lot of HeartWare Ventricular Assist Device (HVAD) System batteries because of welding defects that may cause separation of the two cell battery packs used to power the system, according to an alert on the Food and Drug Administration website.
“The welding defect may cause the battery to malfunction and no longer provide power or prevent the battery from holding a full charge or properly recharging,” the FDA said.
The agency has identified this as a class I recall, the most serious type because of the potential for serious injury or death.
Medtronic reports one death associated with this recall and two complaints in the affected lot.
Back in April, as reported by this news organization, Medtronic alerted providers that patients implanted with the Medtronic HVAD System who develop pump thrombosis could have a welding defect in the internal pump that causes the pump to malfunction.
The batteries from the recalled lot have a model number of 1650DE, were manufactured from April 13 to 19, 2021 and distributed from April 20 to July 19, 2021. The recall affects a total of 429 devices.
On May 5, 2022, Medtronic sent an urgent medical device correction notice to customers asking them to identify and quarantine all affected batteries and notify affected patients. The notice includes a patient template to help communicate directly with patients.
It also includes a customer confirmation form to initiate an exchange. The completed form should be returned to [email protected].
Medtronic is replacing the affected batteries with new product and has implemented actions to improve control of the welding process.
The Medtronic HVAD System was approved as a bridge to heart transplantation in 2012. Since then, it’s been fraught with problems.
Earlier in June, the company announced it was stopping all sales of the device and advised physicians to stop implanting it, as reported by this news organization.
Problems related to the Medtronic HVAD System should be reported to the FDA’s MedWatch program.
A version of this article first appeared on Medscape.com.
Medtronic is recalling a single lot of HeartWare Ventricular Assist Device (HVAD) System batteries because of welding defects that may cause separation of the two cell battery packs used to power the system, according to an alert on the Food and Drug Administration website.
“The welding defect may cause the battery to malfunction and no longer provide power or prevent the battery from holding a full charge or properly recharging,” the FDA said.
The agency has identified this as a class I recall, the most serious type because of the potential for serious injury or death.
Medtronic reports one death associated with this recall and two complaints in the affected lot.
Back in April, as reported by this news organization, Medtronic alerted providers that patients implanted with the Medtronic HVAD System who develop pump thrombosis could have a welding defect in the internal pump that causes the pump to malfunction.
The batteries from the recalled lot have a model number of 1650DE, were manufactured from April 13 to 19, 2021 and distributed from April 20 to July 19, 2021. The recall affects a total of 429 devices.
On May 5, 2022, Medtronic sent an urgent medical device correction notice to customers asking them to identify and quarantine all affected batteries and notify affected patients. The notice includes a patient template to help communicate directly with patients.
It also includes a customer confirmation form to initiate an exchange. The completed form should be returned to [email protected].
Medtronic is replacing the affected batteries with new product and has implemented actions to improve control of the welding process.
The Medtronic HVAD System was approved as a bridge to heart transplantation in 2012. Since then, it’s been fraught with problems.
Earlier in June, the company announced it was stopping all sales of the device and advised physicians to stop implanting it, as reported by this news organization.
Problems related to the Medtronic HVAD System should be reported to the FDA’s MedWatch program.
A version of this article first appeared on Medscape.com.
FDA okays cancer drugs faster than EMA. But at what cost?
Over the past decade, the U.S. Food and Drug Administration has approved new cancer drugs twice as fast as the European Medicines Agency (EMA), often using accelerated pathways, a new analysis shows.
Between 2010 and 2019, the FDA approved almost all oncology therapies ahead of the EMA. Drugs entered the United States market about 8 months (241 days) before European market authorization.
“The faster FDA approval process potentially provides earlier access to potentially life-prolonging medications for patients with cancer in the United States,” Ali Raza Khaki, MD, department of oncology, Stanford (Calif.) University School of Medicine, told this news organization. “On the surface, this is a good thing. However, it comes with limitations.”
Earlier drug approval often means greater uncertainty about an agent’s benefit – most notably, whether it will improve a patient’s survival or quality of life. Dr. Khaki pointed to a study published in JAMA Internal Medicine, which found that only 19 of 93 (20%) cancer drugs that had been recently approved through the FDA’s accelerated approval pathway demonstrated an improvement in overall survival.
In the new study, published online in JAMA Network Open, Dr. Khaki and colleagues found that among the 89 cancer drugs approved in the United States and Europe between January 2010 and December 2019, the FDA approved 85 (95%) before European authorization and four (5%) after.
The researchers found that the median FDA review time was half that of the EMA’s (200 vs. 426 days). Furthermore, 64 new drug applications (72%) were submitted to the FDA first, compared with 21 (23%) to the EMA.
Of the drugs approved through an accelerated pathway, three were ultimately pulled from the U.S. market, compared with one in Europe.
“These early drug approvals that later lead to withdrawal expose many more patients to toxicity, including financial toxicity, given the high cost of cancer medications,” Dr. Khaki commented.
In addition, 35 oncology therapies (39%) were approved by the FDA before trial results were published, compared with only eight (9%) by the EMA. Although FDA drug labels contain some information about efficacy and toxicity, scientific publications often have much more, including details about study populations and toxicities.
“Without this information, providers may be limited in their knowledge about patient selection, clinical benefit, and optimal toxicity management,” Dr. Khaki said.
Jeff Allen PhD, president and CEO of the nonprofit Friends of Cancer Research, who wasn’t involved in the study, believes that an FDA approval before publication shouldn’t be “particularly concerning.”
“Peer-reviewed publication is an important component of validating and communicating scientific findings, but the processes and time lines for individual journals can be highly variable,” he said. “I don’t think we would want to see a situation where potential beneficial treatments are held up due to unrelated publication processes.”
The author of an invited commentary in JAMA Network Open had a different take on the study findings.
“A tempting interpretation” of this study is that the FDA is a “superior agency for expedited review times that bring cancer drugs to patients earlier,” Kristina Jenei, BSN, MSc, with the University of British Columbia School of Population and Public Health, writes. In addition, the fact that more drugs were pulled from the market after approval in the United States than in Europe could be interpreted to mean that the system is working as it should.
Although the speed of FDA reviews and the number of subsequent approvals have increased over time, the proportion of cancer drugs that improve survival has declined. In addition, because the FDA’s follow-up of postmarketing studies has been “inconsistent,” a substantial number of cancer drugs that were approved through accelerated pathways have remained on the market for years without confirmation of their benefit.
Although regulatory agencies must balance earlier patient access to novel treatments with evidence that the therapies are effective and safe, “faster review times and approvals are not cause for celebration; better patient outcomes are,” Ms. Jenei writes. “In other words, quality over quantity.”
The study was supported by the National Cancer Institute. Dr. Khaki reported stock ownership from Merck and stock ownership from Sanofi outside the submitted work. Dr. Allen and Ms. Jenei have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Over the past decade, the U.S. Food and Drug Administration has approved new cancer drugs twice as fast as the European Medicines Agency (EMA), often using accelerated pathways, a new analysis shows.
Between 2010 and 2019, the FDA approved almost all oncology therapies ahead of the EMA. Drugs entered the United States market about 8 months (241 days) before European market authorization.
“The faster FDA approval process potentially provides earlier access to potentially life-prolonging medications for patients with cancer in the United States,” Ali Raza Khaki, MD, department of oncology, Stanford (Calif.) University School of Medicine, told this news organization. “On the surface, this is a good thing. However, it comes with limitations.”
Earlier drug approval often means greater uncertainty about an agent’s benefit – most notably, whether it will improve a patient’s survival or quality of life. Dr. Khaki pointed to a study published in JAMA Internal Medicine, which found that only 19 of 93 (20%) cancer drugs that had been recently approved through the FDA’s accelerated approval pathway demonstrated an improvement in overall survival.
In the new study, published online in JAMA Network Open, Dr. Khaki and colleagues found that among the 89 cancer drugs approved in the United States and Europe between January 2010 and December 2019, the FDA approved 85 (95%) before European authorization and four (5%) after.
The researchers found that the median FDA review time was half that of the EMA’s (200 vs. 426 days). Furthermore, 64 new drug applications (72%) were submitted to the FDA first, compared with 21 (23%) to the EMA.
Of the drugs approved through an accelerated pathway, three were ultimately pulled from the U.S. market, compared with one in Europe.
“These early drug approvals that later lead to withdrawal expose many more patients to toxicity, including financial toxicity, given the high cost of cancer medications,” Dr. Khaki commented.
In addition, 35 oncology therapies (39%) were approved by the FDA before trial results were published, compared with only eight (9%) by the EMA. Although FDA drug labels contain some information about efficacy and toxicity, scientific publications often have much more, including details about study populations and toxicities.
“Without this information, providers may be limited in their knowledge about patient selection, clinical benefit, and optimal toxicity management,” Dr. Khaki said.
Jeff Allen PhD, president and CEO of the nonprofit Friends of Cancer Research, who wasn’t involved in the study, believes that an FDA approval before publication shouldn’t be “particularly concerning.”
“Peer-reviewed publication is an important component of validating and communicating scientific findings, but the processes and time lines for individual journals can be highly variable,” he said. “I don’t think we would want to see a situation where potential beneficial treatments are held up due to unrelated publication processes.”
The author of an invited commentary in JAMA Network Open had a different take on the study findings.
“A tempting interpretation” of this study is that the FDA is a “superior agency for expedited review times that bring cancer drugs to patients earlier,” Kristina Jenei, BSN, MSc, with the University of British Columbia School of Population and Public Health, writes. In addition, the fact that more drugs were pulled from the market after approval in the United States than in Europe could be interpreted to mean that the system is working as it should.
Although the speed of FDA reviews and the number of subsequent approvals have increased over time, the proportion of cancer drugs that improve survival has declined. In addition, because the FDA’s follow-up of postmarketing studies has been “inconsistent,” a substantial number of cancer drugs that were approved through accelerated pathways have remained on the market for years without confirmation of their benefit.
Although regulatory agencies must balance earlier patient access to novel treatments with evidence that the therapies are effective and safe, “faster review times and approvals are not cause for celebration; better patient outcomes are,” Ms. Jenei writes. “In other words, quality over quantity.”
The study was supported by the National Cancer Institute. Dr. Khaki reported stock ownership from Merck and stock ownership from Sanofi outside the submitted work. Dr. Allen and Ms. Jenei have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Over the past decade, the U.S. Food and Drug Administration has approved new cancer drugs twice as fast as the European Medicines Agency (EMA), often using accelerated pathways, a new analysis shows.
Between 2010 and 2019, the FDA approved almost all oncology therapies ahead of the EMA. Drugs entered the United States market about 8 months (241 days) before European market authorization.
“The faster FDA approval process potentially provides earlier access to potentially life-prolonging medications for patients with cancer in the United States,” Ali Raza Khaki, MD, department of oncology, Stanford (Calif.) University School of Medicine, told this news organization. “On the surface, this is a good thing. However, it comes with limitations.”
Earlier drug approval often means greater uncertainty about an agent’s benefit – most notably, whether it will improve a patient’s survival or quality of life. Dr. Khaki pointed to a study published in JAMA Internal Medicine, which found that only 19 of 93 (20%) cancer drugs that had been recently approved through the FDA’s accelerated approval pathway demonstrated an improvement in overall survival.
In the new study, published online in JAMA Network Open, Dr. Khaki and colleagues found that among the 89 cancer drugs approved in the United States and Europe between January 2010 and December 2019, the FDA approved 85 (95%) before European authorization and four (5%) after.
The researchers found that the median FDA review time was half that of the EMA’s (200 vs. 426 days). Furthermore, 64 new drug applications (72%) were submitted to the FDA first, compared with 21 (23%) to the EMA.
Of the drugs approved through an accelerated pathway, three were ultimately pulled from the U.S. market, compared with one in Europe.
“These early drug approvals that later lead to withdrawal expose many more patients to toxicity, including financial toxicity, given the high cost of cancer medications,” Dr. Khaki commented.
In addition, 35 oncology therapies (39%) were approved by the FDA before trial results were published, compared with only eight (9%) by the EMA. Although FDA drug labels contain some information about efficacy and toxicity, scientific publications often have much more, including details about study populations and toxicities.
“Without this information, providers may be limited in their knowledge about patient selection, clinical benefit, and optimal toxicity management,” Dr. Khaki said.
Jeff Allen PhD, president and CEO of the nonprofit Friends of Cancer Research, who wasn’t involved in the study, believes that an FDA approval before publication shouldn’t be “particularly concerning.”
“Peer-reviewed publication is an important component of validating and communicating scientific findings, but the processes and time lines for individual journals can be highly variable,” he said. “I don’t think we would want to see a situation where potential beneficial treatments are held up due to unrelated publication processes.”
The author of an invited commentary in JAMA Network Open had a different take on the study findings.
“A tempting interpretation” of this study is that the FDA is a “superior agency for expedited review times that bring cancer drugs to patients earlier,” Kristina Jenei, BSN, MSc, with the University of British Columbia School of Population and Public Health, writes. In addition, the fact that more drugs were pulled from the market after approval in the United States than in Europe could be interpreted to mean that the system is working as it should.
Although the speed of FDA reviews and the number of subsequent approvals have increased over time, the proportion of cancer drugs that improve survival has declined. In addition, because the FDA’s follow-up of postmarketing studies has been “inconsistent,” a substantial number of cancer drugs that were approved through accelerated pathways have remained on the market for years without confirmation of their benefit.
Although regulatory agencies must balance earlier patient access to novel treatments with evidence that the therapies are effective and safe, “faster review times and approvals are not cause for celebration; better patient outcomes are,” Ms. Jenei writes. “In other words, quality over quantity.”
The study was supported by the National Cancer Institute. Dr. Khaki reported stock ownership from Merck and stock ownership from Sanofi outside the submitted work. Dr. Allen and Ms. Jenei have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JAMA NETWORK OPEN
FDA approves risankizumab (Skyrizi) for Crohn’s disease
The U.S. Food and Drug Administration – making it the first specific anti–interleukin-23 monoclonal antibody indicated for Crohn’s disease.
The safety and efficacy of risankizumab in Crohn’s disease is supported by data from two induction clinical trials (ADVANCE and MOTIVATE) and one maintenance clinical trial (FORTIFY).
Results of the three studies were presented at the annual scientific meeting of the American College of Gastroenterology in 2021.
“In both the induction and maintenance clinical trials, a significantly greater number of adult patients saw few or no symptoms and a meaningful reduction of visible signs of intestinal inflammation, compared to placebo,” Marla Dubinsky, MD, gastroenterologist with the Mount Sinai Health System and codirector of the IBD Center at Mount Sinai, New York, said in a news release from AbbVie.
“This approval provides health care professionals with a greatly needed additional option for treating the disruptive symptoms of Crohn’s disease,” Dr. Dubinsky said.
For the treatment of Crohn’s disease, risankizumab is dosed at 600 mg administered by intravenous infusion over at least 1 hour at week 0, 4, and 8, followed by 360 mg self-administered by subcutaneous injection at week 12, and every 8 weeks thereafter.
Risankizumab is already approved in the United States for the treatment of adults with active psoriatic arthritis and moderate to severe plaque psoriasis.
A version of this article first appeared on Medscape.com.
The U.S. Food and Drug Administration – making it the first specific anti–interleukin-23 monoclonal antibody indicated for Crohn’s disease.
The safety and efficacy of risankizumab in Crohn’s disease is supported by data from two induction clinical trials (ADVANCE and MOTIVATE) and one maintenance clinical trial (FORTIFY).
Results of the three studies were presented at the annual scientific meeting of the American College of Gastroenterology in 2021.
“In both the induction and maintenance clinical trials, a significantly greater number of adult patients saw few or no symptoms and a meaningful reduction of visible signs of intestinal inflammation, compared to placebo,” Marla Dubinsky, MD, gastroenterologist with the Mount Sinai Health System and codirector of the IBD Center at Mount Sinai, New York, said in a news release from AbbVie.
“This approval provides health care professionals with a greatly needed additional option for treating the disruptive symptoms of Crohn’s disease,” Dr. Dubinsky said.
For the treatment of Crohn’s disease, risankizumab is dosed at 600 mg administered by intravenous infusion over at least 1 hour at week 0, 4, and 8, followed by 360 mg self-administered by subcutaneous injection at week 12, and every 8 weeks thereafter.
Risankizumab is already approved in the United States for the treatment of adults with active psoriatic arthritis and moderate to severe plaque psoriasis.
A version of this article first appeared on Medscape.com.
The U.S. Food and Drug Administration – making it the first specific anti–interleukin-23 monoclonal antibody indicated for Crohn’s disease.
The safety and efficacy of risankizumab in Crohn’s disease is supported by data from two induction clinical trials (ADVANCE and MOTIVATE) and one maintenance clinical trial (FORTIFY).
Results of the three studies were presented at the annual scientific meeting of the American College of Gastroenterology in 2021.
“In both the induction and maintenance clinical trials, a significantly greater number of adult patients saw few or no symptoms and a meaningful reduction of visible signs of intestinal inflammation, compared to placebo,” Marla Dubinsky, MD, gastroenterologist with the Mount Sinai Health System and codirector of the IBD Center at Mount Sinai, New York, said in a news release from AbbVie.
“This approval provides health care professionals with a greatly needed additional option for treating the disruptive symptoms of Crohn’s disease,” Dr. Dubinsky said.
For the treatment of Crohn’s disease, risankizumab is dosed at 600 mg administered by intravenous infusion over at least 1 hour at week 0, 4, and 8, followed by 360 mg self-administered by subcutaneous injection at week 12, and every 8 weeks thereafter.
Risankizumab is already approved in the United States for the treatment of adults with active psoriatic arthritis and moderate to severe plaque psoriasis.
A version of this article first appeared on Medscape.com.
Snoring may lead to a sedentary lifestyle
“People who snore are also likely to have sleep apnea, but those who snore and don’t have sleep apnea are a largely understudied group,” senior author Michael Grandner, PhD, told this news organization.
“We found that even just snoring alone can impact health and well-being,” said Dr. Grandner, director of the sleep and health research program at the University of Arizona, Tucson.
The findings were presented at the annual meeting of the Associated Professional Sleep Societies.
A viscous cycle
Frequent snoring can signal sleep-disordered breathing, which is associated with a myriad of comorbidities, including increased risk for cardiovascular disease.
Prior studies have shown that sleep-disordered breathing is associated with less physical activity, but few studies have examined this at the population level or in relation to primary snoring.
Dr. Grandner and colleagues evaluated the relationship between snoring frequency and minutes of sedentary activity using 3 years’ worth of data from the National Health and Nutrition Examination Survey. Participants reported snoring frequency and sedentary activity.
After adjusting for sex, age, race, education level, and marital status, adults who were frequent snorers (5+ nights per week) spent about 36 more minutes per day sedentary, compared with peers who reported never snoring.
In addition, those individuals who were determined to be at increased risk of having sleep apnea had about 54 more minutes per day of sedentary time in the adjusted model.
“Snoring is very common, and it doesn’t just affect the nighttime,” said Dr. Grandner.
Snoring can lead to “more tiredness and less energy, which can impact everything from mood to stress to – as we saw – activity level,” he noted.
Commenting on the results for this news organization, Raman Malhotra, MD, of the Washington University Sleep Center in St. Louis, said this study clearly demonstrates how people who snore and people who are at risk for sleep apnea are more sedentary.
This could explain the “vicious cycle” that these patients suffer from, inasmuch as having obesity can lead to sleep apnea, and having sleep apnea can lead to further sedentary lifestyle and weight gain, owing to lack of energy and feeling tired, Dr. Malhotra told this news organization.
“It is important to intervene and treat the sleep disorder to hopefully make people more active,” he added.
The study had no specific funding. Dr. Grandner and Dr. Malhotra disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
“People who snore are also likely to have sleep apnea, but those who snore and don’t have sleep apnea are a largely understudied group,” senior author Michael Grandner, PhD, told this news organization.
“We found that even just snoring alone can impact health and well-being,” said Dr. Grandner, director of the sleep and health research program at the University of Arizona, Tucson.
The findings were presented at the annual meeting of the Associated Professional Sleep Societies.
A viscous cycle
Frequent snoring can signal sleep-disordered breathing, which is associated with a myriad of comorbidities, including increased risk for cardiovascular disease.
Prior studies have shown that sleep-disordered breathing is associated with less physical activity, but few studies have examined this at the population level or in relation to primary snoring.
Dr. Grandner and colleagues evaluated the relationship between snoring frequency and minutes of sedentary activity using 3 years’ worth of data from the National Health and Nutrition Examination Survey. Participants reported snoring frequency and sedentary activity.
After adjusting for sex, age, race, education level, and marital status, adults who were frequent snorers (5+ nights per week) spent about 36 more minutes per day sedentary, compared with peers who reported never snoring.
In addition, those individuals who were determined to be at increased risk of having sleep apnea had about 54 more minutes per day of sedentary time in the adjusted model.
“Snoring is very common, and it doesn’t just affect the nighttime,” said Dr. Grandner.
Snoring can lead to “more tiredness and less energy, which can impact everything from mood to stress to – as we saw – activity level,” he noted.
Commenting on the results for this news organization, Raman Malhotra, MD, of the Washington University Sleep Center in St. Louis, said this study clearly demonstrates how people who snore and people who are at risk for sleep apnea are more sedentary.
This could explain the “vicious cycle” that these patients suffer from, inasmuch as having obesity can lead to sleep apnea, and having sleep apnea can lead to further sedentary lifestyle and weight gain, owing to lack of energy and feeling tired, Dr. Malhotra told this news organization.
“It is important to intervene and treat the sleep disorder to hopefully make people more active,” he added.
The study had no specific funding. Dr. Grandner and Dr. Malhotra disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
“People who snore are also likely to have sleep apnea, but those who snore and don’t have sleep apnea are a largely understudied group,” senior author Michael Grandner, PhD, told this news organization.
“We found that even just snoring alone can impact health and well-being,” said Dr. Grandner, director of the sleep and health research program at the University of Arizona, Tucson.
The findings were presented at the annual meeting of the Associated Professional Sleep Societies.
A viscous cycle
Frequent snoring can signal sleep-disordered breathing, which is associated with a myriad of comorbidities, including increased risk for cardiovascular disease.
Prior studies have shown that sleep-disordered breathing is associated with less physical activity, but few studies have examined this at the population level or in relation to primary snoring.
Dr. Grandner and colleagues evaluated the relationship between snoring frequency and minutes of sedentary activity using 3 years’ worth of data from the National Health and Nutrition Examination Survey. Participants reported snoring frequency and sedentary activity.
After adjusting for sex, age, race, education level, and marital status, adults who were frequent snorers (5+ nights per week) spent about 36 more minutes per day sedentary, compared with peers who reported never snoring.
In addition, those individuals who were determined to be at increased risk of having sleep apnea had about 54 more minutes per day of sedentary time in the adjusted model.
“Snoring is very common, and it doesn’t just affect the nighttime,” said Dr. Grandner.
Snoring can lead to “more tiredness and less energy, which can impact everything from mood to stress to – as we saw – activity level,” he noted.
Commenting on the results for this news organization, Raman Malhotra, MD, of the Washington University Sleep Center in St. Louis, said this study clearly demonstrates how people who snore and people who are at risk for sleep apnea are more sedentary.
This could explain the “vicious cycle” that these patients suffer from, inasmuch as having obesity can lead to sleep apnea, and having sleep apnea can lead to further sedentary lifestyle and weight gain, owing to lack of energy and feeling tired, Dr. Malhotra told this news organization.
“It is important to intervene and treat the sleep disorder to hopefully make people more active,” he added.
The study had no specific funding. Dr. Grandner and Dr. Malhotra disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM SLEEP 2022