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Treating sleep apnea lowers MI and stroke risk
particularly for patients with moderate to severe OSA and those who are more adherent to CPAP therapy, a new study suggests.
“Most clinical trials on the effect of CPAP on CV diseases to date have focused on secondary CV prevention. This study contributes another piece of evidence about the role of CPAP therapy to prevent CV diseases,” said Diego R. Mazzotti, PhD, an assistant professor at the University of Kansas Medical Center, Kansas City.
“Our study, while observational, suggests that clinical trials focused on understanding how to sustain long-term CPAP adherence in obstructive sleep apnea patients are necessary and could be critical for optimizing comorbidity risk reduction,” Dr. Mazzotti said.
The study was presented at the virtual annual meeting of the Associated Professional Sleep Societies.
Good adherence important
The researchers analyzed the electronic health records of adults referred for a sleep study through the Kaiser Permanente Southern California health system. The sample included 11,145 adults without OSA, 13,898 with OSA who used CPAP, and 20,884 adults with OSA who did not use CPAP. None of them had CV disease at baseline. Median follow-up was 262 days.
The primary outcome was first occurrence of myocardial infarction, stroke, unstable angina, heart failure, or death caused by CV disease.
In adjusted models, adults with moderate to severe OSA (apnea-hypopnea index ≥15) who did not use CPAP were 71% more likely than those without OSA to have a first CV event (hazard ratio, 1.71; 95% CI, 1.11-2.64). However, the risk for a CV event during follow-up was 32% lower among OSA patients with any CPAP use (HR, 0.68; 95% CI, 0.50-0.93; P = .016).
The effect was mostly driven by those who used CPAP for at least 4 hours per night (HR, 0.60; 95% CI, 0.39-0.95). This association was stronger for those with moderate to severe OSA (HR, 0.56; 95% CI, 0.39-0.81).
“This study highlights the importance of long-term management of CPAP therapy in patients with moderate-severe OSA,” Dr. Mazzotti said in an interview.
“It suggests that maintaining good CPAP adherence might be beneficial for cardiovascular health, besides the already established benefits on quality of life, sleepiness, and other cardiometabolic functions,” he said.
Dr. Mazzotti said several mechanisms might explain the association between CPAP use and lower risk for CV events. “CPAP treats OSA by preventing respiratory pauses that occur during sleep, therefore preventing arousals, sleep fragmentation, and decreases in blood oxygen. These improved cardiorespiratory functions can be beneficial to avoid certain molecular changes that are known to contribute to cardiovascular risk, such as oxidative stress and inflammation,” he explained.
“However, specific studies fully understanding these mechanisms are necessary,” Dr. Mazzotti added.
In a comment, Nitun Verma, MD, a spokesperson for the American Academy of Sleep Medicine, said that “the frequent decreases in oxygen levels and fragmented sleep from apnea are associated with cardiovascular disorders. We know this from multiple studies. This, however, was a large study and strengthens the association between improving apnea and reduced serious cardiovascular events.”
Funding for the study was provided by the American Academy of Sleep Medicine Foundation and the American Heart Association. Dr. Mazzotti and Dr. Verma disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
particularly for patients with moderate to severe OSA and those who are more adherent to CPAP therapy, a new study suggests.
“Most clinical trials on the effect of CPAP on CV diseases to date have focused on secondary CV prevention. This study contributes another piece of evidence about the role of CPAP therapy to prevent CV diseases,” said Diego R. Mazzotti, PhD, an assistant professor at the University of Kansas Medical Center, Kansas City.
“Our study, while observational, suggests that clinical trials focused on understanding how to sustain long-term CPAP adherence in obstructive sleep apnea patients are necessary and could be critical for optimizing comorbidity risk reduction,” Dr. Mazzotti said.
The study was presented at the virtual annual meeting of the Associated Professional Sleep Societies.
Good adherence important
The researchers analyzed the electronic health records of adults referred for a sleep study through the Kaiser Permanente Southern California health system. The sample included 11,145 adults without OSA, 13,898 with OSA who used CPAP, and 20,884 adults with OSA who did not use CPAP. None of them had CV disease at baseline. Median follow-up was 262 days.
The primary outcome was first occurrence of myocardial infarction, stroke, unstable angina, heart failure, or death caused by CV disease.
In adjusted models, adults with moderate to severe OSA (apnea-hypopnea index ≥15) who did not use CPAP were 71% more likely than those without OSA to have a first CV event (hazard ratio, 1.71; 95% CI, 1.11-2.64). However, the risk for a CV event during follow-up was 32% lower among OSA patients with any CPAP use (HR, 0.68; 95% CI, 0.50-0.93; P = .016).
The effect was mostly driven by those who used CPAP for at least 4 hours per night (HR, 0.60; 95% CI, 0.39-0.95). This association was stronger for those with moderate to severe OSA (HR, 0.56; 95% CI, 0.39-0.81).
“This study highlights the importance of long-term management of CPAP therapy in patients with moderate-severe OSA,” Dr. Mazzotti said in an interview.
“It suggests that maintaining good CPAP adherence might be beneficial for cardiovascular health, besides the already established benefits on quality of life, sleepiness, and other cardiometabolic functions,” he said.
Dr. Mazzotti said several mechanisms might explain the association between CPAP use and lower risk for CV events. “CPAP treats OSA by preventing respiratory pauses that occur during sleep, therefore preventing arousals, sleep fragmentation, and decreases in blood oxygen. These improved cardiorespiratory functions can be beneficial to avoid certain molecular changes that are known to contribute to cardiovascular risk, such as oxidative stress and inflammation,” he explained.
“However, specific studies fully understanding these mechanisms are necessary,” Dr. Mazzotti added.
In a comment, Nitun Verma, MD, a spokesperson for the American Academy of Sleep Medicine, said that “the frequent decreases in oxygen levels and fragmented sleep from apnea are associated with cardiovascular disorders. We know this from multiple studies. This, however, was a large study and strengthens the association between improving apnea and reduced serious cardiovascular events.”
Funding for the study was provided by the American Academy of Sleep Medicine Foundation and the American Heart Association. Dr. Mazzotti and Dr. Verma disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
particularly for patients with moderate to severe OSA and those who are more adherent to CPAP therapy, a new study suggests.
“Most clinical trials on the effect of CPAP on CV diseases to date have focused on secondary CV prevention. This study contributes another piece of evidence about the role of CPAP therapy to prevent CV diseases,” said Diego R. Mazzotti, PhD, an assistant professor at the University of Kansas Medical Center, Kansas City.
“Our study, while observational, suggests that clinical trials focused on understanding how to sustain long-term CPAP adherence in obstructive sleep apnea patients are necessary and could be critical for optimizing comorbidity risk reduction,” Dr. Mazzotti said.
The study was presented at the virtual annual meeting of the Associated Professional Sleep Societies.
Good adherence important
The researchers analyzed the electronic health records of adults referred for a sleep study through the Kaiser Permanente Southern California health system. The sample included 11,145 adults without OSA, 13,898 with OSA who used CPAP, and 20,884 adults with OSA who did not use CPAP. None of them had CV disease at baseline. Median follow-up was 262 days.
The primary outcome was first occurrence of myocardial infarction, stroke, unstable angina, heart failure, or death caused by CV disease.
In adjusted models, adults with moderate to severe OSA (apnea-hypopnea index ≥15) who did not use CPAP were 71% more likely than those without OSA to have a first CV event (hazard ratio, 1.71; 95% CI, 1.11-2.64). However, the risk for a CV event during follow-up was 32% lower among OSA patients with any CPAP use (HR, 0.68; 95% CI, 0.50-0.93; P = .016).
The effect was mostly driven by those who used CPAP for at least 4 hours per night (HR, 0.60; 95% CI, 0.39-0.95). This association was stronger for those with moderate to severe OSA (HR, 0.56; 95% CI, 0.39-0.81).
“This study highlights the importance of long-term management of CPAP therapy in patients with moderate-severe OSA,” Dr. Mazzotti said in an interview.
“It suggests that maintaining good CPAP adherence might be beneficial for cardiovascular health, besides the already established benefits on quality of life, sleepiness, and other cardiometabolic functions,” he said.
Dr. Mazzotti said several mechanisms might explain the association between CPAP use and lower risk for CV events. “CPAP treats OSA by preventing respiratory pauses that occur during sleep, therefore preventing arousals, sleep fragmentation, and decreases in blood oxygen. These improved cardiorespiratory functions can be beneficial to avoid certain molecular changes that are known to contribute to cardiovascular risk, such as oxidative stress and inflammation,” he explained.
“However, specific studies fully understanding these mechanisms are necessary,” Dr. Mazzotti added.
In a comment, Nitun Verma, MD, a spokesperson for the American Academy of Sleep Medicine, said that “the frequent decreases in oxygen levels and fragmented sleep from apnea are associated with cardiovascular disorders. We know this from multiple studies. This, however, was a large study and strengthens the association between improving apnea and reduced serious cardiovascular events.”
Funding for the study was provided by the American Academy of Sleep Medicine Foundation and the American Heart Association. Dr. Mazzotti and Dr. Verma disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM SLEEP 2021
Potential first-in-class, targeted therapy for myasthenia gravis
(gMG), new research suggests. Results from the phase 3, randomized, placebo-controlled ADAPT trial showed that reduction in disease burden and improvement in strength and quality of life in patients with gMG were consistent across four MG-specific scales for those receiving the novel treatment. In addition, these benefits were observed early and were reproducible and durable, the researchers noted.
Efgartigimod is a “very rapidly acting drug relative to other treatments that may take 4, 6, sometimes 10 months before they start to work, and the side effect profile is much like placebo,” said principal investigator James Howard, Jr., MD, Distinguished Professor of Neuromuscular Disease, department of neurology, University of North Carolina at Chapel Hill.
The ADAPT results are “important for the MG community, and I am hopeful efgartigimod will provide a first-in-class targeted therapy that can be dosed in an individual way for people living with this chronic autoimmune disease,” Dr. Howard added in a news release.
The findings were published online June 17 in Lancet Neurology.
Targeted molecular therapy
The rare and chronic autoimmune neuromuscular disorder of gMG causes debilitating and potentially life-threatening muscle weakness and significantly impaired independence and quality of life. Most patients with gMG have immunoglobulin G (IgG) antibodies, which are most often directed against skeletal muscle nicotinic acetylcholine receptors.
Efgartigimod is an investigational antibody fragment designed to reduce pathogenic IgG antibodies and block the IgG recycling process in patients with gMG.
The novel agent binds to the neonatal Fc receptor (FcRn), which is widely expressed throughout the body and plays a central role in rescuing IgG antibodies from degradation. Blocking FcRn reduces IgG antibody levels.
The ADAPT trial was conducted at 56 neuromuscular academic and community centers in 15 countries in North America, Europe, and Japan. The study included 167 adults with gMG, regardless of acetylcholine receptor antibody status. All had a Myasthenia Gravis Activities of Daily Living (MG-ADL) score of at least 5 (greater than 50% non-ocular) on a background of a stable dose of at least one MG drug.
For 26 weeks, 84 patients were randomly assigned to receive efgartigimod 10 mg/kg and 83 to receive matching placebo. Both treatments were administered as four infusions per cycle at one infusion per week. The process was repeated as needed depending on clinical response no sooner than 8 weeks after initiation of the previous cycle.
ADAPT was designed to allow an individualized treatment approach with an initial treatment cycle followed by a variable number of subsequent treatment cycles, the investigators noted.
Primary endpoint met
The primary efficacy endpoint was number of acetylcholine receptor antibody-positive (AChR-Ab+) patients who achieved a clinically meaningful response on the MG-ADL score. This was defined as at least a 2-point improvement from baseline for 4 or more consecutive weeks. Forty-four (68%) of 65 AChR-Ab+ patients treated with efgartigimod met this endpoint versus 19 (30%) of 64 patients treated with placebo (odds ratio, 4.95; 95% confidence interval, 2.21-11.53; P < .0001).
Many of the patients treated with efgartigimod showed improvement “beyond the clinically meaningful threshold, achieving up to 9-point reductions in MG-ADL,” the investigators reported. In addition, 40% of the efgartigimod group attained an MG-ADL score of 0 or 1 (minimal symptom expression) in cycle 1 versus 11% of the placebo group (P < .0001).
Nearly two-thirds (63%) of AChR-Ab+ patients responded to the first cycle of efgartigimod, and most of these patients (83%) responded to treatment within the first 2 weeks. Among the AChR-Ab+ participants who responded to efgartigimod in cycle 1, the duration of responder status was 6 to 7 weeks in 32% of patients, 8 to 11 weeks in 23% of patients, and 12 weeks or more in 34% of patients.
Safety profile
“Some patients never required retreatment over the 26-week period that they were under observation,” Dr. Howard said. “Patients want to be individuals. They don’t want to be assigned to a regimented therapy, and I think these results show that this therapy can be tailored to the individual patient, rather than simply giving it to them in a cookbook fashion,” he added.
The safety profile of efgartigimod was comparable to placebo. Most adverse events were mild or moderate in severity. The most commonly reported adverse events were headache, nasopharyngitis, nausea, diarrhea, upper respiratory tract infection, and urinary tract infection.
Four (5%) efgartigimod-treated patients had a serious adverse event, which included thrombocytosis, rectal adenocarcinoma, worsening MG, and depression.
The novel agent is currently under review with the U.S. Food and Drug Administration for the treatment of gMG, with a Prescription Drug User Fee Act target action date of Dec. 17. If approved, it would become the first FDA-approved FcRn antagonist.
Expanding therapeutic landscape
In a linked commentary, Shigeaki Suzuki, MD, PhD, department of neurology, Keio University School of Medicine, Tokyo, noted that the therapeutic landscape for patients with MG is “expanding year by year,” with several additional complement inhibitors and FcRn antagonists now in phase 3 testing.
“Biological drugs should be preferentially used as the treatment for patients with refractory myasthenia gravis, although the definition of refractory myasthenia gravis is different depending on the criteria used,” Dr. Suzuki wrote.
He noted that when “cost-effectiveness is not taken into account, targeted molecular therapy might be used widely” in patients with MG.
“Risks of myasthenic exacerbation and crises should be substantially decreased, particularly in patients with refractory myasthenia gravis,” Dr. Suzuki added.
The ADAPT study was supported by argenx. Dr. Howard has reported receiving research support from argenx, Alexion Pharmaceuticals, the Centers for Disease Control and Prevention, the Muscular Dystrophy Association, the National Institutes of Health, Patient-Centered Outcomes Research Institute, and Ra Pharmaceuticals; honoraria from argenx, Alexion, Immunovant, Ra, Regeneron Pharmaceuticals, and Viela Bio; and nonfinancial support from argenx, Alexion, Ra, and Toleranzia. Disclosures for the other investigators are listed in the original article. Dr. Suzuki has reported relationships with Alexion Pharmaceuticals, Japan Blood Products Organization, and Asahi Kasei Medical.
A version of this article first appeared on Medscape.com.
(gMG), new research suggests. Results from the phase 3, randomized, placebo-controlled ADAPT trial showed that reduction in disease burden and improvement in strength and quality of life in patients with gMG were consistent across four MG-specific scales for those receiving the novel treatment. In addition, these benefits were observed early and were reproducible and durable, the researchers noted.
Efgartigimod is a “very rapidly acting drug relative to other treatments that may take 4, 6, sometimes 10 months before they start to work, and the side effect profile is much like placebo,” said principal investigator James Howard, Jr., MD, Distinguished Professor of Neuromuscular Disease, department of neurology, University of North Carolina at Chapel Hill.
The ADAPT results are “important for the MG community, and I am hopeful efgartigimod will provide a first-in-class targeted therapy that can be dosed in an individual way for people living with this chronic autoimmune disease,” Dr. Howard added in a news release.
The findings were published online June 17 in Lancet Neurology.
Targeted molecular therapy
The rare and chronic autoimmune neuromuscular disorder of gMG causes debilitating and potentially life-threatening muscle weakness and significantly impaired independence and quality of life. Most patients with gMG have immunoglobulin G (IgG) antibodies, which are most often directed against skeletal muscle nicotinic acetylcholine receptors.
Efgartigimod is an investigational antibody fragment designed to reduce pathogenic IgG antibodies and block the IgG recycling process in patients with gMG.
The novel agent binds to the neonatal Fc receptor (FcRn), which is widely expressed throughout the body and plays a central role in rescuing IgG antibodies from degradation. Blocking FcRn reduces IgG antibody levels.
The ADAPT trial was conducted at 56 neuromuscular academic and community centers in 15 countries in North America, Europe, and Japan. The study included 167 adults with gMG, regardless of acetylcholine receptor antibody status. All had a Myasthenia Gravis Activities of Daily Living (MG-ADL) score of at least 5 (greater than 50% non-ocular) on a background of a stable dose of at least one MG drug.
For 26 weeks, 84 patients were randomly assigned to receive efgartigimod 10 mg/kg and 83 to receive matching placebo. Both treatments were administered as four infusions per cycle at one infusion per week. The process was repeated as needed depending on clinical response no sooner than 8 weeks after initiation of the previous cycle.
ADAPT was designed to allow an individualized treatment approach with an initial treatment cycle followed by a variable number of subsequent treatment cycles, the investigators noted.
Primary endpoint met
The primary efficacy endpoint was number of acetylcholine receptor antibody-positive (AChR-Ab+) patients who achieved a clinically meaningful response on the MG-ADL score. This was defined as at least a 2-point improvement from baseline for 4 or more consecutive weeks. Forty-four (68%) of 65 AChR-Ab+ patients treated with efgartigimod met this endpoint versus 19 (30%) of 64 patients treated with placebo (odds ratio, 4.95; 95% confidence interval, 2.21-11.53; P < .0001).
Many of the patients treated with efgartigimod showed improvement “beyond the clinically meaningful threshold, achieving up to 9-point reductions in MG-ADL,” the investigators reported. In addition, 40% of the efgartigimod group attained an MG-ADL score of 0 or 1 (minimal symptom expression) in cycle 1 versus 11% of the placebo group (P < .0001).
Nearly two-thirds (63%) of AChR-Ab+ patients responded to the first cycle of efgartigimod, and most of these patients (83%) responded to treatment within the first 2 weeks. Among the AChR-Ab+ participants who responded to efgartigimod in cycle 1, the duration of responder status was 6 to 7 weeks in 32% of patients, 8 to 11 weeks in 23% of patients, and 12 weeks or more in 34% of patients.
Safety profile
“Some patients never required retreatment over the 26-week period that they were under observation,” Dr. Howard said. “Patients want to be individuals. They don’t want to be assigned to a regimented therapy, and I think these results show that this therapy can be tailored to the individual patient, rather than simply giving it to them in a cookbook fashion,” he added.
The safety profile of efgartigimod was comparable to placebo. Most adverse events were mild or moderate in severity. The most commonly reported adverse events were headache, nasopharyngitis, nausea, diarrhea, upper respiratory tract infection, and urinary tract infection.
Four (5%) efgartigimod-treated patients had a serious adverse event, which included thrombocytosis, rectal adenocarcinoma, worsening MG, and depression.
The novel agent is currently under review with the U.S. Food and Drug Administration for the treatment of gMG, with a Prescription Drug User Fee Act target action date of Dec. 17. If approved, it would become the first FDA-approved FcRn antagonist.
Expanding therapeutic landscape
In a linked commentary, Shigeaki Suzuki, MD, PhD, department of neurology, Keio University School of Medicine, Tokyo, noted that the therapeutic landscape for patients with MG is “expanding year by year,” with several additional complement inhibitors and FcRn antagonists now in phase 3 testing.
“Biological drugs should be preferentially used as the treatment for patients with refractory myasthenia gravis, although the definition of refractory myasthenia gravis is different depending on the criteria used,” Dr. Suzuki wrote.
He noted that when “cost-effectiveness is not taken into account, targeted molecular therapy might be used widely” in patients with MG.
“Risks of myasthenic exacerbation and crises should be substantially decreased, particularly in patients with refractory myasthenia gravis,” Dr. Suzuki added.
The ADAPT study was supported by argenx. Dr. Howard has reported receiving research support from argenx, Alexion Pharmaceuticals, the Centers for Disease Control and Prevention, the Muscular Dystrophy Association, the National Institutes of Health, Patient-Centered Outcomes Research Institute, and Ra Pharmaceuticals; honoraria from argenx, Alexion, Immunovant, Ra, Regeneron Pharmaceuticals, and Viela Bio; and nonfinancial support from argenx, Alexion, Ra, and Toleranzia. Disclosures for the other investigators are listed in the original article. Dr. Suzuki has reported relationships with Alexion Pharmaceuticals, Japan Blood Products Organization, and Asahi Kasei Medical.
A version of this article first appeared on Medscape.com.
(gMG), new research suggests. Results from the phase 3, randomized, placebo-controlled ADAPT trial showed that reduction in disease burden and improvement in strength and quality of life in patients with gMG were consistent across four MG-specific scales for those receiving the novel treatment. In addition, these benefits were observed early and were reproducible and durable, the researchers noted.
Efgartigimod is a “very rapidly acting drug relative to other treatments that may take 4, 6, sometimes 10 months before they start to work, and the side effect profile is much like placebo,” said principal investigator James Howard, Jr., MD, Distinguished Professor of Neuromuscular Disease, department of neurology, University of North Carolina at Chapel Hill.
The ADAPT results are “important for the MG community, and I am hopeful efgartigimod will provide a first-in-class targeted therapy that can be dosed in an individual way for people living with this chronic autoimmune disease,” Dr. Howard added in a news release.
The findings were published online June 17 in Lancet Neurology.
Targeted molecular therapy
The rare and chronic autoimmune neuromuscular disorder of gMG causes debilitating and potentially life-threatening muscle weakness and significantly impaired independence and quality of life. Most patients with gMG have immunoglobulin G (IgG) antibodies, which are most often directed against skeletal muscle nicotinic acetylcholine receptors.
Efgartigimod is an investigational antibody fragment designed to reduce pathogenic IgG antibodies and block the IgG recycling process in patients with gMG.
The novel agent binds to the neonatal Fc receptor (FcRn), which is widely expressed throughout the body and plays a central role in rescuing IgG antibodies from degradation. Blocking FcRn reduces IgG antibody levels.
The ADAPT trial was conducted at 56 neuromuscular academic and community centers in 15 countries in North America, Europe, and Japan. The study included 167 adults with gMG, regardless of acetylcholine receptor antibody status. All had a Myasthenia Gravis Activities of Daily Living (MG-ADL) score of at least 5 (greater than 50% non-ocular) on a background of a stable dose of at least one MG drug.
For 26 weeks, 84 patients were randomly assigned to receive efgartigimod 10 mg/kg and 83 to receive matching placebo. Both treatments were administered as four infusions per cycle at one infusion per week. The process was repeated as needed depending on clinical response no sooner than 8 weeks after initiation of the previous cycle.
ADAPT was designed to allow an individualized treatment approach with an initial treatment cycle followed by a variable number of subsequent treatment cycles, the investigators noted.
Primary endpoint met
The primary efficacy endpoint was number of acetylcholine receptor antibody-positive (AChR-Ab+) patients who achieved a clinically meaningful response on the MG-ADL score. This was defined as at least a 2-point improvement from baseline for 4 or more consecutive weeks. Forty-four (68%) of 65 AChR-Ab+ patients treated with efgartigimod met this endpoint versus 19 (30%) of 64 patients treated with placebo (odds ratio, 4.95; 95% confidence interval, 2.21-11.53; P < .0001).
Many of the patients treated with efgartigimod showed improvement “beyond the clinically meaningful threshold, achieving up to 9-point reductions in MG-ADL,” the investigators reported. In addition, 40% of the efgartigimod group attained an MG-ADL score of 0 or 1 (minimal symptom expression) in cycle 1 versus 11% of the placebo group (P < .0001).
Nearly two-thirds (63%) of AChR-Ab+ patients responded to the first cycle of efgartigimod, and most of these patients (83%) responded to treatment within the first 2 weeks. Among the AChR-Ab+ participants who responded to efgartigimod in cycle 1, the duration of responder status was 6 to 7 weeks in 32% of patients, 8 to 11 weeks in 23% of patients, and 12 weeks or more in 34% of patients.
Safety profile
“Some patients never required retreatment over the 26-week period that they were under observation,” Dr. Howard said. “Patients want to be individuals. They don’t want to be assigned to a regimented therapy, and I think these results show that this therapy can be tailored to the individual patient, rather than simply giving it to them in a cookbook fashion,” he added.
The safety profile of efgartigimod was comparable to placebo. Most adverse events were mild or moderate in severity. The most commonly reported adverse events were headache, nasopharyngitis, nausea, diarrhea, upper respiratory tract infection, and urinary tract infection.
Four (5%) efgartigimod-treated patients had a serious adverse event, which included thrombocytosis, rectal adenocarcinoma, worsening MG, and depression.
The novel agent is currently under review with the U.S. Food and Drug Administration for the treatment of gMG, with a Prescription Drug User Fee Act target action date of Dec. 17. If approved, it would become the first FDA-approved FcRn antagonist.
Expanding therapeutic landscape
In a linked commentary, Shigeaki Suzuki, MD, PhD, department of neurology, Keio University School of Medicine, Tokyo, noted that the therapeutic landscape for patients with MG is “expanding year by year,” with several additional complement inhibitors and FcRn antagonists now in phase 3 testing.
“Biological drugs should be preferentially used as the treatment for patients with refractory myasthenia gravis, although the definition of refractory myasthenia gravis is different depending on the criteria used,” Dr. Suzuki wrote.
He noted that when “cost-effectiveness is not taken into account, targeted molecular therapy might be used widely” in patients with MG.
“Risks of myasthenic exacerbation and crises should be substantially decreased, particularly in patients with refractory myasthenia gravis,” Dr. Suzuki added.
The ADAPT study was supported by argenx. Dr. Howard has reported receiving research support from argenx, Alexion Pharmaceuticals, the Centers for Disease Control and Prevention, the Muscular Dystrophy Association, the National Institutes of Health, Patient-Centered Outcomes Research Institute, and Ra Pharmaceuticals; honoraria from argenx, Alexion, Immunovant, Ra, Regeneron Pharmaceuticals, and Viela Bio; and nonfinancial support from argenx, Alexion, Ra, and Toleranzia. Disclosures for the other investigators are listed in the original article. Dr. Suzuki has reported relationships with Alexion Pharmaceuticals, Japan Blood Products Organization, and Asahi Kasei Medical.
A version of this article first appeared on Medscape.com.
From Lancet Neurology
Is trouble falling asleep a modifiable risk factor for dementia?
, new research suggests.
Trouble falling asleep “may be a modifiable risk factor for later-life cognitive impairment and dementia,” said lead author Afsara Zaheed, a PhD candidate in clinical science, department of psychology, University of Michigan, Ann Arbor.
“Patients should also be aware of the importance of insomnia on cognitive functioning so that they can bring up these concerns with their providers early,” she said.
The findings were presented at Virtual SLEEP 2021, the 35th Annual Meeting of the Associated Professional Sleep Societies.
Poor sleep common with age
As many as one-half of older adults report having poor sleep quality and insomnia, and growing evidence suggests that insomnia may be a unique risk factor for cognitive decline in later life, Ms. Zaheed explained.
To investigate further, the researchers analyzed data on 2,496 adults aged 51 years and older who were participants in the Health and Retirement Study, a longitudinal study of aging in a nationally representative population of older adults.
In 2002, participants were asked how often they had trouble falling asleep, woke up during the night, woke up too early, and were not able to fall asleep again and how often they felt really rested when they woke up in the morning.
In 2016, participants’ cognition was assessed using a battery of neuropsychological tests that gauged episodic memory, executive function, language, visuospatial/construction, and processing speed.
Analyses controlled for sociodemographics, baseline global cognitive performance, and the influence of depressive symptoms and vascular disease.
Compared with other insomnia symptoms, having difficulty falling asleep in 2002 was the main insomnia symptom that was predictive of cognitive impairment 14 years later, in 2016.
More frequent trouble falling asleep was predictive of poorer episodic memory, executive function, language, processing speed, and visuospatial performance.
The associations between sleep initiation and later cognitive impairment were partially explained by depressive symptoms and vascular disease burden for all domains except episodic memory, which was only partially explained by depressive symptoms.
Unclear mechanism
Ms. Zaheed said research is needed to uncover neurophysiologic mechanisms underlying the observed associations. “It may be that chronic difficulty with falling asleep is associated with inflammatory or metabolic processes that negatively affect brain structure and function over time,” she said.
“Insomnia has also been linked with higher accumulation of protein aggregates in the brain that disrupt cell communication and are characteristic of late-life disorders such as Alzheimer’s disease,” she added.
“While our project did not directly investigate these potential causal pathways between insomnia and cognition, our results suggest that investigating these potential mechanisms is an important area for future research,” Ms. Zaheed said.
“While additional intervention research is needed to determine whether targeting insomnia in older patients can have lasting cognitive benefits, results from this study suggest that discussing insomnia symptoms at the primary care level may be beneficial for both doctors and patients,” she added.
“By targeting insomnia – for example, through an evidence-based cognitive–behavioral therapy approach – individuals may improve various mental and physical health outcomes in addition to improving their sleep quality,” Ms. Zaheed said.
Reached for comment, Shaheen E. Lakhan, MD, PhD, neurologist in Newton, Massachusetts, said, “There is a strong link between chronic sleep disturbances and cognitive impairment, including dementia.”
“This study further supports this link and specifically calls out initiating sleep (as opposed to staying asleep) as the culprit. It also raises the hypothesis that the link is primarily mediated by depression and vascular disease; however, the verdict is still out,” said Dr. Lakhan.
The study was funded by the National Institute on Aging. Ms. Zaheed and Dr. Lakhan have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, new research suggests.
Trouble falling asleep “may be a modifiable risk factor for later-life cognitive impairment and dementia,” said lead author Afsara Zaheed, a PhD candidate in clinical science, department of psychology, University of Michigan, Ann Arbor.
“Patients should also be aware of the importance of insomnia on cognitive functioning so that they can bring up these concerns with their providers early,” she said.
The findings were presented at Virtual SLEEP 2021, the 35th Annual Meeting of the Associated Professional Sleep Societies.
Poor sleep common with age
As many as one-half of older adults report having poor sleep quality and insomnia, and growing evidence suggests that insomnia may be a unique risk factor for cognitive decline in later life, Ms. Zaheed explained.
To investigate further, the researchers analyzed data on 2,496 adults aged 51 years and older who were participants in the Health and Retirement Study, a longitudinal study of aging in a nationally representative population of older adults.
In 2002, participants were asked how often they had trouble falling asleep, woke up during the night, woke up too early, and were not able to fall asleep again and how often they felt really rested when they woke up in the morning.
In 2016, participants’ cognition was assessed using a battery of neuropsychological tests that gauged episodic memory, executive function, language, visuospatial/construction, and processing speed.
Analyses controlled for sociodemographics, baseline global cognitive performance, and the influence of depressive symptoms and vascular disease.
Compared with other insomnia symptoms, having difficulty falling asleep in 2002 was the main insomnia symptom that was predictive of cognitive impairment 14 years later, in 2016.
More frequent trouble falling asleep was predictive of poorer episodic memory, executive function, language, processing speed, and visuospatial performance.
The associations between sleep initiation and later cognitive impairment were partially explained by depressive symptoms and vascular disease burden for all domains except episodic memory, which was only partially explained by depressive symptoms.
Unclear mechanism
Ms. Zaheed said research is needed to uncover neurophysiologic mechanisms underlying the observed associations. “It may be that chronic difficulty with falling asleep is associated with inflammatory or metabolic processes that negatively affect brain structure and function over time,” she said.
“Insomnia has also been linked with higher accumulation of protein aggregates in the brain that disrupt cell communication and are characteristic of late-life disorders such as Alzheimer’s disease,” she added.
“While our project did not directly investigate these potential causal pathways between insomnia and cognition, our results suggest that investigating these potential mechanisms is an important area for future research,” Ms. Zaheed said.
“While additional intervention research is needed to determine whether targeting insomnia in older patients can have lasting cognitive benefits, results from this study suggest that discussing insomnia symptoms at the primary care level may be beneficial for both doctors and patients,” she added.
“By targeting insomnia – for example, through an evidence-based cognitive–behavioral therapy approach – individuals may improve various mental and physical health outcomes in addition to improving their sleep quality,” Ms. Zaheed said.
Reached for comment, Shaheen E. Lakhan, MD, PhD, neurologist in Newton, Massachusetts, said, “There is a strong link between chronic sleep disturbances and cognitive impairment, including dementia.”
“This study further supports this link and specifically calls out initiating sleep (as opposed to staying asleep) as the culprit. It also raises the hypothesis that the link is primarily mediated by depression and vascular disease; however, the verdict is still out,” said Dr. Lakhan.
The study was funded by the National Institute on Aging. Ms. Zaheed and Dr. Lakhan have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, new research suggests.
Trouble falling asleep “may be a modifiable risk factor for later-life cognitive impairment and dementia,” said lead author Afsara Zaheed, a PhD candidate in clinical science, department of psychology, University of Michigan, Ann Arbor.
“Patients should also be aware of the importance of insomnia on cognitive functioning so that they can bring up these concerns with their providers early,” she said.
The findings were presented at Virtual SLEEP 2021, the 35th Annual Meeting of the Associated Professional Sleep Societies.
Poor sleep common with age
As many as one-half of older adults report having poor sleep quality and insomnia, and growing evidence suggests that insomnia may be a unique risk factor for cognitive decline in later life, Ms. Zaheed explained.
To investigate further, the researchers analyzed data on 2,496 adults aged 51 years and older who were participants in the Health and Retirement Study, a longitudinal study of aging in a nationally representative population of older adults.
In 2002, participants were asked how often they had trouble falling asleep, woke up during the night, woke up too early, and were not able to fall asleep again and how often they felt really rested when they woke up in the morning.
In 2016, participants’ cognition was assessed using a battery of neuropsychological tests that gauged episodic memory, executive function, language, visuospatial/construction, and processing speed.
Analyses controlled for sociodemographics, baseline global cognitive performance, and the influence of depressive symptoms and vascular disease.
Compared with other insomnia symptoms, having difficulty falling asleep in 2002 was the main insomnia symptom that was predictive of cognitive impairment 14 years later, in 2016.
More frequent trouble falling asleep was predictive of poorer episodic memory, executive function, language, processing speed, and visuospatial performance.
The associations between sleep initiation and later cognitive impairment were partially explained by depressive symptoms and vascular disease burden for all domains except episodic memory, which was only partially explained by depressive symptoms.
Unclear mechanism
Ms. Zaheed said research is needed to uncover neurophysiologic mechanisms underlying the observed associations. “It may be that chronic difficulty with falling asleep is associated with inflammatory or metabolic processes that negatively affect brain structure and function over time,” she said.
“Insomnia has also been linked with higher accumulation of protein aggregates in the brain that disrupt cell communication and are characteristic of late-life disorders such as Alzheimer’s disease,” she added.
“While our project did not directly investigate these potential causal pathways between insomnia and cognition, our results suggest that investigating these potential mechanisms is an important area for future research,” Ms. Zaheed said.
“While additional intervention research is needed to determine whether targeting insomnia in older patients can have lasting cognitive benefits, results from this study suggest that discussing insomnia symptoms at the primary care level may be beneficial for both doctors and patients,” she added.
“By targeting insomnia – for example, through an evidence-based cognitive–behavioral therapy approach – individuals may improve various mental and physical health outcomes in addition to improving their sleep quality,” Ms. Zaheed said.
Reached for comment, Shaheen E. Lakhan, MD, PhD, neurologist in Newton, Massachusetts, said, “There is a strong link between chronic sleep disturbances and cognitive impairment, including dementia.”
“This study further supports this link and specifically calls out initiating sleep (as opposed to staying asleep) as the culprit. It also raises the hypothesis that the link is primarily mediated by depression and vascular disease; however, the verdict is still out,” said Dr. Lakhan.
The study was funded by the National Institute on Aging. Ms. Zaheed and Dr. Lakhan have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Insomnia in children tied to mood and anxiety disorders in adulthood
, new research indicates. However, insomnia symptoms in childhood that remit in the transition to adolescence do not confer increased risk of mood or anxiety disorders later on, the study found.
“As insomnia symptoms may precipitate or maintain internalizing disorders, our findings further reinforce the need for early sleep interventions to prevent future mental health disorders,” said lead investigator Julio Fernandez-Mendoza, PhD, associate professor at Penn State University, Hershey.
He presented his research at Virtual SLEEP 2021, the 35th annual meeting of the Associated Professional Sleep Societies.
Results ‘very clear’
The findings are based on data from the Penn State Child Cohort, a longitudinal, population-based sample of 700 children with a median age of 9 years, including 421 who were followed up 8 years later as adolescents (median age, 16 years) and 502 who were followed up 15 years later as young adults (median age, 24 years).
The data are “very clear that the risk of having internalizing disorders in young adulthood associated with having persistent insomnia symptoms, since childhood through adolescence into young adulthood,” Dr. Fernandez-Mendoza said in his presentation.
A persistent developmental trajectory was associated with a threefold increased risk of adult internalizing disorder (hazard ratio, 3.19).
The risk of having an internalizing disorder in young adulthood associated with newly developing (incident) insomnia symptoms is about twofold higher (HR, 1.94), whereas the risk associated with the waxing and waning pattern of insomnia is 1.5-fold (HR, 1.53) higher and only marginally significant, he reported.
An equally important finding, said Dr. Fernandez-Mendoza, is that those who had remitted insomnia symptoms in the transition to adolescence and throughout young adulthood were not at increased risk of having an internalizing disorder in young adulthood.
“Insomnia symptoms in a persistent manner associated with long-term adverse mental health outcomes, but remission of those insomnia symptoms associated with a good prognosis,” he said.
It’s also important to note, he said, that about 40% of children do not outgrow their insomnia symptoms in the transition to adolescence and are at risk of developing mental health disorders later on during early adulthood.
Reached for comment, Nitun Verma, MD, a spokesperson for the American Academy of Sleep Medicine, said: “There is a connection with mood and anxiety disorders with sleep, especially insomnia. This is a good reminder that reviewing someone’s sleep habits should always be a part of assessing someone’s mental health.”
A version of this article first appeared on Medscape.com.
, new research indicates. However, insomnia symptoms in childhood that remit in the transition to adolescence do not confer increased risk of mood or anxiety disorders later on, the study found.
“As insomnia symptoms may precipitate or maintain internalizing disorders, our findings further reinforce the need for early sleep interventions to prevent future mental health disorders,” said lead investigator Julio Fernandez-Mendoza, PhD, associate professor at Penn State University, Hershey.
He presented his research at Virtual SLEEP 2021, the 35th annual meeting of the Associated Professional Sleep Societies.
Results ‘very clear’
The findings are based on data from the Penn State Child Cohort, a longitudinal, population-based sample of 700 children with a median age of 9 years, including 421 who were followed up 8 years later as adolescents (median age, 16 years) and 502 who were followed up 15 years later as young adults (median age, 24 years).
The data are “very clear that the risk of having internalizing disorders in young adulthood associated with having persistent insomnia symptoms, since childhood through adolescence into young adulthood,” Dr. Fernandez-Mendoza said in his presentation.
A persistent developmental trajectory was associated with a threefold increased risk of adult internalizing disorder (hazard ratio, 3.19).
The risk of having an internalizing disorder in young adulthood associated with newly developing (incident) insomnia symptoms is about twofold higher (HR, 1.94), whereas the risk associated with the waxing and waning pattern of insomnia is 1.5-fold (HR, 1.53) higher and only marginally significant, he reported.
An equally important finding, said Dr. Fernandez-Mendoza, is that those who had remitted insomnia symptoms in the transition to adolescence and throughout young adulthood were not at increased risk of having an internalizing disorder in young adulthood.
“Insomnia symptoms in a persistent manner associated with long-term adverse mental health outcomes, but remission of those insomnia symptoms associated with a good prognosis,” he said.
It’s also important to note, he said, that about 40% of children do not outgrow their insomnia symptoms in the transition to adolescence and are at risk of developing mental health disorders later on during early adulthood.
Reached for comment, Nitun Verma, MD, a spokesperson for the American Academy of Sleep Medicine, said: “There is a connection with mood and anxiety disorders with sleep, especially insomnia. This is a good reminder that reviewing someone’s sleep habits should always be a part of assessing someone’s mental health.”
A version of this article first appeared on Medscape.com.
, new research indicates. However, insomnia symptoms in childhood that remit in the transition to adolescence do not confer increased risk of mood or anxiety disorders later on, the study found.
“As insomnia symptoms may precipitate or maintain internalizing disorders, our findings further reinforce the need for early sleep interventions to prevent future mental health disorders,” said lead investigator Julio Fernandez-Mendoza, PhD, associate professor at Penn State University, Hershey.
He presented his research at Virtual SLEEP 2021, the 35th annual meeting of the Associated Professional Sleep Societies.
Results ‘very clear’
The findings are based on data from the Penn State Child Cohort, a longitudinal, population-based sample of 700 children with a median age of 9 years, including 421 who were followed up 8 years later as adolescents (median age, 16 years) and 502 who were followed up 15 years later as young adults (median age, 24 years).
The data are “very clear that the risk of having internalizing disorders in young adulthood associated with having persistent insomnia symptoms, since childhood through adolescence into young adulthood,” Dr. Fernandez-Mendoza said in his presentation.
A persistent developmental trajectory was associated with a threefold increased risk of adult internalizing disorder (hazard ratio, 3.19).
The risk of having an internalizing disorder in young adulthood associated with newly developing (incident) insomnia symptoms is about twofold higher (HR, 1.94), whereas the risk associated with the waxing and waning pattern of insomnia is 1.5-fold (HR, 1.53) higher and only marginally significant, he reported.
An equally important finding, said Dr. Fernandez-Mendoza, is that those who had remitted insomnia symptoms in the transition to adolescence and throughout young adulthood were not at increased risk of having an internalizing disorder in young adulthood.
“Insomnia symptoms in a persistent manner associated with long-term adverse mental health outcomes, but remission of those insomnia symptoms associated with a good prognosis,” he said.
It’s also important to note, he said, that about 40% of children do not outgrow their insomnia symptoms in the transition to adolescence and are at risk of developing mental health disorders later on during early adulthood.
Reached for comment, Nitun Verma, MD, a spokesperson for the American Academy of Sleep Medicine, said: “There is a connection with mood and anxiety disorders with sleep, especially insomnia. This is a good reminder that reviewing someone’s sleep habits should always be a part of assessing someone’s mental health.”
A version of this article first appeared on Medscape.com.
AHA: Don’t delay COVID shot while CDC reviews myocarditis cases
While the investigation into cases of myocarditis possibly associated with COVID vaccines proceeds, the American Heart Association/American Stroke Association (ASA) continue to urge everyone who is eligible for the vaccine to get it without delay.
“We remain confident that the benefits of vaccination far exceed the very unusual risks,” the leadership of the AHA/ASA said in a statement issued June 12.
“The risks of COVID-19 infection include its potentially fatal consequences and the potential long-term health effects that are still revealing themselves, including lingering consequences affecting the heart, brain, vascular system, and other organs after infection,” they point out.
Late last week, the Centers for Disease Control and Prevention alerted health care providers that the COVID-19 Vaccine Safety Technical Work Group (VaST) of the Advisory Committee on Immunization Practices (ACIP) will meet June 18 to review cases of myocarditis reported in adolescents and young adults after they received a COVID-19 vaccine manufactured by Pfizer-BioNTech or Moderna.
The CDC is monitoring the Vaccine Adverse Events Reporting System (VAERS) and the Vaccine Safety Datalink (VSD) for cases of myocarditis that have been associated with the mRNA vaccines against SARS-CoV-2 from Pfizer and Moderna.
These cases may occur more often in males than females and more frequently after the second dose than the first dose of either mRNA vaccine. Symptoms typically occur in the 3 days after administration.
“The CDC’s ongoing investigation into cases of suspected myocarditis reflects a strong and steadfast commitment to transparency and the importance of scientific rigor on all fronts. We applaud the CDC’s unwavering efforts to lead our nation’s scientific and public health efforts, including ensuring the continued safety of the COVID-19 vaccines,” the AHA/ASA states.
They emphasize that vaccinations should continue, and say it’s important to consider the details of the suspected myocarditis cases being investigated by the CDC.
As of June 11, more than 306 million doses of COVID-19 vaccines have been administered in the United States (since Dec. 14, 2020) and nearly 43% of Americans – more than 142 million people – are now fully vaccinated.
According to the June 10 CDC VAERS report detailing adverse events through May 31:
- 789 cases of suspected myocarditis have been reported, with 475 involving people younger than 30 years; 79 cases reported were in patients 16 or 17 years old.
- The vast majority (81%) of the 270 patients younger than 30 years who were discharged from care after suspected myocarditis related to COVID-19 vaccination have recovered fully; the remaining 19% of patients report ongoing symptoms or complete data are missing.
- 196 cases of suspected myocarditis after a COVID-19 vaccine were reported in young adults 18 to 24 years of age, which is higher than expected for this age group.
As of May 31, only about 9% of the COVID-19 vaccine doses administered were to people 16 to 24 years of age, which is why this “higher-than-normal rate of possible myocarditis cases” warrants investigation, the AHA/ASA says.
They note that these suspected myocarditis cases were reported to VAERS because of their proximity to COVID-19 vaccine administration.
It remains to be determined which cases meet the clinical criteria for a diagnosis of myocarditis and whether they have any direct connection to the COVID-19 vaccine, the AHA/ASA says.
They urge all health care professionals to be aware of “very rare” adverse events that could be related to a COVID-19 vaccine, including myocarditis, blood clots, low platelets, and symptoms of severe inflammation.
They advise asking patients who present with symptoms related to these conditions about the timing of recent COVID vaccinations, as needed, to confirm the diagnosis and provide appropriate treatment quickly.
The AHA will be at the CDC’s June 18 meeting to review the latest evidence on cases of suspected myocarditis after the COVID-19 vaccine, the statement adds.
The statement notes that it reflects the views of the AHA/ASA and its scientific leadership, including current president Mitchel S.V. Elkind, MD, PhD; immediate past-president Robert A. Harrington, MD; president-elect Donald M. Lloyd-Jones, MD; AHA/ASA chief science and medical officer Mariell Jessup, MD; and chief medical officer for prevention Eduardo Sanchez, MD, MPH.
A version of this article first appeared on Medscape.com.
While the investigation into cases of myocarditis possibly associated with COVID vaccines proceeds, the American Heart Association/American Stroke Association (ASA) continue to urge everyone who is eligible for the vaccine to get it without delay.
“We remain confident that the benefits of vaccination far exceed the very unusual risks,” the leadership of the AHA/ASA said in a statement issued June 12.
“The risks of COVID-19 infection include its potentially fatal consequences and the potential long-term health effects that are still revealing themselves, including lingering consequences affecting the heart, brain, vascular system, and other organs after infection,” they point out.
Late last week, the Centers for Disease Control and Prevention alerted health care providers that the COVID-19 Vaccine Safety Technical Work Group (VaST) of the Advisory Committee on Immunization Practices (ACIP) will meet June 18 to review cases of myocarditis reported in adolescents and young adults after they received a COVID-19 vaccine manufactured by Pfizer-BioNTech or Moderna.
The CDC is monitoring the Vaccine Adverse Events Reporting System (VAERS) and the Vaccine Safety Datalink (VSD) for cases of myocarditis that have been associated with the mRNA vaccines against SARS-CoV-2 from Pfizer and Moderna.
These cases may occur more often in males than females and more frequently after the second dose than the first dose of either mRNA vaccine. Symptoms typically occur in the 3 days after administration.
“The CDC’s ongoing investigation into cases of suspected myocarditis reflects a strong and steadfast commitment to transparency and the importance of scientific rigor on all fronts. We applaud the CDC’s unwavering efforts to lead our nation’s scientific and public health efforts, including ensuring the continued safety of the COVID-19 vaccines,” the AHA/ASA states.
They emphasize that vaccinations should continue, and say it’s important to consider the details of the suspected myocarditis cases being investigated by the CDC.
As of June 11, more than 306 million doses of COVID-19 vaccines have been administered in the United States (since Dec. 14, 2020) and nearly 43% of Americans – more than 142 million people – are now fully vaccinated.
According to the June 10 CDC VAERS report detailing adverse events through May 31:
- 789 cases of suspected myocarditis have been reported, with 475 involving people younger than 30 years; 79 cases reported were in patients 16 or 17 years old.
- The vast majority (81%) of the 270 patients younger than 30 years who were discharged from care after suspected myocarditis related to COVID-19 vaccination have recovered fully; the remaining 19% of patients report ongoing symptoms or complete data are missing.
- 196 cases of suspected myocarditis after a COVID-19 vaccine were reported in young adults 18 to 24 years of age, which is higher than expected for this age group.
As of May 31, only about 9% of the COVID-19 vaccine doses administered were to people 16 to 24 years of age, which is why this “higher-than-normal rate of possible myocarditis cases” warrants investigation, the AHA/ASA says.
They note that these suspected myocarditis cases were reported to VAERS because of their proximity to COVID-19 vaccine administration.
It remains to be determined which cases meet the clinical criteria for a diagnosis of myocarditis and whether they have any direct connection to the COVID-19 vaccine, the AHA/ASA says.
They urge all health care professionals to be aware of “very rare” adverse events that could be related to a COVID-19 vaccine, including myocarditis, blood clots, low platelets, and symptoms of severe inflammation.
They advise asking patients who present with symptoms related to these conditions about the timing of recent COVID vaccinations, as needed, to confirm the diagnosis and provide appropriate treatment quickly.
The AHA will be at the CDC’s June 18 meeting to review the latest evidence on cases of suspected myocarditis after the COVID-19 vaccine, the statement adds.
The statement notes that it reflects the views of the AHA/ASA and its scientific leadership, including current president Mitchel S.V. Elkind, MD, PhD; immediate past-president Robert A. Harrington, MD; president-elect Donald M. Lloyd-Jones, MD; AHA/ASA chief science and medical officer Mariell Jessup, MD; and chief medical officer for prevention Eduardo Sanchez, MD, MPH.
A version of this article first appeared on Medscape.com.
While the investigation into cases of myocarditis possibly associated with COVID vaccines proceeds, the American Heart Association/American Stroke Association (ASA) continue to urge everyone who is eligible for the vaccine to get it without delay.
“We remain confident that the benefits of vaccination far exceed the very unusual risks,” the leadership of the AHA/ASA said in a statement issued June 12.
“The risks of COVID-19 infection include its potentially fatal consequences and the potential long-term health effects that are still revealing themselves, including lingering consequences affecting the heart, brain, vascular system, and other organs after infection,” they point out.
Late last week, the Centers for Disease Control and Prevention alerted health care providers that the COVID-19 Vaccine Safety Technical Work Group (VaST) of the Advisory Committee on Immunization Practices (ACIP) will meet June 18 to review cases of myocarditis reported in adolescents and young adults after they received a COVID-19 vaccine manufactured by Pfizer-BioNTech or Moderna.
The CDC is monitoring the Vaccine Adverse Events Reporting System (VAERS) and the Vaccine Safety Datalink (VSD) for cases of myocarditis that have been associated with the mRNA vaccines against SARS-CoV-2 from Pfizer and Moderna.
These cases may occur more often in males than females and more frequently after the second dose than the first dose of either mRNA vaccine. Symptoms typically occur in the 3 days after administration.
“The CDC’s ongoing investigation into cases of suspected myocarditis reflects a strong and steadfast commitment to transparency and the importance of scientific rigor on all fronts. We applaud the CDC’s unwavering efforts to lead our nation’s scientific and public health efforts, including ensuring the continued safety of the COVID-19 vaccines,” the AHA/ASA states.
They emphasize that vaccinations should continue, and say it’s important to consider the details of the suspected myocarditis cases being investigated by the CDC.
As of June 11, more than 306 million doses of COVID-19 vaccines have been administered in the United States (since Dec. 14, 2020) and nearly 43% of Americans – more than 142 million people – are now fully vaccinated.
According to the June 10 CDC VAERS report detailing adverse events through May 31:
- 789 cases of suspected myocarditis have been reported, with 475 involving people younger than 30 years; 79 cases reported were in patients 16 or 17 years old.
- The vast majority (81%) of the 270 patients younger than 30 years who were discharged from care after suspected myocarditis related to COVID-19 vaccination have recovered fully; the remaining 19% of patients report ongoing symptoms or complete data are missing.
- 196 cases of suspected myocarditis after a COVID-19 vaccine were reported in young adults 18 to 24 years of age, which is higher than expected for this age group.
As of May 31, only about 9% of the COVID-19 vaccine doses administered were to people 16 to 24 years of age, which is why this “higher-than-normal rate of possible myocarditis cases” warrants investigation, the AHA/ASA says.
They note that these suspected myocarditis cases were reported to VAERS because of their proximity to COVID-19 vaccine administration.
It remains to be determined which cases meet the clinical criteria for a diagnosis of myocarditis and whether they have any direct connection to the COVID-19 vaccine, the AHA/ASA says.
They urge all health care professionals to be aware of “very rare” adverse events that could be related to a COVID-19 vaccine, including myocarditis, blood clots, low platelets, and symptoms of severe inflammation.
They advise asking patients who present with symptoms related to these conditions about the timing of recent COVID vaccinations, as needed, to confirm the diagnosis and provide appropriate treatment quickly.
The AHA will be at the CDC’s June 18 meeting to review the latest evidence on cases of suspected myocarditis after the COVID-19 vaccine, the statement adds.
The statement notes that it reflects the views of the AHA/ASA and its scientific leadership, including current president Mitchel S.V. Elkind, MD, PhD; immediate past-president Robert A. Harrington, MD; president-elect Donald M. Lloyd-Jones, MD; AHA/ASA chief science and medical officer Mariell Jessup, MD; and chief medical officer for prevention Eduardo Sanchez, MD, MPH.
A version of this article first appeared on Medscape.com.
COVID-19 tied to spike in suspected suicide attempts by girls
Suspected suicide attempts by teenage girls have increased significantly during the COVID-19 pandemic, according to data released today by the U.S. Centers for Disease Control and Prevention.
Among children and adolescents aged 12-17 years, the average weekly number of emergency department visits for suspected suicide attempts was 22.3% higher during summer 2020 and 39.1% higher during winter 2021 than during the corresponding periods in 2019.
The increase was most evident among young girls.
Between Feb. 21 and March 20, 2021, the number of ED visits for suspected suicide attempts was about 51% higher among girls aged 12-17 years than during the same period in 2019. Among boys aged 12-17 years, ED visits for suspected suicide attempts increased 4%, the CDC reports.
“Young persons might represent a group at high risk because they might have been particularly affected by mitigation measures, such as physical distancing (including a lack of connectedness to schools, teachers, and peers); barriers to mental health treatment; increases in substance use; and anxiety about family health and economic problems, which are all risk factors for suicide,” write the authors, led by Ellen Yard, PhD, with the CDC’s National Center for Injury Prevention and Control.
In addition, the findings from this study suggest there has been “more severe distress among young females than has been identified in previous reports during the pandemic, reinforcing the need for increased attention to, and prevention for, this population,” they point out.
The results were published June 11 in Morbidity and Mortality Weekly Report.
The findings are based on data for ED visits for suspected suicide from the National Syndromic Surveillance Program, which includes about 71% of the nation’s EDs in 49 states (all except Hawaii) and the District of Columbia.
Earlier data reported by the CDC showed that the proportion of mental health–related ED visits among children and adolescents aged 12-17 years increased by 31% during 2020, compared with 2019.
‘Time for action is now’
These new findings underscore the “enormous impact the COVID-19 pandemic is having on our country’s overall emotional wellbeing, especially among young people,” the National Action Alliance for Suicide Prevention (Action Alliance) Media Messaging Work Group said in a statement responding to the newly released data.
“Just as we have taken steps to protect our physical health throughout the pandemic, we must also take steps to protect our mental and emotional health,” the group says.
The data, the group says, specifically speak to the importance of improving suicide care both during and after ED visits by scaling up the adoption of best practices, such as the Recommended Standard Care for People with Suicide Risk: Making Health Care Suicide Safe and Best Practices in Care Transitions for Individuals with Suicide Risk: Inpatient Care to Outpatient Care.
“These and other evidence-based best practices must be adopted by health care systems nationwide to ensure safe, effective suicide care for all,” the group says.
“However, health care systems cannot address this issue alone. Suicide is a complex public health issue that also requires a comprehensive, community-based approach to addressing it. We must ensure suicide prevention is infused into a variety of community-based settings – such as schools, workplaces, and places of worship – to ensure people are connected with prevention activities and resources before a crisis occurs,” the group says.
It also highlights the crucial role of social connectedness as a protective factor against suicide.
“Research indicates that a sense of belonging and social connectedness improves physical, mental, and emotional wellbeing. Everyone can play a role in being there for each other and helping to build resiliency. Having real, honest conversations about our own mental health opens the door for connection and social support,” the group says.
It calls on leaders from all sectors and industries to make suicide prevention “a national priority by becoming engaged in the issue and bringing resources to bear. The time for action is now.”
A version of this article first appeared on Medscape.com.
Suspected suicide attempts by teenage girls have increased significantly during the COVID-19 pandemic, according to data released today by the U.S. Centers for Disease Control and Prevention.
Among children and adolescents aged 12-17 years, the average weekly number of emergency department visits for suspected suicide attempts was 22.3% higher during summer 2020 and 39.1% higher during winter 2021 than during the corresponding periods in 2019.
The increase was most evident among young girls.
Between Feb. 21 and March 20, 2021, the number of ED visits for suspected suicide attempts was about 51% higher among girls aged 12-17 years than during the same period in 2019. Among boys aged 12-17 years, ED visits for suspected suicide attempts increased 4%, the CDC reports.
“Young persons might represent a group at high risk because they might have been particularly affected by mitigation measures, such as physical distancing (including a lack of connectedness to schools, teachers, and peers); barriers to mental health treatment; increases in substance use; and anxiety about family health and economic problems, which are all risk factors for suicide,” write the authors, led by Ellen Yard, PhD, with the CDC’s National Center for Injury Prevention and Control.
In addition, the findings from this study suggest there has been “more severe distress among young females than has been identified in previous reports during the pandemic, reinforcing the need for increased attention to, and prevention for, this population,” they point out.
The results were published June 11 in Morbidity and Mortality Weekly Report.
The findings are based on data for ED visits for suspected suicide from the National Syndromic Surveillance Program, which includes about 71% of the nation’s EDs in 49 states (all except Hawaii) and the District of Columbia.
Earlier data reported by the CDC showed that the proportion of mental health–related ED visits among children and adolescents aged 12-17 years increased by 31% during 2020, compared with 2019.
‘Time for action is now’
These new findings underscore the “enormous impact the COVID-19 pandemic is having on our country’s overall emotional wellbeing, especially among young people,” the National Action Alliance for Suicide Prevention (Action Alliance) Media Messaging Work Group said in a statement responding to the newly released data.
“Just as we have taken steps to protect our physical health throughout the pandemic, we must also take steps to protect our mental and emotional health,” the group says.
The data, the group says, specifically speak to the importance of improving suicide care both during and after ED visits by scaling up the adoption of best practices, such as the Recommended Standard Care for People with Suicide Risk: Making Health Care Suicide Safe and Best Practices in Care Transitions for Individuals with Suicide Risk: Inpatient Care to Outpatient Care.
“These and other evidence-based best practices must be adopted by health care systems nationwide to ensure safe, effective suicide care for all,” the group says.
“However, health care systems cannot address this issue alone. Suicide is a complex public health issue that also requires a comprehensive, community-based approach to addressing it. We must ensure suicide prevention is infused into a variety of community-based settings – such as schools, workplaces, and places of worship – to ensure people are connected with prevention activities and resources before a crisis occurs,” the group says.
It also highlights the crucial role of social connectedness as a protective factor against suicide.
“Research indicates that a sense of belonging and social connectedness improves physical, mental, and emotional wellbeing. Everyone can play a role in being there for each other and helping to build resiliency. Having real, honest conversations about our own mental health opens the door for connection and social support,” the group says.
It calls on leaders from all sectors and industries to make suicide prevention “a national priority by becoming engaged in the issue and bringing resources to bear. The time for action is now.”
A version of this article first appeared on Medscape.com.
Suspected suicide attempts by teenage girls have increased significantly during the COVID-19 pandemic, according to data released today by the U.S. Centers for Disease Control and Prevention.
Among children and adolescents aged 12-17 years, the average weekly number of emergency department visits for suspected suicide attempts was 22.3% higher during summer 2020 and 39.1% higher during winter 2021 than during the corresponding periods in 2019.
The increase was most evident among young girls.
Between Feb. 21 and March 20, 2021, the number of ED visits for suspected suicide attempts was about 51% higher among girls aged 12-17 years than during the same period in 2019. Among boys aged 12-17 years, ED visits for suspected suicide attempts increased 4%, the CDC reports.
“Young persons might represent a group at high risk because they might have been particularly affected by mitigation measures, such as physical distancing (including a lack of connectedness to schools, teachers, and peers); barriers to mental health treatment; increases in substance use; and anxiety about family health and economic problems, which are all risk factors for suicide,” write the authors, led by Ellen Yard, PhD, with the CDC’s National Center for Injury Prevention and Control.
In addition, the findings from this study suggest there has been “more severe distress among young females than has been identified in previous reports during the pandemic, reinforcing the need for increased attention to, and prevention for, this population,” they point out.
The results were published June 11 in Morbidity and Mortality Weekly Report.
The findings are based on data for ED visits for suspected suicide from the National Syndromic Surveillance Program, which includes about 71% of the nation’s EDs in 49 states (all except Hawaii) and the District of Columbia.
Earlier data reported by the CDC showed that the proportion of mental health–related ED visits among children and adolescents aged 12-17 years increased by 31% during 2020, compared with 2019.
‘Time for action is now’
These new findings underscore the “enormous impact the COVID-19 pandemic is having on our country’s overall emotional wellbeing, especially among young people,” the National Action Alliance for Suicide Prevention (Action Alliance) Media Messaging Work Group said in a statement responding to the newly released data.
“Just as we have taken steps to protect our physical health throughout the pandemic, we must also take steps to protect our mental and emotional health,” the group says.
The data, the group says, specifically speak to the importance of improving suicide care both during and after ED visits by scaling up the adoption of best practices, such as the Recommended Standard Care for People with Suicide Risk: Making Health Care Suicide Safe and Best Practices in Care Transitions for Individuals with Suicide Risk: Inpatient Care to Outpatient Care.
“These and other evidence-based best practices must be adopted by health care systems nationwide to ensure safe, effective suicide care for all,” the group says.
“However, health care systems cannot address this issue alone. Suicide is a complex public health issue that also requires a comprehensive, community-based approach to addressing it. We must ensure suicide prevention is infused into a variety of community-based settings – such as schools, workplaces, and places of worship – to ensure people are connected with prevention activities and resources before a crisis occurs,” the group says.
It also highlights the crucial role of social connectedness as a protective factor against suicide.
“Research indicates that a sense of belonging and social connectedness improves physical, mental, and emotional wellbeing. Everyone can play a role in being there for each other and helping to build resiliency. Having real, honest conversations about our own mental health opens the door for connection and social support,” the group says.
It calls on leaders from all sectors and industries to make suicide prevention “a national priority by becoming engaged in the issue and bringing resources to bear. The time for action is now.”
A version of this article first appeared on Medscape.com.
‘COVID toes’ chilblain-like lesions not related to COVID-19
from Italy.
These lesions are “most likely are benign” and resolve on their own after 2-6 weeks, Valentina Discepolo, MD, PhD, University of Naples Federico II, told this news organization.
“They do not seem to be the manifestation of systemic inflammatory or autoimmune phenomena. According to our experience, they should not require a SARS-CoV-2–specific molecular or serological test since in all cases in our series they were negative,” said Dr. Discepolo.
The study was published online June 10, 2021, in JAMA Network Open.
‘COVID toes’ a fallacy?
The temporal association between the COVID-19 pandemic and the increasing number of chilblain-like lesions has led some in the media to call it “COVID toes,” the investigators wrote. However, data on the association with SARS-CoV-2 are controversial.
For this report, Dr. Discepolo and colleagues evaluated 17 adolescents who presented with chilblain-like lesions of the toes during the first wave of the pandemic in southern Italy.
None had evidence of current, past, or local SARS-CoV-2 infection.
“In our experience, chilblain-like lesions are not a manifestation of COVID-19, as shown by negative serological and molecular specific for SARS-CoV2,” Dr. Discepolo said in an interview.
The lesions were bilaterally distributed in 16 adolescents (94.1%) and heel skin was involved in 7 (41.2%). Ulceration complicated one patient during the active phase of the disease, and desquamation developed over time in three patients (17.6%). Only two patients (11.8%) had concurrent involvement of the fingers.
Self-administered therapies included topical antibiotics and/or corticosteroids, disinfectants, and antifungal agents; systemic antibiotics or corticosteroids were used rarely.
None of the therapies substantially changed the course of the lesions. Duration was “extremely variable,” ranging from 49 to 145 days; however, at follow-up, all patients had full resolution.
Almost invariably, the lesions were characterized by a triad of red dots, white rosettes, and white streaks on an erythematous background, the investigators reported.
In more than half the patients (56%), red dots often appeared as dotted and comma-shaped congested vessels that surrounded the rosettes in the early stage of the lesions. In later stages, red dots were still present, but the rosettes had disappeared.
Although found inconsistently in inflammatory cutaneous conditions, these three signs do not characterize the dermoscopic picture of perniosis, suggesting a distinct disease process, the investigators said.
Don’t blame it on ischemia, clots
Histologic analysis revealed “remodeling of the dermal blood vessels with a lobular arrangement, wall thickening, and a mild perivascular lymphocytic infiltrate,” they noted.
Punch biopsy of the involved skin mostly showed endothelial hyperplasia, mild lymphocytic infiltrate, and vessels’ architecture disruption with no papillary dermal edema or eosinophilic or neutrophilic infiltrate.
Pathology did not reveal any ischemic changes, which argues against systemic vasculopathy, Farzam Gorouhi, MD, from Kaiser Permanente, South Sacramento Medical Center, noted in a linked editorial. “Thus, this study provides further evidence against the thromboembolic nature of the presented pattern in adolescents during the COVID-19 pandemic.”
Results of capillaroscopy, used to investigate structural changes in peripheral microcirculation, were either completely normal or showed rare ectasias, supporting a lack of systemic inflammatory process.
“The lack of capillaroscopic features of a major vasculopathic event in the study by Discepolo et al. argues against the ischemic nature of this disease and, thus, indicates that this presentation is not associated with systemic ischemia or an embolic event,” Dr. Gorouhi noted.
Chilblain-like lesions have been one of the most commonly described cutaneous manifestations during the COVID-19 pandemic, but their etiopathogenesis, including the role of SARS-CoV-2, has remained elusive, the investigators wrote.
The findings in this case series do not support the association of the lesions with SARS-CoV-2 infection, they concluded.
The fact that only three new cases of chilblain-like lesions were reported during the highest peaks of the pandemic further supports a lack of association with SARS-CoV-2 infection, they noted.
In addition, none of these patients tested positive for SARS-CoV-2 and all three cases during the second wave occurred in the winter months, suggesting that exposure to the cold might, at least in some cases, trigger the skin lesions, the investigators said.
In line with this hypothesis, seven of the adolescents in this case series (41.2%) relapsed during the winter months while again testing negative for SARS-CoV-2.
“We believe that lifestyle modifications [reduced physical activity, microtraumatisms caused by walking barefoot at home] during the first strict lockdown played a role, likely promoting a local inflammatory process promoted by vascular stasis that led in genetically susceptible individuals to the onset of these lesions,” Dr. Discepolo said in an interview.
This research had no specific funding. The investigators and Dr. Gorouhi declared no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
from Italy.
These lesions are “most likely are benign” and resolve on their own after 2-6 weeks, Valentina Discepolo, MD, PhD, University of Naples Federico II, told this news organization.
“They do not seem to be the manifestation of systemic inflammatory or autoimmune phenomena. According to our experience, they should not require a SARS-CoV-2–specific molecular or serological test since in all cases in our series they were negative,” said Dr. Discepolo.
The study was published online June 10, 2021, in JAMA Network Open.
‘COVID toes’ a fallacy?
The temporal association between the COVID-19 pandemic and the increasing number of chilblain-like lesions has led some in the media to call it “COVID toes,” the investigators wrote. However, data on the association with SARS-CoV-2 are controversial.
For this report, Dr. Discepolo and colleagues evaluated 17 adolescents who presented with chilblain-like lesions of the toes during the first wave of the pandemic in southern Italy.
None had evidence of current, past, or local SARS-CoV-2 infection.
“In our experience, chilblain-like lesions are not a manifestation of COVID-19, as shown by negative serological and molecular specific for SARS-CoV2,” Dr. Discepolo said in an interview.
The lesions were bilaterally distributed in 16 adolescents (94.1%) and heel skin was involved in 7 (41.2%). Ulceration complicated one patient during the active phase of the disease, and desquamation developed over time in three patients (17.6%). Only two patients (11.8%) had concurrent involvement of the fingers.
Self-administered therapies included topical antibiotics and/or corticosteroids, disinfectants, and antifungal agents; systemic antibiotics or corticosteroids were used rarely.
None of the therapies substantially changed the course of the lesions. Duration was “extremely variable,” ranging from 49 to 145 days; however, at follow-up, all patients had full resolution.
Almost invariably, the lesions were characterized by a triad of red dots, white rosettes, and white streaks on an erythematous background, the investigators reported.
In more than half the patients (56%), red dots often appeared as dotted and comma-shaped congested vessels that surrounded the rosettes in the early stage of the lesions. In later stages, red dots were still present, but the rosettes had disappeared.
Although found inconsistently in inflammatory cutaneous conditions, these three signs do not characterize the dermoscopic picture of perniosis, suggesting a distinct disease process, the investigators said.
Don’t blame it on ischemia, clots
Histologic analysis revealed “remodeling of the dermal blood vessels with a lobular arrangement, wall thickening, and a mild perivascular lymphocytic infiltrate,” they noted.
Punch biopsy of the involved skin mostly showed endothelial hyperplasia, mild lymphocytic infiltrate, and vessels’ architecture disruption with no papillary dermal edema or eosinophilic or neutrophilic infiltrate.
Pathology did not reveal any ischemic changes, which argues against systemic vasculopathy, Farzam Gorouhi, MD, from Kaiser Permanente, South Sacramento Medical Center, noted in a linked editorial. “Thus, this study provides further evidence against the thromboembolic nature of the presented pattern in adolescents during the COVID-19 pandemic.”
Results of capillaroscopy, used to investigate structural changes in peripheral microcirculation, were either completely normal or showed rare ectasias, supporting a lack of systemic inflammatory process.
“The lack of capillaroscopic features of a major vasculopathic event in the study by Discepolo et al. argues against the ischemic nature of this disease and, thus, indicates that this presentation is not associated with systemic ischemia or an embolic event,” Dr. Gorouhi noted.
Chilblain-like lesions have been one of the most commonly described cutaneous manifestations during the COVID-19 pandemic, but their etiopathogenesis, including the role of SARS-CoV-2, has remained elusive, the investigators wrote.
The findings in this case series do not support the association of the lesions with SARS-CoV-2 infection, they concluded.
The fact that only three new cases of chilblain-like lesions were reported during the highest peaks of the pandemic further supports a lack of association with SARS-CoV-2 infection, they noted.
In addition, none of these patients tested positive for SARS-CoV-2 and all three cases during the second wave occurred in the winter months, suggesting that exposure to the cold might, at least in some cases, trigger the skin lesions, the investigators said.
In line with this hypothesis, seven of the adolescents in this case series (41.2%) relapsed during the winter months while again testing negative for SARS-CoV-2.
“We believe that lifestyle modifications [reduced physical activity, microtraumatisms caused by walking barefoot at home] during the first strict lockdown played a role, likely promoting a local inflammatory process promoted by vascular stasis that led in genetically susceptible individuals to the onset of these lesions,” Dr. Discepolo said in an interview.
This research had no specific funding. The investigators and Dr. Gorouhi declared no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
from Italy.
These lesions are “most likely are benign” and resolve on their own after 2-6 weeks, Valentina Discepolo, MD, PhD, University of Naples Federico II, told this news organization.
“They do not seem to be the manifestation of systemic inflammatory or autoimmune phenomena. According to our experience, they should not require a SARS-CoV-2–specific molecular or serological test since in all cases in our series they were negative,” said Dr. Discepolo.
The study was published online June 10, 2021, in JAMA Network Open.
‘COVID toes’ a fallacy?
The temporal association between the COVID-19 pandemic and the increasing number of chilblain-like lesions has led some in the media to call it “COVID toes,” the investigators wrote. However, data on the association with SARS-CoV-2 are controversial.
For this report, Dr. Discepolo and colleagues evaluated 17 adolescents who presented with chilblain-like lesions of the toes during the first wave of the pandemic in southern Italy.
None had evidence of current, past, or local SARS-CoV-2 infection.
“In our experience, chilblain-like lesions are not a manifestation of COVID-19, as shown by negative serological and molecular specific for SARS-CoV2,” Dr. Discepolo said in an interview.
The lesions were bilaterally distributed in 16 adolescents (94.1%) and heel skin was involved in 7 (41.2%). Ulceration complicated one patient during the active phase of the disease, and desquamation developed over time in three patients (17.6%). Only two patients (11.8%) had concurrent involvement of the fingers.
Self-administered therapies included topical antibiotics and/or corticosteroids, disinfectants, and antifungal agents; systemic antibiotics or corticosteroids were used rarely.
None of the therapies substantially changed the course of the lesions. Duration was “extremely variable,” ranging from 49 to 145 days; however, at follow-up, all patients had full resolution.
Almost invariably, the lesions were characterized by a triad of red dots, white rosettes, and white streaks on an erythematous background, the investigators reported.
In more than half the patients (56%), red dots often appeared as dotted and comma-shaped congested vessels that surrounded the rosettes in the early stage of the lesions. In later stages, red dots were still present, but the rosettes had disappeared.
Although found inconsistently in inflammatory cutaneous conditions, these three signs do not characterize the dermoscopic picture of perniosis, suggesting a distinct disease process, the investigators said.
Don’t blame it on ischemia, clots
Histologic analysis revealed “remodeling of the dermal blood vessels with a lobular arrangement, wall thickening, and a mild perivascular lymphocytic infiltrate,” they noted.
Punch biopsy of the involved skin mostly showed endothelial hyperplasia, mild lymphocytic infiltrate, and vessels’ architecture disruption with no papillary dermal edema or eosinophilic or neutrophilic infiltrate.
Pathology did not reveal any ischemic changes, which argues against systemic vasculopathy, Farzam Gorouhi, MD, from Kaiser Permanente, South Sacramento Medical Center, noted in a linked editorial. “Thus, this study provides further evidence against the thromboembolic nature of the presented pattern in adolescents during the COVID-19 pandemic.”
Results of capillaroscopy, used to investigate structural changes in peripheral microcirculation, were either completely normal or showed rare ectasias, supporting a lack of systemic inflammatory process.
“The lack of capillaroscopic features of a major vasculopathic event in the study by Discepolo et al. argues against the ischemic nature of this disease and, thus, indicates that this presentation is not associated with systemic ischemia or an embolic event,” Dr. Gorouhi noted.
Chilblain-like lesions have been one of the most commonly described cutaneous manifestations during the COVID-19 pandemic, but their etiopathogenesis, including the role of SARS-CoV-2, has remained elusive, the investigators wrote.
The findings in this case series do not support the association of the lesions with SARS-CoV-2 infection, they concluded.
The fact that only three new cases of chilblain-like lesions were reported during the highest peaks of the pandemic further supports a lack of association with SARS-CoV-2 infection, they noted.
In addition, none of these patients tested positive for SARS-CoV-2 and all three cases during the second wave occurred in the winter months, suggesting that exposure to the cold might, at least in some cases, trigger the skin lesions, the investigators said.
In line with this hypothesis, seven of the adolescents in this case series (41.2%) relapsed during the winter months while again testing negative for SARS-CoV-2.
“We believe that lifestyle modifications [reduced physical activity, microtraumatisms caused by walking barefoot at home] during the first strict lockdown played a role, likely promoting a local inflammatory process promoted by vascular stasis that led in genetically susceptible individuals to the onset of these lesions,” Dr. Discepolo said in an interview.
This research had no specific funding. The investigators and Dr. Gorouhi declared no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
AHA: Physical activity best first-line for high BP, cholesterol
The optimal first step to address mild to moderately elevated blood pressure and cholesterol in otherwise healthy adults is a “prescription” to sit less and move more, the American Heart Association says in a new scientific statement.
“The current American Heart Association guidelines for diagnosing high blood pressure and cholesterol recognize that otherwise healthy individuals with mildly or moderately elevated levels of these cardiovascular risk factors should actively attempt to reduce these risks,” Bethany Barone Gibbs, PhD, chair of the statement writing group, said in an AHA news release.
“The first treatment strategy for many of these patients should be healthy lifestyle changes beginning with increasing physical activity,” said Dr. Gibbs, from the University of Pittsburgh.
The 12-page AHA scientific statement – Physical Activity as a Critical Component of First-Line Treatment for Elevated Blood Pressure or Cholesterol: Who, What, and How? – was published online June 2 in Hypertension.
Every little bit helps
According to the AHA, about 21% of American adults have systolic blood pressure between 120 and 139 mm Hg, or diastolic blood pressure between 80 and 89 mm Hg, which meets the criteria for lifestyle-only treatment for elevated BP outlined in the American College of Cardiology (ACC)/AHA high blood pressure guideline.
In addition, about 28% of American adults have LDL cholesterol above 70 mg/dL and otherwise meet the low-risk criteria for heart disease or stroke. These individuals would meet the criteria for lifestyle-only treatment outlined in the 2018 ACC/AHA cholesterol treatment guidelines, which include increased physical activity, weight loss, better diet, smoking cessation, and moderating alcohol intake.
“Of the recommended lifestyle changes, increasing physical activity has extensive benefits, including improving both blood pressure and blood cholesterol, that are comparable, superior, or complementary to other healthy lifestyle changes,” the writing group says.
“Physical activity assessment and prescription are an excellent lifestyle behavior treatment option for all patients, including for the large population of mild-moderate-risk patients with elevated blood pressure and blood cholesterol,” they note.
Research has shown that increasing physical activity can lead to clinically meaningful 3 or 4 mm Hg reductions in systolic and diastolic blood pressure, and 3 to 6 mg/dL decreases in LDL cholesterol, the authors point out.
Previous evidence also shows that physically active people have a 21% lower risk of developing cardiovascular disease and a 36% lower risk for death from cardiovascular diseases than those who are not physically active.
Physical activity also has benefits beyond heart health, including a lower risk for some cancers; improved bone, brain, and mental health; and better sleep, they note.
The U.S. Department of Health and Human Services 2018 physical activity guidelines advise Americans to log 150 minutes of moderate-intensity aerobic exercise or 75 minutes of vigorous aerobic activity each week and to participate in two or more weekly strength training sessions.
However, there is no minimum amount of time to receive benefits from physical activity.
“Every little bit of activity is better than none. Even small initial increases of 5 to 10 minutes a day can yield health benefits,” Dr. Gibbs said.
Translational advice for clinicians
The AHA statement encourages clinicians to ask patients about their physical activity at every interaction; provide ideas and resources to help patients improve and sustain regular life-long physical activity; and encourage and celebrate small increases in activity, such as walking more or taking the stairs, to help with motivation.
“In our world where physical activity is increasingly engineered out of our lives and the overwhelming default is to sit – and even more so now as the nation and the world is practicing quarantine and isolation to reduce the spread of coronavirus – the message that we must be relentless in our pursuit to ‘sit less and move more’ throughout the day is more important than ever,” said Dr. Gibbs.
The statement was prepared by a volunteer writing group on behalf of the AHA Council on Lifestyle and Cardiometabolic Health; the Council on Cardiovascular and Stroke Nursing; and the Council on Clinical Cardiology.
This research had no commercial funding. A list of disclosures for the writing group is available with the original article.
A version of this article first appeared on Medscape.com.
The optimal first step to address mild to moderately elevated blood pressure and cholesterol in otherwise healthy adults is a “prescription” to sit less and move more, the American Heart Association says in a new scientific statement.
“The current American Heart Association guidelines for diagnosing high blood pressure and cholesterol recognize that otherwise healthy individuals with mildly or moderately elevated levels of these cardiovascular risk factors should actively attempt to reduce these risks,” Bethany Barone Gibbs, PhD, chair of the statement writing group, said in an AHA news release.
“The first treatment strategy for many of these patients should be healthy lifestyle changes beginning with increasing physical activity,” said Dr. Gibbs, from the University of Pittsburgh.
The 12-page AHA scientific statement – Physical Activity as a Critical Component of First-Line Treatment for Elevated Blood Pressure or Cholesterol: Who, What, and How? – was published online June 2 in Hypertension.
Every little bit helps
According to the AHA, about 21% of American adults have systolic blood pressure between 120 and 139 mm Hg, or diastolic blood pressure between 80 and 89 mm Hg, which meets the criteria for lifestyle-only treatment for elevated BP outlined in the American College of Cardiology (ACC)/AHA high blood pressure guideline.
In addition, about 28% of American adults have LDL cholesterol above 70 mg/dL and otherwise meet the low-risk criteria for heart disease or stroke. These individuals would meet the criteria for lifestyle-only treatment outlined in the 2018 ACC/AHA cholesterol treatment guidelines, which include increased physical activity, weight loss, better diet, smoking cessation, and moderating alcohol intake.
“Of the recommended lifestyle changes, increasing physical activity has extensive benefits, including improving both blood pressure and blood cholesterol, that are comparable, superior, or complementary to other healthy lifestyle changes,” the writing group says.
“Physical activity assessment and prescription are an excellent lifestyle behavior treatment option for all patients, including for the large population of mild-moderate-risk patients with elevated blood pressure and blood cholesterol,” they note.
Research has shown that increasing physical activity can lead to clinically meaningful 3 or 4 mm Hg reductions in systolic and diastolic blood pressure, and 3 to 6 mg/dL decreases in LDL cholesterol, the authors point out.
Previous evidence also shows that physically active people have a 21% lower risk of developing cardiovascular disease and a 36% lower risk for death from cardiovascular diseases than those who are not physically active.
Physical activity also has benefits beyond heart health, including a lower risk for some cancers; improved bone, brain, and mental health; and better sleep, they note.
The U.S. Department of Health and Human Services 2018 physical activity guidelines advise Americans to log 150 minutes of moderate-intensity aerobic exercise or 75 minutes of vigorous aerobic activity each week and to participate in two or more weekly strength training sessions.
However, there is no minimum amount of time to receive benefits from physical activity.
“Every little bit of activity is better than none. Even small initial increases of 5 to 10 minutes a day can yield health benefits,” Dr. Gibbs said.
Translational advice for clinicians
The AHA statement encourages clinicians to ask patients about their physical activity at every interaction; provide ideas and resources to help patients improve and sustain regular life-long physical activity; and encourage and celebrate small increases in activity, such as walking more or taking the stairs, to help with motivation.
“In our world where physical activity is increasingly engineered out of our lives and the overwhelming default is to sit – and even more so now as the nation and the world is practicing quarantine and isolation to reduce the spread of coronavirus – the message that we must be relentless in our pursuit to ‘sit less and move more’ throughout the day is more important than ever,” said Dr. Gibbs.
The statement was prepared by a volunteer writing group on behalf of the AHA Council on Lifestyle and Cardiometabolic Health; the Council on Cardiovascular and Stroke Nursing; and the Council on Clinical Cardiology.
This research had no commercial funding. A list of disclosures for the writing group is available with the original article.
A version of this article first appeared on Medscape.com.
The optimal first step to address mild to moderately elevated blood pressure and cholesterol in otherwise healthy adults is a “prescription” to sit less and move more, the American Heart Association says in a new scientific statement.
“The current American Heart Association guidelines for diagnosing high blood pressure and cholesterol recognize that otherwise healthy individuals with mildly or moderately elevated levels of these cardiovascular risk factors should actively attempt to reduce these risks,” Bethany Barone Gibbs, PhD, chair of the statement writing group, said in an AHA news release.
“The first treatment strategy for many of these patients should be healthy lifestyle changes beginning with increasing physical activity,” said Dr. Gibbs, from the University of Pittsburgh.
The 12-page AHA scientific statement – Physical Activity as a Critical Component of First-Line Treatment for Elevated Blood Pressure or Cholesterol: Who, What, and How? – was published online June 2 in Hypertension.
Every little bit helps
According to the AHA, about 21% of American adults have systolic blood pressure between 120 and 139 mm Hg, or diastolic blood pressure between 80 and 89 mm Hg, which meets the criteria for lifestyle-only treatment for elevated BP outlined in the American College of Cardiology (ACC)/AHA high blood pressure guideline.
In addition, about 28% of American adults have LDL cholesterol above 70 mg/dL and otherwise meet the low-risk criteria for heart disease or stroke. These individuals would meet the criteria for lifestyle-only treatment outlined in the 2018 ACC/AHA cholesterol treatment guidelines, which include increased physical activity, weight loss, better diet, smoking cessation, and moderating alcohol intake.
“Of the recommended lifestyle changes, increasing physical activity has extensive benefits, including improving both blood pressure and blood cholesterol, that are comparable, superior, or complementary to other healthy lifestyle changes,” the writing group says.
“Physical activity assessment and prescription are an excellent lifestyle behavior treatment option for all patients, including for the large population of mild-moderate-risk patients with elevated blood pressure and blood cholesterol,” they note.
Research has shown that increasing physical activity can lead to clinically meaningful 3 or 4 mm Hg reductions in systolic and diastolic blood pressure, and 3 to 6 mg/dL decreases in LDL cholesterol, the authors point out.
Previous evidence also shows that physically active people have a 21% lower risk of developing cardiovascular disease and a 36% lower risk for death from cardiovascular diseases than those who are not physically active.
Physical activity also has benefits beyond heart health, including a lower risk for some cancers; improved bone, brain, and mental health; and better sleep, they note.
The U.S. Department of Health and Human Services 2018 physical activity guidelines advise Americans to log 150 minutes of moderate-intensity aerobic exercise or 75 minutes of vigorous aerobic activity each week and to participate in two or more weekly strength training sessions.
However, there is no minimum amount of time to receive benefits from physical activity.
“Every little bit of activity is better than none. Even small initial increases of 5 to 10 minutes a day can yield health benefits,” Dr. Gibbs said.
Translational advice for clinicians
The AHA statement encourages clinicians to ask patients about their physical activity at every interaction; provide ideas and resources to help patients improve and sustain regular life-long physical activity; and encourage and celebrate small increases in activity, such as walking more or taking the stairs, to help with motivation.
“In our world where physical activity is increasingly engineered out of our lives and the overwhelming default is to sit – and even more so now as the nation and the world is practicing quarantine and isolation to reduce the spread of coronavirus – the message that we must be relentless in our pursuit to ‘sit less and move more’ throughout the day is more important than ever,” said Dr. Gibbs.
The statement was prepared by a volunteer writing group on behalf of the AHA Council on Lifestyle and Cardiometabolic Health; the Council on Cardiovascular and Stroke Nursing; and the Council on Clinical Cardiology.
This research had no commercial funding. A list of disclosures for the writing group is available with the original article.
A version of this article first appeared on Medscape.com.
Cortical thinning in adolescence ‘definitively’ tied to subsequent psychosis
Subtle differences in brain morphometric features present in adolescence were associated with the subsequent development of psychosis in what is believed to be the largest neuroimaging investigation to date involving people at clinical high risk (CHR).
Investigators found widespread lower cortical thickness (CT) in individuals at CHR, consistent with previously reported CT differences in individuals with an established psychotic disorder.
“This is the first study to definitively show that there are subtle, widespread structural brain differences in high-risk youth before they develop psychosis,” study investigator Maria Jalbrzikowski, PhD, assistant professor of psychiatry, University of Pittsburgh, said in an interview.
The findings also suggest that there are developmental periods during which certain brain abnormalities may be more apparent, “highlighting the need to consider developmental period when developing objective, biological risk factors for early intervention in psychosis,” Dr. Jalbrzikowski said.
The study was published online May 5 in JAMA Psychiatry.
‘Sobering’ results
The findings are based on pooled structural MRI scans from 3,169 individuals recruited at 31 international sites participating in the Enhancing Neuro Imaging Genetics Through Meta-Analysis (ENIGMA) Clinical High Risk for Psychosis Working Group.
Forty-five percent of the participants were female; the mean age was 21 years (range, 9.5 to 39.9 years).
The cohort included 1,792 individuals at CHR for psychosis and 1,377 healthy control persons. Using longitudinal clinical information, the researchers identified 253 individuals at CHR who went on to develop a psychotic disorder (CHR-PS+) and 1,234 at CHR who did not develop a psychotic disorder (CHR-PS-). For the remaining 305 individuals at CHR, follow-up data were unavailable.
Compared with healthy control persons, individuals at CHR had widespread lower CT measures but not lower surface area or subcortical volume. Lower CT measures in the fusiform, superior temporal, and paracentral regions were associated with conversion to psychosis.
The pattern of differences in cortical thickness in those in the CHR-PS+ group mirrored patterns seen in people with schizophrenia and in people with 22q11.2 microdeletion syndrome who developed a psychotic disorder.
The researchers note that although all individuals experience cortical thinning as they move into adulthood, in their study, cortical thinning was already present in participants aged 12 to 16 years who developed psychosis.
“We don’t yet know exactly what this means, but adolescence is a critical time in a child’s life – it’s a time of opportunity to take risks and explore, but also a period of vulnerability,” Dr. Jalbrzikowski said in a news release.
“We could be seeing the result of something that happened even earlier in brain development but only begins to influence behavior during this developmental stage,” she noted.
This analysis represents the largest-ever pooling of brain scans in children and young adults who were determined by psychiatric assessment to be at high risk of developing psychosis.
“These results were, in a sense, sobering. On the one hand, our dataset includes 600% more high-risk youth who developed psychosis than any existing study, allowing us to see statistically significant results in brain structure.”
“But the variance between whether or not a high-risk youth develops psychosis is so small that it would be impossible to see a difference at the individual level,” Dr. Jalbrzikowski said.
More work is needed in order for the findings to be translated into clinical care, she added.
Definitive findings
Commenting on the findings for an interview, Russell Margolis, MD, clinical director, Johns Hopkins Schizophrenia Center, said that “it’s not so much that the findings are novel but rather that they’re fairly definitive in that this is by far the largest study of its kind looking at this particular question, and that gives it power. The problem with imaging studies has often been inconsistent results from study to study because of small sample size.”
“In order to see these differences in a robust way, you need a large sample size, meaning that for any one individual, this kind of structural imaging is not going to add much to the prediction of whether someone will eventually develop a schizophrenia-like illness,” said Dr. Margolis, professor of psychiatry and behavioral sciences, Johns Hopkins University, Baltimore.
From a clinical standpoint,
“The predominant hypothesis in the field is that early developmental abnormalities are the root cause of schizophrenia and related disorders, and this study is consistent with that, particularly the age-related differences, which are suggestive of neurodevelopmental abnormalities preceding the development of overt symptoms, which many other findings have also suggested,” Dr. Margolis said.
“Abnormalities in cortical thickness could be from a number of different neurobiological processes, and research into those processes are worth investigating,” he added.
The researchers received support from numerous funders, all of which are listed in the original article, along with author disclosures for ENIGMA working group members. Dr. Margolis has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Subtle differences in brain morphometric features present in adolescence were associated with the subsequent development of psychosis in what is believed to be the largest neuroimaging investigation to date involving people at clinical high risk (CHR).
Investigators found widespread lower cortical thickness (CT) in individuals at CHR, consistent with previously reported CT differences in individuals with an established psychotic disorder.
“This is the first study to definitively show that there are subtle, widespread structural brain differences in high-risk youth before they develop psychosis,” study investigator Maria Jalbrzikowski, PhD, assistant professor of psychiatry, University of Pittsburgh, said in an interview.
The findings also suggest that there are developmental periods during which certain brain abnormalities may be more apparent, “highlighting the need to consider developmental period when developing objective, biological risk factors for early intervention in psychosis,” Dr. Jalbrzikowski said.
The study was published online May 5 in JAMA Psychiatry.
‘Sobering’ results
The findings are based on pooled structural MRI scans from 3,169 individuals recruited at 31 international sites participating in the Enhancing Neuro Imaging Genetics Through Meta-Analysis (ENIGMA) Clinical High Risk for Psychosis Working Group.
Forty-five percent of the participants were female; the mean age was 21 years (range, 9.5 to 39.9 years).
The cohort included 1,792 individuals at CHR for psychosis and 1,377 healthy control persons. Using longitudinal clinical information, the researchers identified 253 individuals at CHR who went on to develop a psychotic disorder (CHR-PS+) and 1,234 at CHR who did not develop a psychotic disorder (CHR-PS-). For the remaining 305 individuals at CHR, follow-up data were unavailable.
Compared with healthy control persons, individuals at CHR had widespread lower CT measures but not lower surface area or subcortical volume. Lower CT measures in the fusiform, superior temporal, and paracentral regions were associated with conversion to psychosis.
The pattern of differences in cortical thickness in those in the CHR-PS+ group mirrored patterns seen in people with schizophrenia and in people with 22q11.2 microdeletion syndrome who developed a psychotic disorder.
The researchers note that although all individuals experience cortical thinning as they move into adulthood, in their study, cortical thinning was already present in participants aged 12 to 16 years who developed psychosis.
“We don’t yet know exactly what this means, but adolescence is a critical time in a child’s life – it’s a time of opportunity to take risks and explore, but also a period of vulnerability,” Dr. Jalbrzikowski said in a news release.
“We could be seeing the result of something that happened even earlier in brain development but only begins to influence behavior during this developmental stage,” she noted.
This analysis represents the largest-ever pooling of brain scans in children and young adults who were determined by psychiatric assessment to be at high risk of developing psychosis.
“These results were, in a sense, sobering. On the one hand, our dataset includes 600% more high-risk youth who developed psychosis than any existing study, allowing us to see statistically significant results in brain structure.”
“But the variance between whether or not a high-risk youth develops psychosis is so small that it would be impossible to see a difference at the individual level,” Dr. Jalbrzikowski said.
More work is needed in order for the findings to be translated into clinical care, she added.
Definitive findings
Commenting on the findings for an interview, Russell Margolis, MD, clinical director, Johns Hopkins Schizophrenia Center, said that “it’s not so much that the findings are novel but rather that they’re fairly definitive in that this is by far the largest study of its kind looking at this particular question, and that gives it power. The problem with imaging studies has often been inconsistent results from study to study because of small sample size.”
“In order to see these differences in a robust way, you need a large sample size, meaning that for any one individual, this kind of structural imaging is not going to add much to the prediction of whether someone will eventually develop a schizophrenia-like illness,” said Dr. Margolis, professor of psychiatry and behavioral sciences, Johns Hopkins University, Baltimore.
From a clinical standpoint,
“The predominant hypothesis in the field is that early developmental abnormalities are the root cause of schizophrenia and related disorders, and this study is consistent with that, particularly the age-related differences, which are suggestive of neurodevelopmental abnormalities preceding the development of overt symptoms, which many other findings have also suggested,” Dr. Margolis said.
“Abnormalities in cortical thickness could be from a number of different neurobiological processes, and research into those processes are worth investigating,” he added.
The researchers received support from numerous funders, all of which are listed in the original article, along with author disclosures for ENIGMA working group members. Dr. Margolis has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Subtle differences in brain morphometric features present in adolescence were associated with the subsequent development of psychosis in what is believed to be the largest neuroimaging investigation to date involving people at clinical high risk (CHR).
Investigators found widespread lower cortical thickness (CT) in individuals at CHR, consistent with previously reported CT differences in individuals with an established psychotic disorder.
“This is the first study to definitively show that there are subtle, widespread structural brain differences in high-risk youth before they develop psychosis,” study investigator Maria Jalbrzikowski, PhD, assistant professor of psychiatry, University of Pittsburgh, said in an interview.
The findings also suggest that there are developmental periods during which certain brain abnormalities may be more apparent, “highlighting the need to consider developmental period when developing objective, biological risk factors for early intervention in psychosis,” Dr. Jalbrzikowski said.
The study was published online May 5 in JAMA Psychiatry.
‘Sobering’ results
The findings are based on pooled structural MRI scans from 3,169 individuals recruited at 31 international sites participating in the Enhancing Neuro Imaging Genetics Through Meta-Analysis (ENIGMA) Clinical High Risk for Psychosis Working Group.
Forty-five percent of the participants were female; the mean age was 21 years (range, 9.5 to 39.9 years).
The cohort included 1,792 individuals at CHR for psychosis and 1,377 healthy control persons. Using longitudinal clinical information, the researchers identified 253 individuals at CHR who went on to develop a psychotic disorder (CHR-PS+) and 1,234 at CHR who did not develop a psychotic disorder (CHR-PS-). For the remaining 305 individuals at CHR, follow-up data were unavailable.
Compared with healthy control persons, individuals at CHR had widespread lower CT measures but not lower surface area or subcortical volume. Lower CT measures in the fusiform, superior temporal, and paracentral regions were associated with conversion to psychosis.
The pattern of differences in cortical thickness in those in the CHR-PS+ group mirrored patterns seen in people with schizophrenia and in people with 22q11.2 microdeletion syndrome who developed a psychotic disorder.
The researchers note that although all individuals experience cortical thinning as they move into adulthood, in their study, cortical thinning was already present in participants aged 12 to 16 years who developed psychosis.
“We don’t yet know exactly what this means, but adolescence is a critical time in a child’s life – it’s a time of opportunity to take risks and explore, but also a period of vulnerability,” Dr. Jalbrzikowski said in a news release.
“We could be seeing the result of something that happened even earlier in brain development but only begins to influence behavior during this developmental stage,” she noted.
This analysis represents the largest-ever pooling of brain scans in children and young adults who were determined by psychiatric assessment to be at high risk of developing psychosis.
“These results were, in a sense, sobering. On the one hand, our dataset includes 600% more high-risk youth who developed psychosis than any existing study, allowing us to see statistically significant results in brain structure.”
“But the variance between whether or not a high-risk youth develops psychosis is so small that it would be impossible to see a difference at the individual level,” Dr. Jalbrzikowski said.
More work is needed in order for the findings to be translated into clinical care, she added.
Definitive findings
Commenting on the findings for an interview, Russell Margolis, MD, clinical director, Johns Hopkins Schizophrenia Center, said that “it’s not so much that the findings are novel but rather that they’re fairly definitive in that this is by far the largest study of its kind looking at this particular question, and that gives it power. The problem with imaging studies has often been inconsistent results from study to study because of small sample size.”
“In order to see these differences in a robust way, you need a large sample size, meaning that for any one individual, this kind of structural imaging is not going to add much to the prediction of whether someone will eventually develop a schizophrenia-like illness,” said Dr. Margolis, professor of psychiatry and behavioral sciences, Johns Hopkins University, Baltimore.
From a clinical standpoint,
“The predominant hypothesis in the field is that early developmental abnormalities are the root cause of schizophrenia and related disorders, and this study is consistent with that, particularly the age-related differences, which are suggestive of neurodevelopmental abnormalities preceding the development of overt symptoms, which many other findings have also suggested,” Dr. Margolis said.
“Abnormalities in cortical thickness could be from a number of different neurobiological processes, and research into those processes are worth investigating,” he added.
The researchers received support from numerous funders, all of which are listed in the original article, along with author disclosures for ENIGMA working group members. Dr. Margolis has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FDA clears next-generation DBS system for movement disorders
The SenSight Directional Lead System for DBS therapy combines two recent advancements: sensing capability that allows real-time monitoring of brain signals to optimize settings for stimulation, and a “directional lead” that enables steering of electric current for more precise targeting of stimulation through the electrode.
“Until now, sensing capability and directional leads have not been available in the same DBS system, so we have had to choose one technology or the other, based on the predicted needs of each patient,” neurosurgeon Kelly Foote, MD, who performed the first implant of the SenSight System at University of Florida (UF) Health, said in a news release.
“Now, by coupling this new directional lead with a pulse generator capable of brain sensing, we are excited to be able to offer our patients the synergistic benefits of both technologies,” added Dr. Foote, codirector of the Norman Fixel Institute for Neurological Diseases at UF Health.
Dr. Foote said DBS systems capable of adjusting therapeutic stimulation in response to continuously recorded brain signals may lead to better DBS outcomes with fewer adverse effects.
“Adding a directional lead to such a system will improve our ability to localize abnormal signals and enable us to steer current more effectively to areas in the brain where it is most beneficial,” Dr. Foote said.
“We are excited to see the clinical benefits that the new SenSight directional lead system will provide to patients and physicians in the U.S.,” added Mike Daly, vice president and general manager of brain modulation at Medtronic.
Medtronic’s SenSight directional lead DBS system received CE Mark approval in Europe in March.
A version of this article first appeared on Medscape.com.
The SenSight Directional Lead System for DBS therapy combines two recent advancements: sensing capability that allows real-time monitoring of brain signals to optimize settings for stimulation, and a “directional lead” that enables steering of electric current for more precise targeting of stimulation through the electrode.
“Until now, sensing capability and directional leads have not been available in the same DBS system, so we have had to choose one technology or the other, based on the predicted needs of each patient,” neurosurgeon Kelly Foote, MD, who performed the first implant of the SenSight System at University of Florida (UF) Health, said in a news release.
“Now, by coupling this new directional lead with a pulse generator capable of brain sensing, we are excited to be able to offer our patients the synergistic benefits of both technologies,” added Dr. Foote, codirector of the Norman Fixel Institute for Neurological Diseases at UF Health.
Dr. Foote said DBS systems capable of adjusting therapeutic stimulation in response to continuously recorded brain signals may lead to better DBS outcomes with fewer adverse effects.
“Adding a directional lead to such a system will improve our ability to localize abnormal signals and enable us to steer current more effectively to areas in the brain where it is most beneficial,” Dr. Foote said.
“We are excited to see the clinical benefits that the new SenSight directional lead system will provide to patients and physicians in the U.S.,” added Mike Daly, vice president and general manager of brain modulation at Medtronic.
Medtronic’s SenSight directional lead DBS system received CE Mark approval in Europe in March.
A version of this article first appeared on Medscape.com.
The SenSight Directional Lead System for DBS therapy combines two recent advancements: sensing capability that allows real-time monitoring of brain signals to optimize settings for stimulation, and a “directional lead” that enables steering of electric current for more precise targeting of stimulation through the electrode.
“Until now, sensing capability and directional leads have not been available in the same DBS system, so we have had to choose one technology or the other, based on the predicted needs of each patient,” neurosurgeon Kelly Foote, MD, who performed the first implant of the SenSight System at University of Florida (UF) Health, said in a news release.
“Now, by coupling this new directional lead with a pulse generator capable of brain sensing, we are excited to be able to offer our patients the synergistic benefits of both technologies,” added Dr. Foote, codirector of the Norman Fixel Institute for Neurological Diseases at UF Health.
Dr. Foote said DBS systems capable of adjusting therapeutic stimulation in response to continuously recorded brain signals may lead to better DBS outcomes with fewer adverse effects.
“Adding a directional lead to such a system will improve our ability to localize abnormal signals and enable us to steer current more effectively to areas in the brain where it is most beneficial,” Dr. Foote said.
“We are excited to see the clinical benefits that the new SenSight directional lead system will provide to patients and physicians in the U.S.,” added Mike Daly, vice president and general manager of brain modulation at Medtronic.
Medtronic’s SenSight directional lead DBS system received CE Mark approval in Europe in March.
A version of this article first appeared on Medscape.com.