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Growing evidence supports repurposing antidepressants to treat COVID-19
Mounting evidence suggests selective serotonin reuptake inhibitors (SSRI) are associated with lower COVID-19 severity.
A large analysis of health records shows patients with COVID-19 taking an SSRI were significantly less likely to die of COVID-19 than a matched control group.
“We can’t tell if the drugs are causing these effects, but the statistical analysis is showing significant association. There’s power in the numbers,” Marina Sirota, PhD, University of California, San Francisco (UCSF), said in a statement.
The study was published online Nov. 15 in JAMA Network Open.
Data-driven approach
, including 3,401 patients who were prescribed SSRIs.
When compared with matched patients with COVID-19 taking SSRIs, patients taking fluoxetine were 28% less likely to die (relative risk, 0.72; 95% CI, 0.54-0.97; adjusted P = .03) and those taking either fluoxetine or fluvoxamine were 26% less likely to die (RR, 0.74; 95% CI, 0.55-0.99; adjusted P = .04) versus those not on these medications.
Patients with COVID-19 taking any kind of SSRI were 8% less likely to die than the matched controls (RR, 0.92; 95% CI, 0.85-0.99; adjusted P = .03).
“We observed a statistically significant reduction in mortality of COVID-19 patients who were already taking SSRIs. This is a demonstration of a data-driven approach for identifying new uses for existing drugs,” Dr. Sirota said in an interview.
“Our study simply shows an association between SSRIs and COVID-19 outcomes and doesn’t investigate the mechanism of action of why the drugs might work. Additional clinical trials need to be carried out before these drugs can be used in patients going forward,” she cautioned.
“There is currently an open-label trial investigating fluoxetine to reduce intubation and death after COVID-19. To our knowledge, there are no phase 3 randomized controlled trials taking place or planned,” study investigator Tomiko Oskotsky, MD, with UCSF, told this news organization.
Urgent need
The current results “confirm and expand on prior findings from observational, preclinical, and clinical studies suggesting that certain SSRI antidepressants, including fluoxetine or fluvoxamine, could be beneficial against COVID-19,” Nicolas Hoertel, MD, PhD, MPH, with Paris University and Corentin-Celton Hospital, France, writes in a linked editorial.
Dr. Hoertel notes that the anti-inflammatory properties of SSRIs may underlie their potential action against COVID-19, and other potential mechanisms may include reduction in platelet aggregation, decreased mast cell degranulation, increased melatonin levels, interference with endolysosomal viral trafficking, and antioxidant activities.
“Because most of the world’s population is currently unvaccinated and the COVID-19 pandemic is still active, effective treatments of COVID-19 – especially those that are easy to use, show good tolerability, can be administered orally, and have widespread availability at low cost to allow their use in resource-poor countries – are urgently needed to reduce COVID-19-related mortality and morbidity,” Dr. Hoertel points out.
“In this context, short-term use of fluoxetine or fluvoxamine, if proven effective, should be considered as a potential means of reaching this goal,” he adds.
The study was supported by the Christopher Hess Research Fund and, in part, by UCSF and the National Institutes of Health. Dr. Sirota has reported serving as a scientific advisor at Aria Pharmaceuticals. Dr. Hoertel has reported being listed as an inventor on a patent application related to methods of treating COVID-19, filed by Assistance Publique-Hopitaux de Paris, and receiving consulting fees and nonfinancial support from Lundbeck.
A version of this article first appeared on Medscape.com.
Mounting evidence suggests selective serotonin reuptake inhibitors (SSRI) are associated with lower COVID-19 severity.
A large analysis of health records shows patients with COVID-19 taking an SSRI were significantly less likely to die of COVID-19 than a matched control group.
“We can’t tell if the drugs are causing these effects, but the statistical analysis is showing significant association. There’s power in the numbers,” Marina Sirota, PhD, University of California, San Francisco (UCSF), said in a statement.
The study was published online Nov. 15 in JAMA Network Open.
Data-driven approach
, including 3,401 patients who were prescribed SSRIs.
When compared with matched patients with COVID-19 taking SSRIs, patients taking fluoxetine were 28% less likely to die (relative risk, 0.72; 95% CI, 0.54-0.97; adjusted P = .03) and those taking either fluoxetine or fluvoxamine were 26% less likely to die (RR, 0.74; 95% CI, 0.55-0.99; adjusted P = .04) versus those not on these medications.
Patients with COVID-19 taking any kind of SSRI were 8% less likely to die than the matched controls (RR, 0.92; 95% CI, 0.85-0.99; adjusted P = .03).
“We observed a statistically significant reduction in mortality of COVID-19 patients who were already taking SSRIs. This is a demonstration of a data-driven approach for identifying new uses for existing drugs,” Dr. Sirota said in an interview.
“Our study simply shows an association between SSRIs and COVID-19 outcomes and doesn’t investigate the mechanism of action of why the drugs might work. Additional clinical trials need to be carried out before these drugs can be used in patients going forward,” she cautioned.
“There is currently an open-label trial investigating fluoxetine to reduce intubation and death after COVID-19. To our knowledge, there are no phase 3 randomized controlled trials taking place or planned,” study investigator Tomiko Oskotsky, MD, with UCSF, told this news organization.
Urgent need
The current results “confirm and expand on prior findings from observational, preclinical, and clinical studies suggesting that certain SSRI antidepressants, including fluoxetine or fluvoxamine, could be beneficial against COVID-19,” Nicolas Hoertel, MD, PhD, MPH, with Paris University and Corentin-Celton Hospital, France, writes in a linked editorial.
Dr. Hoertel notes that the anti-inflammatory properties of SSRIs may underlie their potential action against COVID-19, and other potential mechanisms may include reduction in platelet aggregation, decreased mast cell degranulation, increased melatonin levels, interference with endolysosomal viral trafficking, and antioxidant activities.
“Because most of the world’s population is currently unvaccinated and the COVID-19 pandemic is still active, effective treatments of COVID-19 – especially those that are easy to use, show good tolerability, can be administered orally, and have widespread availability at low cost to allow their use in resource-poor countries – are urgently needed to reduce COVID-19-related mortality and morbidity,” Dr. Hoertel points out.
“In this context, short-term use of fluoxetine or fluvoxamine, if proven effective, should be considered as a potential means of reaching this goal,” he adds.
The study was supported by the Christopher Hess Research Fund and, in part, by UCSF and the National Institutes of Health. Dr. Sirota has reported serving as a scientific advisor at Aria Pharmaceuticals. Dr. Hoertel has reported being listed as an inventor on a patent application related to methods of treating COVID-19, filed by Assistance Publique-Hopitaux de Paris, and receiving consulting fees and nonfinancial support from Lundbeck.
A version of this article first appeared on Medscape.com.
Mounting evidence suggests selective serotonin reuptake inhibitors (SSRI) are associated with lower COVID-19 severity.
A large analysis of health records shows patients with COVID-19 taking an SSRI were significantly less likely to die of COVID-19 than a matched control group.
“We can’t tell if the drugs are causing these effects, but the statistical analysis is showing significant association. There’s power in the numbers,” Marina Sirota, PhD, University of California, San Francisco (UCSF), said in a statement.
The study was published online Nov. 15 in JAMA Network Open.
Data-driven approach
, including 3,401 patients who were prescribed SSRIs.
When compared with matched patients with COVID-19 taking SSRIs, patients taking fluoxetine were 28% less likely to die (relative risk, 0.72; 95% CI, 0.54-0.97; adjusted P = .03) and those taking either fluoxetine or fluvoxamine were 26% less likely to die (RR, 0.74; 95% CI, 0.55-0.99; adjusted P = .04) versus those not on these medications.
Patients with COVID-19 taking any kind of SSRI were 8% less likely to die than the matched controls (RR, 0.92; 95% CI, 0.85-0.99; adjusted P = .03).
“We observed a statistically significant reduction in mortality of COVID-19 patients who were already taking SSRIs. This is a demonstration of a data-driven approach for identifying new uses for existing drugs,” Dr. Sirota said in an interview.
“Our study simply shows an association between SSRIs and COVID-19 outcomes and doesn’t investigate the mechanism of action of why the drugs might work. Additional clinical trials need to be carried out before these drugs can be used in patients going forward,” she cautioned.
“There is currently an open-label trial investigating fluoxetine to reduce intubation and death after COVID-19. To our knowledge, there are no phase 3 randomized controlled trials taking place or planned,” study investigator Tomiko Oskotsky, MD, with UCSF, told this news organization.
Urgent need
The current results “confirm and expand on prior findings from observational, preclinical, and clinical studies suggesting that certain SSRI antidepressants, including fluoxetine or fluvoxamine, could be beneficial against COVID-19,” Nicolas Hoertel, MD, PhD, MPH, with Paris University and Corentin-Celton Hospital, France, writes in a linked editorial.
Dr. Hoertel notes that the anti-inflammatory properties of SSRIs may underlie their potential action against COVID-19, and other potential mechanisms may include reduction in platelet aggregation, decreased mast cell degranulation, increased melatonin levels, interference with endolysosomal viral trafficking, and antioxidant activities.
“Because most of the world’s population is currently unvaccinated and the COVID-19 pandemic is still active, effective treatments of COVID-19 – especially those that are easy to use, show good tolerability, can be administered orally, and have widespread availability at low cost to allow their use in resource-poor countries – are urgently needed to reduce COVID-19-related mortality and morbidity,” Dr. Hoertel points out.
“In this context, short-term use of fluoxetine or fluvoxamine, if proven effective, should be considered as a potential means of reaching this goal,” he adds.
The study was supported by the Christopher Hess Research Fund and, in part, by UCSF and the National Institutes of Health. Dr. Sirota has reported serving as a scientific advisor at Aria Pharmaceuticals. Dr. Hoertel has reported being listed as an inventor on a patent application related to methods of treating COVID-19, filed by Assistance Publique-Hopitaux de Paris, and receiving consulting fees and nonfinancial support from Lundbeck.
A version of this article first appeared on Medscape.com.
Controversial Alzheimer’s drug unlikely to get the OK in Europe
At its November meeting, , making it highly unlikely the drug will be recommended for approval at its December meeting.
In a news release issued Nov. 17, Biogen said the company received a “negative trend vote” on the aducanumab marketing authorization application in Europe.
“While we are disappointed with the trend vote, we strongly believe in the strength of our data and that aducanumab has the potential to make a positive and meaningful difference for people and families affected by Alzheimer’s disease [AD],” Priya Singhal, MD, MPH, head of global safety and regulatory sciences and interim head of research and development at Biogen, said in the release.
The EMA committee is expected to adopt a formal opinion on the marketing application at its December meeting (Dec. 13-16, 2021).
“Biogen will continue to engage with the EMA and CHMP as it considers next steps towards the goal of providing access to aducanumab to patients in Europe,” the company said.
At the recent Clinical Trials on Alzheimer’s Disease conference, Biogen announced new phase 3 findings that “provide further evidence of aducanumab’s effect on lowering amyloid beta plaque and downstream tau pathology, the two defining pathologies of Alzheimer’s disease,” the company said.
No clinically meaningful effect
In a statement from the nonprofit U.K. Science Media Centre, Prof. Robert Howard, from University College London, said the result of the CHMP vote “is absolutely the decision that we should have expected from the EMA’s expert advisory panel and is consistent with the FDA’s [U.S. Food and Drug Administration’s] Advisory Committee who voted unanimously 12 months ago against approval of aducanumab because of a lack of demonstrable efficacy in the pivotal phase 3 trials ENGAGE and EMERGE.”
“The FDA’s accelerated approval of aducanumab, solely on the grounds that it was reasonable to expect that reduction in amyloid would lead to improvement in the course of Alzheimer’s disease, despite all the evidence indicating no meaningful correlation between amyloid reduction and symptom improvement, has been highly controversial and has called into question the impartiality of the FDA and its staff,” Prof. Howard noted.
He anticipates that when the EMA panel meets in December they will not grant a license to aducanumab.
“Aducanumab is a treatment without convincing efficacy, with serious associated adverse effects and a high financial cost. On the basis of the available evidence and in the best interests of people with Alzheimer’s disease, their families and those who care for them, EMA and MHRA [Medicines and Healthcare products Regulatory Agency] should not approve a license for aducanumab,” Prof. Howard said.
Also weighing in, David Thomas, head of policy at Alzheimer’s Research UK, said the need for new AD treatments is “urgent,” but added that “it’s vital that regulators judge that any new treatment is safe and effective.”
“Results of aducanumab’s phase 3 trials, EMERGE and ENGAGE, have sparked much debate among the research community about how to judge the effectiveness of any new Alzheimer’s treatment,” Mr. Thomas noted.
“The FDA’s approval of aducanumab in the U.S. was based on the drug’s ability to clear the hallmark Alzheimer’s protein amyloid from the brain. As part of this approval the regulator now requires further trials to be carried out to ensure that aducanumab brings long-term improvement to people’s memory, thinking and day-to-day lives,” Mr. Thomas said.
EMA is now undertaking its own review of the data and “it’s important that we wait for the committee’s official recommendation, which is expected next month. In the meantime, we must continue to work at pace to ensure researchers are developing a broad pipeline of potential new treatments for diseases like Alzheimer’s, and that health systems like the NHS [National Health Service] will be ready to deliver them in the years ahead,” he added.
‘Reckless’ FDA decision
In related news, the Centers for Medicare and Medicaid Services (CMS) has announced that the Medicare Part B standard premium would rise to $170 per month for all enrollees, a 15% spike over the 2021 premium level.
“All Part B Medicare beneficiaries soon will be forced to bear significant financial burden as a direct result of the FDA’s reckless decision to approve aducanumab, a drug that has not been proven to provide any clinically meaningful benefit to Alzheimer’s patients but nevertheless carries an indefensible annual price tag set by Biogen at $56,000 per year for just the drug alone,” Michael Carome, MD, director of Public Citizen’s Health Research Group, said in a statement.
“To protect the many Medicare beneficiaries who cannot afford the unacceptable 15% jump in Part B premiums, CMS must promptly announce that it will exclude aducanumab from coverage under the Medicare program until there is definitive evidence that the drug provides substantial evidence of cognitive benefit to Alzheimer’s disease patients,” Dr. Carome said.
A version of this article first appeared on Medscape.com.
At its November meeting, , making it highly unlikely the drug will be recommended for approval at its December meeting.
In a news release issued Nov. 17, Biogen said the company received a “negative trend vote” on the aducanumab marketing authorization application in Europe.
“While we are disappointed with the trend vote, we strongly believe in the strength of our data and that aducanumab has the potential to make a positive and meaningful difference for people and families affected by Alzheimer’s disease [AD],” Priya Singhal, MD, MPH, head of global safety and regulatory sciences and interim head of research and development at Biogen, said in the release.
The EMA committee is expected to adopt a formal opinion on the marketing application at its December meeting (Dec. 13-16, 2021).
“Biogen will continue to engage with the EMA and CHMP as it considers next steps towards the goal of providing access to aducanumab to patients in Europe,” the company said.
At the recent Clinical Trials on Alzheimer’s Disease conference, Biogen announced new phase 3 findings that “provide further evidence of aducanumab’s effect on lowering amyloid beta plaque and downstream tau pathology, the two defining pathologies of Alzheimer’s disease,” the company said.
No clinically meaningful effect
In a statement from the nonprofit U.K. Science Media Centre, Prof. Robert Howard, from University College London, said the result of the CHMP vote “is absolutely the decision that we should have expected from the EMA’s expert advisory panel and is consistent with the FDA’s [U.S. Food and Drug Administration’s] Advisory Committee who voted unanimously 12 months ago against approval of aducanumab because of a lack of demonstrable efficacy in the pivotal phase 3 trials ENGAGE and EMERGE.”
“The FDA’s accelerated approval of aducanumab, solely on the grounds that it was reasonable to expect that reduction in amyloid would lead to improvement in the course of Alzheimer’s disease, despite all the evidence indicating no meaningful correlation between amyloid reduction and symptom improvement, has been highly controversial and has called into question the impartiality of the FDA and its staff,” Prof. Howard noted.
He anticipates that when the EMA panel meets in December they will not grant a license to aducanumab.
“Aducanumab is a treatment without convincing efficacy, with serious associated adverse effects and a high financial cost. On the basis of the available evidence and in the best interests of people with Alzheimer’s disease, their families and those who care for them, EMA and MHRA [Medicines and Healthcare products Regulatory Agency] should not approve a license for aducanumab,” Prof. Howard said.
Also weighing in, David Thomas, head of policy at Alzheimer’s Research UK, said the need for new AD treatments is “urgent,” but added that “it’s vital that regulators judge that any new treatment is safe and effective.”
“Results of aducanumab’s phase 3 trials, EMERGE and ENGAGE, have sparked much debate among the research community about how to judge the effectiveness of any new Alzheimer’s treatment,” Mr. Thomas noted.
“The FDA’s approval of aducanumab in the U.S. was based on the drug’s ability to clear the hallmark Alzheimer’s protein amyloid from the brain. As part of this approval the regulator now requires further trials to be carried out to ensure that aducanumab brings long-term improvement to people’s memory, thinking and day-to-day lives,” Mr. Thomas said.
EMA is now undertaking its own review of the data and “it’s important that we wait for the committee’s official recommendation, which is expected next month. In the meantime, we must continue to work at pace to ensure researchers are developing a broad pipeline of potential new treatments for diseases like Alzheimer’s, and that health systems like the NHS [National Health Service] will be ready to deliver them in the years ahead,” he added.
‘Reckless’ FDA decision
In related news, the Centers for Medicare and Medicaid Services (CMS) has announced that the Medicare Part B standard premium would rise to $170 per month for all enrollees, a 15% spike over the 2021 premium level.
“All Part B Medicare beneficiaries soon will be forced to bear significant financial burden as a direct result of the FDA’s reckless decision to approve aducanumab, a drug that has not been proven to provide any clinically meaningful benefit to Alzheimer’s patients but nevertheless carries an indefensible annual price tag set by Biogen at $56,000 per year for just the drug alone,” Michael Carome, MD, director of Public Citizen’s Health Research Group, said in a statement.
“To protect the many Medicare beneficiaries who cannot afford the unacceptable 15% jump in Part B premiums, CMS must promptly announce that it will exclude aducanumab from coverage under the Medicare program until there is definitive evidence that the drug provides substantial evidence of cognitive benefit to Alzheimer’s disease patients,” Dr. Carome said.
A version of this article first appeared on Medscape.com.
At its November meeting, , making it highly unlikely the drug will be recommended for approval at its December meeting.
In a news release issued Nov. 17, Biogen said the company received a “negative trend vote” on the aducanumab marketing authorization application in Europe.
“While we are disappointed with the trend vote, we strongly believe in the strength of our data and that aducanumab has the potential to make a positive and meaningful difference for people and families affected by Alzheimer’s disease [AD],” Priya Singhal, MD, MPH, head of global safety and regulatory sciences and interim head of research and development at Biogen, said in the release.
The EMA committee is expected to adopt a formal opinion on the marketing application at its December meeting (Dec. 13-16, 2021).
“Biogen will continue to engage with the EMA and CHMP as it considers next steps towards the goal of providing access to aducanumab to patients in Europe,” the company said.
At the recent Clinical Trials on Alzheimer’s Disease conference, Biogen announced new phase 3 findings that “provide further evidence of aducanumab’s effect on lowering amyloid beta plaque and downstream tau pathology, the two defining pathologies of Alzheimer’s disease,” the company said.
No clinically meaningful effect
In a statement from the nonprofit U.K. Science Media Centre, Prof. Robert Howard, from University College London, said the result of the CHMP vote “is absolutely the decision that we should have expected from the EMA’s expert advisory panel and is consistent with the FDA’s [U.S. Food and Drug Administration’s] Advisory Committee who voted unanimously 12 months ago against approval of aducanumab because of a lack of demonstrable efficacy in the pivotal phase 3 trials ENGAGE and EMERGE.”
“The FDA’s accelerated approval of aducanumab, solely on the grounds that it was reasonable to expect that reduction in amyloid would lead to improvement in the course of Alzheimer’s disease, despite all the evidence indicating no meaningful correlation between amyloid reduction and symptom improvement, has been highly controversial and has called into question the impartiality of the FDA and its staff,” Prof. Howard noted.
He anticipates that when the EMA panel meets in December they will not grant a license to aducanumab.
“Aducanumab is a treatment without convincing efficacy, with serious associated adverse effects and a high financial cost. On the basis of the available evidence and in the best interests of people with Alzheimer’s disease, their families and those who care for them, EMA and MHRA [Medicines and Healthcare products Regulatory Agency] should not approve a license for aducanumab,” Prof. Howard said.
Also weighing in, David Thomas, head of policy at Alzheimer’s Research UK, said the need for new AD treatments is “urgent,” but added that “it’s vital that regulators judge that any new treatment is safe and effective.”
“Results of aducanumab’s phase 3 trials, EMERGE and ENGAGE, have sparked much debate among the research community about how to judge the effectiveness of any new Alzheimer’s treatment,” Mr. Thomas noted.
“The FDA’s approval of aducanumab in the U.S. was based on the drug’s ability to clear the hallmark Alzheimer’s protein amyloid from the brain. As part of this approval the regulator now requires further trials to be carried out to ensure that aducanumab brings long-term improvement to people’s memory, thinking and day-to-day lives,” Mr. Thomas said.
EMA is now undertaking its own review of the data and “it’s important that we wait for the committee’s official recommendation, which is expected next month. In the meantime, we must continue to work at pace to ensure researchers are developing a broad pipeline of potential new treatments for diseases like Alzheimer’s, and that health systems like the NHS [National Health Service] will be ready to deliver them in the years ahead,” he added.
‘Reckless’ FDA decision
In related news, the Centers for Medicare and Medicaid Services (CMS) has announced that the Medicare Part B standard premium would rise to $170 per month for all enrollees, a 15% spike over the 2021 premium level.
“All Part B Medicare beneficiaries soon will be forced to bear significant financial burden as a direct result of the FDA’s reckless decision to approve aducanumab, a drug that has not been proven to provide any clinically meaningful benefit to Alzheimer’s patients but nevertheless carries an indefensible annual price tag set by Biogen at $56,000 per year for just the drug alone,” Michael Carome, MD, director of Public Citizen’s Health Research Group, said in a statement.
“To protect the many Medicare beneficiaries who cannot afford the unacceptable 15% jump in Part B premiums, CMS must promptly announce that it will exclude aducanumab from coverage under the Medicare program until there is definitive evidence that the drug provides substantial evidence of cognitive benefit to Alzheimer’s disease patients,” Dr. Carome said.
A version of this article first appeared on Medscape.com.
Single infusion of ketamine rapidly reduces suicidal thoughts
A single infusion of ketamine rapidly improves distorted thinking and reasoning to reduce suicidal thoughts, independent of the drug’s effect on severe depression, new research shows.
“Previously it was shown that ketamine rapidly improved depression and that explained part of the rapid improvement in suicidal ideation,” senior author J. John Mann, MD, with Columbia University, New York, said in an interview.
“What was unclear was what else changed that could decrease suicidal ideation and the risk for suicidal behavior. This study identifies a second new domain of improvement – namely rapid improvement in several cognitive functions that can potentially reduce suicide risk,” said Dr. Mann.
The study was published online Nov. 2, 2021, in the Journal of Clinical Psychiatry.
Boosts cognitive function
A total of 78 adults with major depressive disorder and clinically significant suicidal ideation underwent neuropsychological testing before, and 1 day after, double-blind treatment with a single intravenous infusion of ketamine or midazolam.
“Ketamine produced rapid improvement in suicidal ideation and mood” compared with midazolam, the authors reported.
Ketamine was linked to specific improvement in reaction time and cognitive control/interference processing – a measure that has been associated with previous suicide attempt in depression.
A subgroup of patients whose suicidal ideation did not remit on midazolam were later treated with unblinded ketamine and retested. In these individuals, reaction time and cognitive control/interference processing also improved relative to preketamine assessments.
Neurocognitive improvement, however, was not correlated with changes in depression, suicidal thinking, or general mood, the researchers noted.
Nonetheless, they say ketamine had a “positive therapeutic effect” on neurocognition 1 day after treatment on at least one measure associated with suicidal behavior in the context of depression.
The results suggest “additional independent therapeutic effects for ketamine in the treatment of depressed patients at risk for suicidal behavior,” they wrote.
“Ketamine modulates many neurotransmitter systems including glutamate transmission which is crucial for learning and memory. It increases the number of synapses or connections between neurons. These effects are fundamental to cognition and are logical explanations of the beneficial effects observed in this study,” Dr. Mann said in an interview.
“Our study helped us gain a better understanding of how ketamine works in the brain and how quickly it can improve distorted thinking. study investigator Ravi. N. Shah, MD, chief innovation officer, Columbia Psychiatry, said in a news release.
Important research with caveats
In a comment, James Murrough, MD, PhD, director of the Depression and Anxiety Center for Discovery and Treatment at Mount Sinai in New York, said the study is important and “adds to a growing understanding of how ketamine affects brain systems and thinking in the context of depression and suicide risk.”
“One reason this study is significant is that prior studies have shown that ketamine can have harmful effects on cognitive functioning in the context of ketamine misuse and exposures to high doses for long periods of time,” Dr. Murrough, who wasn’t involved in the study, said in an interview.
“In contrast in this study, a single low-dose treatment of ketamine can have the opposite effects, actually boosting some markers of cognitive functioning, at least in the short-term,” he noted.
Dr. Murrough said one caveat to the study is that it only examined the effect of ketamine on cognition once, 1 day after a single treatment.
“While this is an important initial observation, we don’t yet have any understanding of how persistent this effect on cognition is, or how this observed change may be related to any benefit ketamine may have on depression or suicide risk,” Dr. Murrough said.
“In fact, the researchers found that there was no association between change in cognitive functioning following ketamine and change in depression or suicidal thinking. The patients who showed improved cognitive function following ketamine did not differ in terms of mood or suicide risk compared to patients who did not show an improvement in cognition,” Dr. Murrough noted.
“This raises the important question of what is the relevance of change in cognition to the potential benefits of ketamine. This is an important area and should be the focus of future research in order to improve outcomes for patients with depression and who are at risk for suicide,” he added.
Also weighing in, Roger S. McIntyre, MD, professor of psychiatry and pharmacology and head of the mood disorders psychopharmacology unit, University of Toronto, said the study is “very interesting and in keeping” with some previous work that he and his colleagues have done showing that ketamine “seems to benefit aspects of cognition which is a core element in depression.”
“It’s a testable hypothesis that the improvement in cognition now being reported and replicated could play some role in the improved quality of life and functioning with this treatment and as well reduce reducing suicide,” said Dr. McIntyre.
This study was supported by the National Institute of Mental Health. Dr. Mann receives royalties for commercial use of the Columbia-Suicide Severity Rating Scale, which was not used in this study. Dr. Murrough’s institution was involved in research involving esketamine (Spravato) for treatment-resistant depression and receives financial remuneration from the manufacturer of esketamine. Dr. McIntyre has received research grant support from the Canadian Institutes of Health Research/Global Alliance for Chronic Diseases/Chinese National Natural Research Foundation and speaker/consultation fees from Lundbeck, Janssen, Purdue, Pfizer, Otsuka, Allergan, Takeda, Neurocrine, Sunovion, Eisai, Minerva, Intra-Cellular, and AbbVie. Dr. McIntyre is also CEO of AltMed.
A version of this article first appeared on Medscape.com.
A single infusion of ketamine rapidly improves distorted thinking and reasoning to reduce suicidal thoughts, independent of the drug’s effect on severe depression, new research shows.
“Previously it was shown that ketamine rapidly improved depression and that explained part of the rapid improvement in suicidal ideation,” senior author J. John Mann, MD, with Columbia University, New York, said in an interview.
“What was unclear was what else changed that could decrease suicidal ideation and the risk for suicidal behavior. This study identifies a second new domain of improvement – namely rapid improvement in several cognitive functions that can potentially reduce suicide risk,” said Dr. Mann.
The study was published online Nov. 2, 2021, in the Journal of Clinical Psychiatry.
Boosts cognitive function
A total of 78 adults with major depressive disorder and clinically significant suicidal ideation underwent neuropsychological testing before, and 1 day after, double-blind treatment with a single intravenous infusion of ketamine or midazolam.
“Ketamine produced rapid improvement in suicidal ideation and mood” compared with midazolam, the authors reported.
Ketamine was linked to specific improvement in reaction time and cognitive control/interference processing – a measure that has been associated with previous suicide attempt in depression.
A subgroup of patients whose suicidal ideation did not remit on midazolam were later treated with unblinded ketamine and retested. In these individuals, reaction time and cognitive control/interference processing also improved relative to preketamine assessments.
Neurocognitive improvement, however, was not correlated with changes in depression, suicidal thinking, or general mood, the researchers noted.
Nonetheless, they say ketamine had a “positive therapeutic effect” on neurocognition 1 day after treatment on at least one measure associated with suicidal behavior in the context of depression.
The results suggest “additional independent therapeutic effects for ketamine in the treatment of depressed patients at risk for suicidal behavior,” they wrote.
“Ketamine modulates many neurotransmitter systems including glutamate transmission which is crucial for learning and memory. It increases the number of synapses or connections between neurons. These effects are fundamental to cognition and are logical explanations of the beneficial effects observed in this study,” Dr. Mann said in an interview.
“Our study helped us gain a better understanding of how ketamine works in the brain and how quickly it can improve distorted thinking. study investigator Ravi. N. Shah, MD, chief innovation officer, Columbia Psychiatry, said in a news release.
Important research with caveats
In a comment, James Murrough, MD, PhD, director of the Depression and Anxiety Center for Discovery and Treatment at Mount Sinai in New York, said the study is important and “adds to a growing understanding of how ketamine affects brain systems and thinking in the context of depression and suicide risk.”
“One reason this study is significant is that prior studies have shown that ketamine can have harmful effects on cognitive functioning in the context of ketamine misuse and exposures to high doses for long periods of time,” Dr. Murrough, who wasn’t involved in the study, said in an interview.
“In contrast in this study, a single low-dose treatment of ketamine can have the opposite effects, actually boosting some markers of cognitive functioning, at least in the short-term,” he noted.
Dr. Murrough said one caveat to the study is that it only examined the effect of ketamine on cognition once, 1 day after a single treatment.
“While this is an important initial observation, we don’t yet have any understanding of how persistent this effect on cognition is, or how this observed change may be related to any benefit ketamine may have on depression or suicide risk,” Dr. Murrough said.
“In fact, the researchers found that there was no association between change in cognitive functioning following ketamine and change in depression or suicidal thinking. The patients who showed improved cognitive function following ketamine did not differ in terms of mood or suicide risk compared to patients who did not show an improvement in cognition,” Dr. Murrough noted.
“This raises the important question of what is the relevance of change in cognition to the potential benefits of ketamine. This is an important area and should be the focus of future research in order to improve outcomes for patients with depression and who are at risk for suicide,” he added.
Also weighing in, Roger S. McIntyre, MD, professor of psychiatry and pharmacology and head of the mood disorders psychopharmacology unit, University of Toronto, said the study is “very interesting and in keeping” with some previous work that he and his colleagues have done showing that ketamine “seems to benefit aspects of cognition which is a core element in depression.”
“It’s a testable hypothesis that the improvement in cognition now being reported and replicated could play some role in the improved quality of life and functioning with this treatment and as well reduce reducing suicide,” said Dr. McIntyre.
This study was supported by the National Institute of Mental Health. Dr. Mann receives royalties for commercial use of the Columbia-Suicide Severity Rating Scale, which was not used in this study. Dr. Murrough’s institution was involved in research involving esketamine (Spravato) for treatment-resistant depression and receives financial remuneration from the manufacturer of esketamine. Dr. McIntyre has received research grant support from the Canadian Institutes of Health Research/Global Alliance for Chronic Diseases/Chinese National Natural Research Foundation and speaker/consultation fees from Lundbeck, Janssen, Purdue, Pfizer, Otsuka, Allergan, Takeda, Neurocrine, Sunovion, Eisai, Minerva, Intra-Cellular, and AbbVie. Dr. McIntyre is also CEO of AltMed.
A version of this article first appeared on Medscape.com.
A single infusion of ketamine rapidly improves distorted thinking and reasoning to reduce suicidal thoughts, independent of the drug’s effect on severe depression, new research shows.
“Previously it was shown that ketamine rapidly improved depression and that explained part of the rapid improvement in suicidal ideation,” senior author J. John Mann, MD, with Columbia University, New York, said in an interview.
“What was unclear was what else changed that could decrease suicidal ideation and the risk for suicidal behavior. This study identifies a second new domain of improvement – namely rapid improvement in several cognitive functions that can potentially reduce suicide risk,” said Dr. Mann.
The study was published online Nov. 2, 2021, in the Journal of Clinical Psychiatry.
Boosts cognitive function
A total of 78 adults with major depressive disorder and clinically significant suicidal ideation underwent neuropsychological testing before, and 1 day after, double-blind treatment with a single intravenous infusion of ketamine or midazolam.
“Ketamine produced rapid improvement in suicidal ideation and mood” compared with midazolam, the authors reported.
Ketamine was linked to specific improvement in reaction time and cognitive control/interference processing – a measure that has been associated with previous suicide attempt in depression.
A subgroup of patients whose suicidal ideation did not remit on midazolam were later treated with unblinded ketamine and retested. In these individuals, reaction time and cognitive control/interference processing also improved relative to preketamine assessments.
Neurocognitive improvement, however, was not correlated with changes in depression, suicidal thinking, or general mood, the researchers noted.
Nonetheless, they say ketamine had a “positive therapeutic effect” on neurocognition 1 day after treatment on at least one measure associated with suicidal behavior in the context of depression.
The results suggest “additional independent therapeutic effects for ketamine in the treatment of depressed patients at risk for suicidal behavior,” they wrote.
“Ketamine modulates many neurotransmitter systems including glutamate transmission which is crucial for learning and memory. It increases the number of synapses or connections between neurons. These effects are fundamental to cognition and are logical explanations of the beneficial effects observed in this study,” Dr. Mann said in an interview.
“Our study helped us gain a better understanding of how ketamine works in the brain and how quickly it can improve distorted thinking. study investigator Ravi. N. Shah, MD, chief innovation officer, Columbia Psychiatry, said in a news release.
Important research with caveats
In a comment, James Murrough, MD, PhD, director of the Depression and Anxiety Center for Discovery and Treatment at Mount Sinai in New York, said the study is important and “adds to a growing understanding of how ketamine affects brain systems and thinking in the context of depression and suicide risk.”
“One reason this study is significant is that prior studies have shown that ketamine can have harmful effects on cognitive functioning in the context of ketamine misuse and exposures to high doses for long periods of time,” Dr. Murrough, who wasn’t involved in the study, said in an interview.
“In contrast in this study, a single low-dose treatment of ketamine can have the opposite effects, actually boosting some markers of cognitive functioning, at least in the short-term,” he noted.
Dr. Murrough said one caveat to the study is that it only examined the effect of ketamine on cognition once, 1 day after a single treatment.
“While this is an important initial observation, we don’t yet have any understanding of how persistent this effect on cognition is, or how this observed change may be related to any benefit ketamine may have on depression or suicide risk,” Dr. Murrough said.
“In fact, the researchers found that there was no association between change in cognitive functioning following ketamine and change in depression or suicidal thinking. The patients who showed improved cognitive function following ketamine did not differ in terms of mood or suicide risk compared to patients who did not show an improvement in cognition,” Dr. Murrough noted.
“This raises the important question of what is the relevance of change in cognition to the potential benefits of ketamine. This is an important area and should be the focus of future research in order to improve outcomes for patients with depression and who are at risk for suicide,” he added.
Also weighing in, Roger S. McIntyre, MD, professor of psychiatry and pharmacology and head of the mood disorders psychopharmacology unit, University of Toronto, said the study is “very interesting and in keeping” with some previous work that he and his colleagues have done showing that ketamine “seems to benefit aspects of cognition which is a core element in depression.”
“It’s a testable hypothesis that the improvement in cognition now being reported and replicated could play some role in the improved quality of life and functioning with this treatment and as well reduce reducing suicide,” said Dr. McIntyre.
This study was supported by the National Institute of Mental Health. Dr. Mann receives royalties for commercial use of the Columbia-Suicide Severity Rating Scale, which was not used in this study. Dr. Murrough’s institution was involved in research involving esketamine (Spravato) for treatment-resistant depression and receives financial remuneration from the manufacturer of esketamine. Dr. McIntyre has received research grant support from the Canadian Institutes of Health Research/Global Alliance for Chronic Diseases/Chinese National Natural Research Foundation and speaker/consultation fees from Lundbeck, Janssen, Purdue, Pfizer, Otsuka, Allergan, Takeda, Neurocrine, Sunovion, Eisai, Minerva, Intra-Cellular, and AbbVie. Dr. McIntyre is also CEO of AltMed.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF CLINICAL PSYCHIATRY
Parkinson’s death rate rising, reasons unclear
, according to what investigators say is the most comprehensive study in the nation of temporal trends in Parkinson’s disease mortality.
“The reason behind the rising death rates from Parkinson’s disease is not clear at present and warrants further investigation,” Wei Bao, MD, PhD, associate professor in the department of epidemiology at the University of Iowa College of Public Health, in Iowa City, said in an interview. “We know that people are living longer and the general population is getting older, but that doesn’t fully explain the increase we saw in the death rate in people with Parkinson’s disease,” Dr. Bao added in a statement.
“Understanding why more people are dying from this disease is critical if we are going to reverse the trend,” Dr. Bao said.
The study was published online Oct. 27 in Neurology.
Long-term data
The researchers used data from the National Vital Statistics System to determine national trends in Parkinson’s disease mortality overall and in several key subgroups. The analyses included 479,059 people who died of Parkinson’s disease between 1999 and 2019.
Over the 21-year period, the age-adjusted mortality from Parkinson’s disease rose from 5.4 per 100,000 in 1999 to 8.8 per 100,000 in 2019. The average annual percent change (APC) was 2.4% for the entire period.
During the study period, the number of deaths from Parkinson’s disease more than doubled, from 14,593 to 35,311.
The death rate from Parkinson’s disease increased significantly across all age groups. The average APC was 5.0% among adults younger than 65 years, 1.9% among those aged 65-74 years, 2.2% among those 75-84 years, and 2.7% among those 85 and older.
The death rate increased in both men and women, but age-adjusted Parkinson’s disease mortality was twice as high in men as in women. The researchers say one possible explanation for the sex difference is estrogen, which leads to higher dopamine levels in areas of the brain that control motor responses and may protect women from Parkinson’s disease.
The study also showed that White people are more likely to die from Parkinson’s disease than persons of other racial and ethnic groups. In 2019, the death rate per 100,000 was 9.7 for Whites, 6.5 for Hispanics, and 4.7 for non-Hispanic Blacks.
Previous studies have shown that compared with White people, Black and Hispanic people are less likely to see a neurologist, owing to socioeconomic barriers. This suggests that White people may be more likely to receive a Parkinson’s disease diagnosis, the researchers noted.
“It’s important to continue to evaluate long-term trends in Parkinson’s death rates,” Dr. Bao said.
“This can inform future research that may help pinpoint why more people are dying of the disease. Also, updating vital statistics about Parkinson’s death rates may be used for priority setting and financing of health care and policy,” Dr. Bao added.
1.2 million patients by 2030
Reached for comment, James Beck, PhD, chief scientific officer for the Parkinson’s Foundation, said these findings are not surprising. “They are aligned with the work the Parkinson’s Foundation has done to show that the number of people with Parkinson’s disease has increased over time. We are working on an improved estimate of Parkinson’s disease incidence and predict that Parkinson’s disease will continue to rise as the population ages, so an increase in mortality rates would be expected,” Dr. Beck said.
He noted that much of the public health statistics regarding Parkinson’s disease are outdated and that the Parkinson’s Foundation has been partnering with others to update them.
“For instance, to calculate an accurate estimate of the prevalence of Parkinson’s disease, the Parkinson’s Foundation Prevalence Project was formed. The findings from this group demonstrated that the number of people living with Parkinson’s disease will rise to nearly 1.2 million by 2030, a substantial increase from the estimate of 930,000 for 2020,” Dr. Beck said.
“The overarching message is that more people are being diagnosed with Parkinson’s disease, not that more people are dying from the disease,” he added.
“Over the last 20 years, our understanding of Parkinson’s disease has changed and developed, so clinicians are more aware and better able to properly diagnose Parkinson’s disease. This could mean that the cause is likely due to an increase in diagnosis rates and better recognition of Parkinson’s disease, which would lead to higher rates of identifying Parkinson’s disease as a cause of death,” said Dr. Beck.
The study had no targeted funding. Dr. Bao and Dr. Beck have indicated no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, according to what investigators say is the most comprehensive study in the nation of temporal trends in Parkinson’s disease mortality.
“The reason behind the rising death rates from Parkinson’s disease is not clear at present and warrants further investigation,” Wei Bao, MD, PhD, associate professor in the department of epidemiology at the University of Iowa College of Public Health, in Iowa City, said in an interview. “We know that people are living longer and the general population is getting older, but that doesn’t fully explain the increase we saw in the death rate in people with Parkinson’s disease,” Dr. Bao added in a statement.
“Understanding why more people are dying from this disease is critical if we are going to reverse the trend,” Dr. Bao said.
The study was published online Oct. 27 in Neurology.
Long-term data
The researchers used data from the National Vital Statistics System to determine national trends in Parkinson’s disease mortality overall and in several key subgroups. The analyses included 479,059 people who died of Parkinson’s disease between 1999 and 2019.
Over the 21-year period, the age-adjusted mortality from Parkinson’s disease rose from 5.4 per 100,000 in 1999 to 8.8 per 100,000 in 2019. The average annual percent change (APC) was 2.4% for the entire period.
During the study period, the number of deaths from Parkinson’s disease more than doubled, from 14,593 to 35,311.
The death rate from Parkinson’s disease increased significantly across all age groups. The average APC was 5.0% among adults younger than 65 years, 1.9% among those aged 65-74 years, 2.2% among those 75-84 years, and 2.7% among those 85 and older.
The death rate increased in both men and women, but age-adjusted Parkinson’s disease mortality was twice as high in men as in women. The researchers say one possible explanation for the sex difference is estrogen, which leads to higher dopamine levels in areas of the brain that control motor responses and may protect women from Parkinson’s disease.
The study also showed that White people are more likely to die from Parkinson’s disease than persons of other racial and ethnic groups. In 2019, the death rate per 100,000 was 9.7 for Whites, 6.5 for Hispanics, and 4.7 for non-Hispanic Blacks.
Previous studies have shown that compared with White people, Black and Hispanic people are less likely to see a neurologist, owing to socioeconomic barriers. This suggests that White people may be more likely to receive a Parkinson’s disease diagnosis, the researchers noted.
“It’s important to continue to evaluate long-term trends in Parkinson’s death rates,” Dr. Bao said.
“This can inform future research that may help pinpoint why more people are dying of the disease. Also, updating vital statistics about Parkinson’s death rates may be used for priority setting and financing of health care and policy,” Dr. Bao added.
1.2 million patients by 2030
Reached for comment, James Beck, PhD, chief scientific officer for the Parkinson’s Foundation, said these findings are not surprising. “They are aligned with the work the Parkinson’s Foundation has done to show that the number of people with Parkinson’s disease has increased over time. We are working on an improved estimate of Parkinson’s disease incidence and predict that Parkinson’s disease will continue to rise as the population ages, so an increase in mortality rates would be expected,” Dr. Beck said.
He noted that much of the public health statistics regarding Parkinson’s disease are outdated and that the Parkinson’s Foundation has been partnering with others to update them.
“For instance, to calculate an accurate estimate of the prevalence of Parkinson’s disease, the Parkinson’s Foundation Prevalence Project was formed. The findings from this group demonstrated that the number of people living with Parkinson’s disease will rise to nearly 1.2 million by 2030, a substantial increase from the estimate of 930,000 for 2020,” Dr. Beck said.
“The overarching message is that more people are being diagnosed with Parkinson’s disease, not that more people are dying from the disease,” he added.
“Over the last 20 years, our understanding of Parkinson’s disease has changed and developed, so clinicians are more aware and better able to properly diagnose Parkinson’s disease. This could mean that the cause is likely due to an increase in diagnosis rates and better recognition of Parkinson’s disease, which would lead to higher rates of identifying Parkinson’s disease as a cause of death,” said Dr. Beck.
The study had no targeted funding. Dr. Bao and Dr. Beck have indicated no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, according to what investigators say is the most comprehensive study in the nation of temporal trends in Parkinson’s disease mortality.
“The reason behind the rising death rates from Parkinson’s disease is not clear at present and warrants further investigation,” Wei Bao, MD, PhD, associate professor in the department of epidemiology at the University of Iowa College of Public Health, in Iowa City, said in an interview. “We know that people are living longer and the general population is getting older, but that doesn’t fully explain the increase we saw in the death rate in people with Parkinson’s disease,” Dr. Bao added in a statement.
“Understanding why more people are dying from this disease is critical if we are going to reverse the trend,” Dr. Bao said.
The study was published online Oct. 27 in Neurology.
Long-term data
The researchers used data from the National Vital Statistics System to determine national trends in Parkinson’s disease mortality overall and in several key subgroups. The analyses included 479,059 people who died of Parkinson’s disease between 1999 and 2019.
Over the 21-year period, the age-adjusted mortality from Parkinson’s disease rose from 5.4 per 100,000 in 1999 to 8.8 per 100,000 in 2019. The average annual percent change (APC) was 2.4% for the entire period.
During the study period, the number of deaths from Parkinson’s disease more than doubled, from 14,593 to 35,311.
The death rate from Parkinson’s disease increased significantly across all age groups. The average APC was 5.0% among adults younger than 65 years, 1.9% among those aged 65-74 years, 2.2% among those 75-84 years, and 2.7% among those 85 and older.
The death rate increased in both men and women, but age-adjusted Parkinson’s disease mortality was twice as high in men as in women. The researchers say one possible explanation for the sex difference is estrogen, which leads to higher dopamine levels in areas of the brain that control motor responses and may protect women from Parkinson’s disease.
The study also showed that White people are more likely to die from Parkinson’s disease than persons of other racial and ethnic groups. In 2019, the death rate per 100,000 was 9.7 for Whites, 6.5 for Hispanics, and 4.7 for non-Hispanic Blacks.
Previous studies have shown that compared with White people, Black and Hispanic people are less likely to see a neurologist, owing to socioeconomic barriers. This suggests that White people may be more likely to receive a Parkinson’s disease diagnosis, the researchers noted.
“It’s important to continue to evaluate long-term trends in Parkinson’s death rates,” Dr. Bao said.
“This can inform future research that may help pinpoint why more people are dying of the disease. Also, updating vital statistics about Parkinson’s death rates may be used for priority setting and financing of health care and policy,” Dr. Bao added.
1.2 million patients by 2030
Reached for comment, James Beck, PhD, chief scientific officer for the Parkinson’s Foundation, said these findings are not surprising. “They are aligned with the work the Parkinson’s Foundation has done to show that the number of people with Parkinson’s disease has increased over time. We are working on an improved estimate of Parkinson’s disease incidence and predict that Parkinson’s disease will continue to rise as the population ages, so an increase in mortality rates would be expected,” Dr. Beck said.
He noted that much of the public health statistics regarding Parkinson’s disease are outdated and that the Parkinson’s Foundation has been partnering with others to update them.
“For instance, to calculate an accurate estimate of the prevalence of Parkinson’s disease, the Parkinson’s Foundation Prevalence Project was formed. The findings from this group demonstrated that the number of people living with Parkinson’s disease will rise to nearly 1.2 million by 2030, a substantial increase from the estimate of 930,000 for 2020,” Dr. Beck said.
“The overarching message is that more people are being diagnosed with Parkinson’s disease, not that more people are dying from the disease,” he added.
“Over the last 20 years, our understanding of Parkinson’s disease has changed and developed, so clinicians are more aware and better able to properly diagnose Parkinson’s disease. This could mean that the cause is likely due to an increase in diagnosis rates and better recognition of Parkinson’s disease, which would lead to higher rates of identifying Parkinson’s disease as a cause of death,” said Dr. Beck.
The study had no targeted funding. Dr. Bao and Dr. Beck have indicated no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM NEUROLOGY
Texas interventional cardiologist subject of anticompetitive lawsuit
Doctors Hospital of Laredo, Texas, and the Laredo Physicians Group have filed a lawsuit against interventional cardiologist Ricardo Cigarroa, MD, alleging that he engaged in anticompetitive conduct over the availability of cardiologists in Laredo.
Also named in the lawsuit are Cigarroa Heart and Vascular Institute, Laredo Texas Hospital Company (doing business as Laredo Medical Center) and Laredo Physician Associates (LPA).
According to the complaint, in August 2020, Doctors Hospital and Laredo Physicians Group began actively recruiting cardiologists to the city of Laredo.
The complaint states that, with more than 260,000 residents, the city should have a minimum of 20 cardiologists. However, Laredo currently has only eight cardiologists and only six are interventional cardiologists.
The lawsuit alleges that when Dr. Cigarroa got wind of these recruitment efforts, he entered into a conspiracy with the Cigarroa Institute (a cardiology outpatient clinic) and Laredo Medical Center, the largest acute-care hospital in the city, to engage in “anticompetitive and tortious behavior.
“Their conspiracy had a simple but pernicious goal: deprive Doctors Hospital and Physicians Group of the doctors and employees needed to compete and provide interventional cardiology services to the Laredo market,” the complaint reads.
The alleged conspiracy unfolded in multiple steps, it notes, with Dr. Cigarroa issuing threats to Doctors Hospital, Laredo Physicians Group, and prospective interventional cardiologists being recruited.
Through threats and coercion, multiple qualified interventional cardiologists who were interested in joining Laredo Physicians Group, and to whom the group extended employment offers, decided not to join, the complaint states.
It further claims that Dr. Cigarroa, his son, and his nephew – who represent more than half of the interventional cardiologists in Laredo – informed Doctors Hospital that they would “no longer respond” to emergency calls at Doctors Hospital.
The complaint further alleges that after “scaring off competitors and further cementing their dominant market power and position,” the defendants targeted Arthur Santos, MD, Laredo’s only cardiovascular surgeon who was employed by Laredo Physicians Group.
“Defendants successfully induced Dr. Santos to agree to join Defendant Laredo Physicians Associates (LPA), breaching his enforceable noncompete contractual provision,” the complaint states.
The defendants then allegedly induced the cardiothoracic surgery technicians at Doctors Hospital to join Laredo Medical Center (LMC) and work with Dr. Cigarroa and Dr. Santos, the complaint says.
“The conspiracy to monopolize Laredo’s interventional cardiology market is a win-win-win for Defendants. Dr Cigarroa and the clinic avoid competition for interventional cardiological services, while LMC is left as the only provider of acute cardiology services in Laredo, gaining additional patients and corresponding increased revenue,” the complaint reads.
“Meanwhile, Doctors Hospital’s acute-care cardiology program will be threatened with extinction and, critically, Laredo patients are left with higher health care costs and greater health risks and without competitive market alternatives,” it states.
Dr. Cigarroa responds
According to the Laredo Times, in a statement responding to the anticompetitive conduct lawsuit, Dr. Cigarroa said: “This lawsuit is a dispute between a for-profit corporation and a physician who has demonstrated over 30 years of commitment to his patients and patient care in this community.
“It’s unfortunate that the executives [at] Doctors Hospital have chosen to put profit above the well-being of their patients and employees. Their actions confirm that they care more about their bottom line than they do about our residents and reaffirms how disconnected they are from our community,” Dr. Cigarroa said.
“My top priority continues to be the health of all Laredo residents. I will never stop caring for the patients that I love, and I will continue to help save lives,” Dr. Cigarroa said, according to the Times article.
“I am humbled to have received numerous calls of support from many Doctors Hospital employees. Their words of encouragement are a true testament to the strong relationships I have within the medical community,” Dr. Cigarroa added.
A version of this article first appeared on Medscape.com.
Doctors Hospital of Laredo, Texas, and the Laredo Physicians Group have filed a lawsuit against interventional cardiologist Ricardo Cigarroa, MD, alleging that he engaged in anticompetitive conduct over the availability of cardiologists in Laredo.
Also named in the lawsuit are Cigarroa Heart and Vascular Institute, Laredo Texas Hospital Company (doing business as Laredo Medical Center) and Laredo Physician Associates (LPA).
According to the complaint, in August 2020, Doctors Hospital and Laredo Physicians Group began actively recruiting cardiologists to the city of Laredo.
The complaint states that, with more than 260,000 residents, the city should have a minimum of 20 cardiologists. However, Laredo currently has only eight cardiologists and only six are interventional cardiologists.
The lawsuit alleges that when Dr. Cigarroa got wind of these recruitment efforts, he entered into a conspiracy with the Cigarroa Institute (a cardiology outpatient clinic) and Laredo Medical Center, the largest acute-care hospital in the city, to engage in “anticompetitive and tortious behavior.
“Their conspiracy had a simple but pernicious goal: deprive Doctors Hospital and Physicians Group of the doctors and employees needed to compete and provide interventional cardiology services to the Laredo market,” the complaint reads.
The alleged conspiracy unfolded in multiple steps, it notes, with Dr. Cigarroa issuing threats to Doctors Hospital, Laredo Physicians Group, and prospective interventional cardiologists being recruited.
Through threats and coercion, multiple qualified interventional cardiologists who were interested in joining Laredo Physicians Group, and to whom the group extended employment offers, decided not to join, the complaint states.
It further claims that Dr. Cigarroa, his son, and his nephew – who represent more than half of the interventional cardiologists in Laredo – informed Doctors Hospital that they would “no longer respond” to emergency calls at Doctors Hospital.
The complaint further alleges that after “scaring off competitors and further cementing their dominant market power and position,” the defendants targeted Arthur Santos, MD, Laredo’s only cardiovascular surgeon who was employed by Laredo Physicians Group.
“Defendants successfully induced Dr. Santos to agree to join Defendant Laredo Physicians Associates (LPA), breaching his enforceable noncompete contractual provision,” the complaint states.
The defendants then allegedly induced the cardiothoracic surgery technicians at Doctors Hospital to join Laredo Medical Center (LMC) and work with Dr. Cigarroa and Dr. Santos, the complaint says.
“The conspiracy to monopolize Laredo’s interventional cardiology market is a win-win-win for Defendants. Dr Cigarroa and the clinic avoid competition for interventional cardiological services, while LMC is left as the only provider of acute cardiology services in Laredo, gaining additional patients and corresponding increased revenue,” the complaint reads.
“Meanwhile, Doctors Hospital’s acute-care cardiology program will be threatened with extinction and, critically, Laredo patients are left with higher health care costs and greater health risks and without competitive market alternatives,” it states.
Dr. Cigarroa responds
According to the Laredo Times, in a statement responding to the anticompetitive conduct lawsuit, Dr. Cigarroa said: “This lawsuit is a dispute between a for-profit corporation and a physician who has demonstrated over 30 years of commitment to his patients and patient care in this community.
“It’s unfortunate that the executives [at] Doctors Hospital have chosen to put profit above the well-being of their patients and employees. Their actions confirm that they care more about their bottom line than they do about our residents and reaffirms how disconnected they are from our community,” Dr. Cigarroa said.
“My top priority continues to be the health of all Laredo residents. I will never stop caring for the patients that I love, and I will continue to help save lives,” Dr. Cigarroa said, according to the Times article.
“I am humbled to have received numerous calls of support from many Doctors Hospital employees. Their words of encouragement are a true testament to the strong relationships I have within the medical community,” Dr. Cigarroa added.
A version of this article first appeared on Medscape.com.
Doctors Hospital of Laredo, Texas, and the Laredo Physicians Group have filed a lawsuit against interventional cardiologist Ricardo Cigarroa, MD, alleging that he engaged in anticompetitive conduct over the availability of cardiologists in Laredo.
Also named in the lawsuit are Cigarroa Heart and Vascular Institute, Laredo Texas Hospital Company (doing business as Laredo Medical Center) and Laredo Physician Associates (LPA).
According to the complaint, in August 2020, Doctors Hospital and Laredo Physicians Group began actively recruiting cardiologists to the city of Laredo.
The complaint states that, with more than 260,000 residents, the city should have a minimum of 20 cardiologists. However, Laredo currently has only eight cardiologists and only six are interventional cardiologists.
The lawsuit alleges that when Dr. Cigarroa got wind of these recruitment efforts, he entered into a conspiracy with the Cigarroa Institute (a cardiology outpatient clinic) and Laredo Medical Center, the largest acute-care hospital in the city, to engage in “anticompetitive and tortious behavior.
“Their conspiracy had a simple but pernicious goal: deprive Doctors Hospital and Physicians Group of the doctors and employees needed to compete and provide interventional cardiology services to the Laredo market,” the complaint reads.
The alleged conspiracy unfolded in multiple steps, it notes, with Dr. Cigarroa issuing threats to Doctors Hospital, Laredo Physicians Group, and prospective interventional cardiologists being recruited.
Through threats and coercion, multiple qualified interventional cardiologists who were interested in joining Laredo Physicians Group, and to whom the group extended employment offers, decided not to join, the complaint states.
It further claims that Dr. Cigarroa, his son, and his nephew – who represent more than half of the interventional cardiologists in Laredo – informed Doctors Hospital that they would “no longer respond” to emergency calls at Doctors Hospital.
The complaint further alleges that after “scaring off competitors and further cementing their dominant market power and position,” the defendants targeted Arthur Santos, MD, Laredo’s only cardiovascular surgeon who was employed by Laredo Physicians Group.
“Defendants successfully induced Dr. Santos to agree to join Defendant Laredo Physicians Associates (LPA), breaching his enforceable noncompete contractual provision,” the complaint states.
The defendants then allegedly induced the cardiothoracic surgery technicians at Doctors Hospital to join Laredo Medical Center (LMC) and work with Dr. Cigarroa and Dr. Santos, the complaint says.
“The conspiracy to monopolize Laredo’s interventional cardiology market is a win-win-win for Defendants. Dr Cigarroa and the clinic avoid competition for interventional cardiological services, while LMC is left as the only provider of acute cardiology services in Laredo, gaining additional patients and corresponding increased revenue,” the complaint reads.
“Meanwhile, Doctors Hospital’s acute-care cardiology program will be threatened with extinction and, critically, Laredo patients are left with higher health care costs and greater health risks and without competitive market alternatives,” it states.
Dr. Cigarroa responds
According to the Laredo Times, in a statement responding to the anticompetitive conduct lawsuit, Dr. Cigarroa said: “This lawsuit is a dispute between a for-profit corporation and a physician who has demonstrated over 30 years of commitment to his patients and patient care in this community.
“It’s unfortunate that the executives [at] Doctors Hospital have chosen to put profit above the well-being of their patients and employees. Their actions confirm that they care more about their bottom line than they do about our residents and reaffirms how disconnected they are from our community,” Dr. Cigarroa said.
“My top priority continues to be the health of all Laredo residents. I will never stop caring for the patients that I love, and I will continue to help save lives,” Dr. Cigarroa said, according to the Times article.
“I am humbled to have received numerous calls of support from many Doctors Hospital employees. Their words of encouragement are a true testament to the strong relationships I have within the medical community,” Dr. Cigarroa added.
A version of this article first appeared on Medscape.com.
Brain rhythm predicts response to DBS for severe depression
Brain beta rhythm predicts early and robust response to deep brain stimulation (DBS) for severe depression in new findings that could help optimize and personalize DBS treatment protocols, early research suggests.
In a small study, investigators found brief stimulation at the time of implantation of DBS leads induced a rapid and consistent decrease in beta power measured at the site of stimulation, which correlated with significant and sustained decrease in depressive symptoms.
“Patient by patient, the magnitude of the decrease in the left beta power could predict how well they were doing a week later,” study investigator Helen Mayberg, MD, founding director of the Nash Family Center for Advanced Circuit Therapeutics at Mount Sinai in New York, told this news organization.
The study was published online Nov. 3 in Translational Psychiatry.
Optimal targets identified
Eight adults with treatment-resistant depression underwent intraoperative electrophysiological recording at the time that bilateral DBS leads were implanted in the subcallosal cingulate (SCC).
Using patient-specific tractography models prior to surgery, the investigators identified the optimal target within the SCC for lead placement.
During surgery, 20 minutes of stimulation in the optimal tractography-defined targets was delivered, with no stimulation in the 4 weeks after surgery. Local field potentials (LFPs) – electrical signals between neurons deep in the brain – were simultaneously recorded during intraoperative stimulation.
One week after brief intraoperative stimulation, patient depression scores had declined by 45.6% on the 17-item Hamilton Depression Rating Scale (HDRS-17).
This early antidepressant response correlated with a decrease in the beta power recorded from the left hemisphere SCC. The correlation of symptom improvement with reduction in SCC beta power suggests that this electrophysiological finding is a “biomarker for treatment optimization,” the investigators note.
“This study shows reproducible and consistent changes in a brain readout over the first minutes of optimized stimulation in the operating room in individual patients,” Dr. Mayberg said in a press release.
“Within minutes of stimulation inside the operating room, there was a change in the beta brain rhythm. Patients who showed larger changes then experienced greater relief from their depression in the week after surgery,” added Allison Waters, PhD, a co–first author on the study and electrophysiology core leader at Mount Sinai’s Nash Center.
It appears that the early decline in depressive symptoms is “partially but not completely lost” during a postoperative, one-month washout period, the researchers note.
In addition, it remains unknown whether intraoperative stimulation-induced changes in beta power are predictive of eventual sustained clinical response to chronic therapeutic SCC DBS for treatment-resistant depression.
To this point, however, chronic SCC DBS at the tractography-defined “optimal” locations led to a response rate of 88% (7 of 8) after 6 months of treatment, they report.
One step closer to precision psychiatry
“This line of work is moving the field one step closer to precision psychiatry,” Shaheen E. Lakhan, MD, PhD, a neurologist in Newton, Massachusetts, said in an interview.
“Outside of psychiatry, many diseases have measurable biomarkers that correlate with whether the disease is present or its severity. For example, for diabetes there is hemoglobin A1c, and for multiple sclerosis, brain lesions on MRI are both diagnostic and prognostic. Sadly, within psychiatry, biomarkers are few and far between,” said Dr. Lakhan, who wasn’t involved in this study.
“Over the last decades, an interesting phenomenon occurs with DBS for patients with advanced Parkinson’s – often their depression abates and mood improves. Several lines of studies have tried to tease apart whether this was primarily from alleviating the motor symptoms of Parkinson’s or [if] DBS is directly implicated in mood enhancement. Lo and behold a subset of patients with treatment-resistant depression demonstrate improvement on standardized depression testing,” Dr. Lakhan added.
This study now shows that beta rhythm – a signal deep in the brain that traditional EEG can’t pick up – “predicted who would later benefit from DBS right at the time of implantation,” Dr. Lakhan said.
“(deep beta rhythm) in and outside of brain surgery,” he told this news organization.
“Other therapy trials, for instance, with drugs or non-invasive, digital neuroactivation and modulation (DiNaMo), may use this key biomarker to optimize its development and maximize effect, one day, for a given individual,” Dr. Lakhan predicted.
“The challenge remains that these signals are deep in the brain and currently require surgical implantation of electrodes for recordings. However, technologies such as magnetoencephalography (MEG) that use powerful external magnetics may substitute,” he added.
Funding support was provided by the National Institutes of Health, the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, and the Hope for Depression Research Foundation. Implanted devices used in this research were donated by Medtronic. Dr. Mayberg receives consulting and licensing fees from Abbott Labs. Dr. Lakhan has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Brain beta rhythm predicts early and robust response to deep brain stimulation (DBS) for severe depression in new findings that could help optimize and personalize DBS treatment protocols, early research suggests.
In a small study, investigators found brief stimulation at the time of implantation of DBS leads induced a rapid and consistent decrease in beta power measured at the site of stimulation, which correlated with significant and sustained decrease in depressive symptoms.
“Patient by patient, the magnitude of the decrease in the left beta power could predict how well they were doing a week later,” study investigator Helen Mayberg, MD, founding director of the Nash Family Center for Advanced Circuit Therapeutics at Mount Sinai in New York, told this news organization.
The study was published online Nov. 3 in Translational Psychiatry.
Optimal targets identified
Eight adults with treatment-resistant depression underwent intraoperative electrophysiological recording at the time that bilateral DBS leads were implanted in the subcallosal cingulate (SCC).
Using patient-specific tractography models prior to surgery, the investigators identified the optimal target within the SCC for lead placement.
During surgery, 20 minutes of stimulation in the optimal tractography-defined targets was delivered, with no stimulation in the 4 weeks after surgery. Local field potentials (LFPs) – electrical signals between neurons deep in the brain – were simultaneously recorded during intraoperative stimulation.
One week after brief intraoperative stimulation, patient depression scores had declined by 45.6% on the 17-item Hamilton Depression Rating Scale (HDRS-17).
This early antidepressant response correlated with a decrease in the beta power recorded from the left hemisphere SCC. The correlation of symptom improvement with reduction in SCC beta power suggests that this electrophysiological finding is a “biomarker for treatment optimization,” the investigators note.
“This study shows reproducible and consistent changes in a brain readout over the first minutes of optimized stimulation in the operating room in individual patients,” Dr. Mayberg said in a press release.
“Within minutes of stimulation inside the operating room, there was a change in the beta brain rhythm. Patients who showed larger changes then experienced greater relief from their depression in the week after surgery,” added Allison Waters, PhD, a co–first author on the study and electrophysiology core leader at Mount Sinai’s Nash Center.
It appears that the early decline in depressive symptoms is “partially but not completely lost” during a postoperative, one-month washout period, the researchers note.
In addition, it remains unknown whether intraoperative stimulation-induced changes in beta power are predictive of eventual sustained clinical response to chronic therapeutic SCC DBS for treatment-resistant depression.
To this point, however, chronic SCC DBS at the tractography-defined “optimal” locations led to a response rate of 88% (7 of 8) after 6 months of treatment, they report.
One step closer to precision psychiatry
“This line of work is moving the field one step closer to precision psychiatry,” Shaheen E. Lakhan, MD, PhD, a neurologist in Newton, Massachusetts, said in an interview.
“Outside of psychiatry, many diseases have measurable biomarkers that correlate with whether the disease is present or its severity. For example, for diabetes there is hemoglobin A1c, and for multiple sclerosis, brain lesions on MRI are both diagnostic and prognostic. Sadly, within psychiatry, biomarkers are few and far between,” said Dr. Lakhan, who wasn’t involved in this study.
“Over the last decades, an interesting phenomenon occurs with DBS for patients with advanced Parkinson’s – often their depression abates and mood improves. Several lines of studies have tried to tease apart whether this was primarily from alleviating the motor symptoms of Parkinson’s or [if] DBS is directly implicated in mood enhancement. Lo and behold a subset of patients with treatment-resistant depression demonstrate improvement on standardized depression testing,” Dr. Lakhan added.
This study now shows that beta rhythm – a signal deep in the brain that traditional EEG can’t pick up – “predicted who would later benefit from DBS right at the time of implantation,” Dr. Lakhan said.
“(deep beta rhythm) in and outside of brain surgery,” he told this news organization.
“Other therapy trials, for instance, with drugs or non-invasive, digital neuroactivation and modulation (DiNaMo), may use this key biomarker to optimize its development and maximize effect, one day, for a given individual,” Dr. Lakhan predicted.
“The challenge remains that these signals are deep in the brain and currently require surgical implantation of electrodes for recordings. However, technologies such as magnetoencephalography (MEG) that use powerful external magnetics may substitute,” he added.
Funding support was provided by the National Institutes of Health, the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, and the Hope for Depression Research Foundation. Implanted devices used in this research were donated by Medtronic. Dr. Mayberg receives consulting and licensing fees from Abbott Labs. Dr. Lakhan has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Brain beta rhythm predicts early and robust response to deep brain stimulation (DBS) for severe depression in new findings that could help optimize and personalize DBS treatment protocols, early research suggests.
In a small study, investigators found brief stimulation at the time of implantation of DBS leads induced a rapid and consistent decrease in beta power measured at the site of stimulation, which correlated with significant and sustained decrease in depressive symptoms.
“Patient by patient, the magnitude of the decrease in the left beta power could predict how well they were doing a week later,” study investigator Helen Mayberg, MD, founding director of the Nash Family Center for Advanced Circuit Therapeutics at Mount Sinai in New York, told this news organization.
The study was published online Nov. 3 in Translational Psychiatry.
Optimal targets identified
Eight adults with treatment-resistant depression underwent intraoperative electrophysiological recording at the time that bilateral DBS leads were implanted in the subcallosal cingulate (SCC).
Using patient-specific tractography models prior to surgery, the investigators identified the optimal target within the SCC for lead placement.
During surgery, 20 minutes of stimulation in the optimal tractography-defined targets was delivered, with no stimulation in the 4 weeks after surgery. Local field potentials (LFPs) – electrical signals between neurons deep in the brain – were simultaneously recorded during intraoperative stimulation.
One week after brief intraoperative stimulation, patient depression scores had declined by 45.6% on the 17-item Hamilton Depression Rating Scale (HDRS-17).
This early antidepressant response correlated with a decrease in the beta power recorded from the left hemisphere SCC. The correlation of symptom improvement with reduction in SCC beta power suggests that this electrophysiological finding is a “biomarker for treatment optimization,” the investigators note.
“This study shows reproducible and consistent changes in a brain readout over the first minutes of optimized stimulation in the operating room in individual patients,” Dr. Mayberg said in a press release.
“Within minutes of stimulation inside the operating room, there was a change in the beta brain rhythm. Patients who showed larger changes then experienced greater relief from their depression in the week after surgery,” added Allison Waters, PhD, a co–first author on the study and electrophysiology core leader at Mount Sinai’s Nash Center.
It appears that the early decline in depressive symptoms is “partially but not completely lost” during a postoperative, one-month washout period, the researchers note.
In addition, it remains unknown whether intraoperative stimulation-induced changes in beta power are predictive of eventual sustained clinical response to chronic therapeutic SCC DBS for treatment-resistant depression.
To this point, however, chronic SCC DBS at the tractography-defined “optimal” locations led to a response rate of 88% (7 of 8) after 6 months of treatment, they report.
One step closer to precision psychiatry
“This line of work is moving the field one step closer to precision psychiatry,” Shaheen E. Lakhan, MD, PhD, a neurologist in Newton, Massachusetts, said in an interview.
“Outside of psychiatry, many diseases have measurable biomarkers that correlate with whether the disease is present or its severity. For example, for diabetes there is hemoglobin A1c, and for multiple sclerosis, brain lesions on MRI are both diagnostic and prognostic. Sadly, within psychiatry, biomarkers are few and far between,” said Dr. Lakhan, who wasn’t involved in this study.
“Over the last decades, an interesting phenomenon occurs with DBS for patients with advanced Parkinson’s – often their depression abates and mood improves. Several lines of studies have tried to tease apart whether this was primarily from alleviating the motor symptoms of Parkinson’s or [if] DBS is directly implicated in mood enhancement. Lo and behold a subset of patients with treatment-resistant depression demonstrate improvement on standardized depression testing,” Dr. Lakhan added.
This study now shows that beta rhythm – a signal deep in the brain that traditional EEG can’t pick up – “predicted who would later benefit from DBS right at the time of implantation,” Dr. Lakhan said.
“(deep beta rhythm) in and outside of brain surgery,” he told this news organization.
“Other therapy trials, for instance, with drugs or non-invasive, digital neuroactivation and modulation (DiNaMo), may use this key biomarker to optimize its development and maximize effect, one day, for a given individual,” Dr. Lakhan predicted.
“The challenge remains that these signals are deep in the brain and currently require surgical implantation of electrodes for recordings. However, technologies such as magnetoencephalography (MEG) that use powerful external magnetics may substitute,” he added.
Funding support was provided by the National Institutes of Health, the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, and the Hope for Depression Research Foundation. Implanted devices used in this research were donated by Medtronic. Dr. Mayberg receives consulting and licensing fees from Abbott Labs. Dr. Lakhan has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM TRANSLATIONAL PSYCHIATRY
Small fiber neuropathy is rising in the U.S., but why is a mystery
The exact reason for the increase in isolated SFN “remains unclear,” said Christopher J. Klein, MD, of the Mayo Clinic in Rochester, Minn. However, “we noted during the study period the population has had increased BMI, which appears to be a risk factor for this disorder, with many (50%) developing either glucose impairment or frank diabetes during the study period even if not present at first small fiber neuropathy presentation, also with associated higher triglyceride levels,” he explained.
The study was published online October 27 in Neurology.
Significant upward trend
Investigators reviewed the records of all 94 adults diagnosed with pure SFN (no large fiber involvement) between 1998 and 2017 in Olmsted and adjacent counties in Minnesota – and compared them with 282 adults of similar age and gender who did not have neuropathy.
The incidence of SFN over the entire study period was 1.3 per 100,000 per year and the prevalence was 13.3 per 100,000.
There was a “significant upward trend” in SFN incidence over the study period that could not be attributed to the availability of intraepidermal nerve fiber density testing, the authors reported.
The median age of onset of SFN was 54 years and two-thirds were women (67%).
Diabetes, obesity, and hypertriglyceridemia were significantly more common in patients with SFN compared with matched controls. These metabolic risk factors are also associated with peripheral neuropathy regardless of fiber type.
Autonomic symptoms were common and generally mild, affecting 85% of patients with SFN, and included male erectile dysfunction, constipation, light-headedness and palpitations, urinary symptoms, diarrhea, dry eyes and mouth, sweat abnormalities, and gastroparesis.
Insomnia and use of opioid pain medication were more common in those with SFN than matched controls.
More than one-third (36%) of patients with SFN developed large fiber neuropathy an average of 5.3 years after developing SFN.
During an average follow-up of 6.1 years, adults with SFN were significantly more likely to suffer myocardial infarction (46% vs. 27%; odds ratio, 2.0; 95% CI, 1.8-4.9), congestive heart failure (27% vs. 12%; OR, 2.6; 95% CI, 1.4-4.8), peripheral vascular disease (22% vs. 6%; OR, 4.0; 95% CI, 1.9-8.1), stroke (24% vs. 10%; OR, 2.8; 95% CI, 1.5-5.3), diabetes (51% vs. 22%; OR, 4.6; 95% CI, 2.8-7.6) and rheumatologic disease (30% vs. 7%; OR, 5.3; 95% CI, 2.8-10.4).
For 70% of patients, no cause for SFN could be determined. Diabetes (15%) was the most common cause identified. Other less common causes included Sjögren syndrome, lupus, amyloidosis, and Fabry disease.
“It is important to quantitatively diagnose patients with SFN as many non-neurological musculoskeletal causes can mimic the disorder,” said Dr. Klein.
“If rates of progression are rapid, sinister causes such as out-of-control diabetes, hereditary [transthyretin] TTR amyloidosis, and Fabry disease can be responsible. For other patients, rates of progression are slow and generally do not lead to significant neurologic impairments,” he added.
“However,” he said, “internal medicine follow-up is important for all as this disorder associates with development with higher risk of cardiovascular disease, including commonly heart attacks.”
Of note, although mean age at death was not significantly different in patients with SFN than controls (70 vs. 73 years), there was a significantly higher number of deaths in patients with SFN (n = 18; 19%) than in matched controls (n = 35; 12%) from the time of symptom onset, the researchers reported.
Important research
This “important” study sheds light on the comorbidities and longitudinal consequences of SFN, wrote Brian Callaghan, MD, with the University of Michigan, Ann Arbor, and J. Robinson Singleton, MD, with the University of Utah, Salt Lake City, in an accompanying editorial in Neurology.
The study demonstrates clearly that SFN has “metabolic risk factors similar to those seen for sensory predominant peripheral neuropathies affecting a broader range of fiber types. As a result, therapies that address metabolic risk factors are likely to help prevent or treat both conditions,” they wrote.
Dr. Callaghan and Dr. Singleton added that a key strength of the study is the detailed follow-up that examines SFN progression over time. “The authors found that patients with SFN do not report high disability and that progression tends to be slow. Therefore, patients with SFN can be counseled that progression and disability are likely to be modest in most cases. However, when patients do progress quickly, uncommon etiologies should be sought,” the editorialists wrote.
The study was supported by the Mayo Clinic Foundation, Mayo Clinic Center for Individualized Medicine, and Mayo Clinic Center of MS and Autoimmune Neurology. Dr. Klein has received teaching honorarium from Ackea pharmaceuticals for lectures on hereditary transthyretin amyloidosis and Fabry disease, consulted for Pfizer regarding tafamidis (all compensation for consulting activities is paid directly to Mayo Clinic), and participated in the clinical trials for inotersen and patisiran but received no personal compensation for his participation. Dr. Callaghan consults for DynaMed, performs medical legal consultations, including consultations for the Vaccine Injury Compensation Program, and receives research support from the American Academy of Neurology. Dr. Singleton has consulted for Regenacy.
A version of this article first appeared on Medscape.com.
The exact reason for the increase in isolated SFN “remains unclear,” said Christopher J. Klein, MD, of the Mayo Clinic in Rochester, Minn. However, “we noted during the study period the population has had increased BMI, which appears to be a risk factor for this disorder, with many (50%) developing either glucose impairment or frank diabetes during the study period even if not present at first small fiber neuropathy presentation, also with associated higher triglyceride levels,” he explained.
The study was published online October 27 in Neurology.
Significant upward trend
Investigators reviewed the records of all 94 adults diagnosed with pure SFN (no large fiber involvement) between 1998 and 2017 in Olmsted and adjacent counties in Minnesota – and compared them with 282 adults of similar age and gender who did not have neuropathy.
The incidence of SFN over the entire study period was 1.3 per 100,000 per year and the prevalence was 13.3 per 100,000.
There was a “significant upward trend” in SFN incidence over the study period that could not be attributed to the availability of intraepidermal nerve fiber density testing, the authors reported.
The median age of onset of SFN was 54 years and two-thirds were women (67%).
Diabetes, obesity, and hypertriglyceridemia were significantly more common in patients with SFN compared with matched controls. These metabolic risk factors are also associated with peripheral neuropathy regardless of fiber type.
Autonomic symptoms were common and generally mild, affecting 85% of patients with SFN, and included male erectile dysfunction, constipation, light-headedness and palpitations, urinary symptoms, diarrhea, dry eyes and mouth, sweat abnormalities, and gastroparesis.
Insomnia and use of opioid pain medication were more common in those with SFN than matched controls.
More than one-third (36%) of patients with SFN developed large fiber neuropathy an average of 5.3 years after developing SFN.
During an average follow-up of 6.1 years, adults with SFN were significantly more likely to suffer myocardial infarction (46% vs. 27%; odds ratio, 2.0; 95% CI, 1.8-4.9), congestive heart failure (27% vs. 12%; OR, 2.6; 95% CI, 1.4-4.8), peripheral vascular disease (22% vs. 6%; OR, 4.0; 95% CI, 1.9-8.1), stroke (24% vs. 10%; OR, 2.8; 95% CI, 1.5-5.3), diabetes (51% vs. 22%; OR, 4.6; 95% CI, 2.8-7.6) and rheumatologic disease (30% vs. 7%; OR, 5.3; 95% CI, 2.8-10.4).
For 70% of patients, no cause for SFN could be determined. Diabetes (15%) was the most common cause identified. Other less common causes included Sjögren syndrome, lupus, amyloidosis, and Fabry disease.
“It is important to quantitatively diagnose patients with SFN as many non-neurological musculoskeletal causes can mimic the disorder,” said Dr. Klein.
“If rates of progression are rapid, sinister causes such as out-of-control diabetes, hereditary [transthyretin] TTR amyloidosis, and Fabry disease can be responsible. For other patients, rates of progression are slow and generally do not lead to significant neurologic impairments,” he added.
“However,” he said, “internal medicine follow-up is important for all as this disorder associates with development with higher risk of cardiovascular disease, including commonly heart attacks.”
Of note, although mean age at death was not significantly different in patients with SFN than controls (70 vs. 73 years), there was a significantly higher number of deaths in patients with SFN (n = 18; 19%) than in matched controls (n = 35; 12%) from the time of symptom onset, the researchers reported.
Important research
This “important” study sheds light on the comorbidities and longitudinal consequences of SFN, wrote Brian Callaghan, MD, with the University of Michigan, Ann Arbor, and J. Robinson Singleton, MD, with the University of Utah, Salt Lake City, in an accompanying editorial in Neurology.
The study demonstrates clearly that SFN has “metabolic risk factors similar to those seen for sensory predominant peripheral neuropathies affecting a broader range of fiber types. As a result, therapies that address metabolic risk factors are likely to help prevent or treat both conditions,” they wrote.
Dr. Callaghan and Dr. Singleton added that a key strength of the study is the detailed follow-up that examines SFN progression over time. “The authors found that patients with SFN do not report high disability and that progression tends to be slow. Therefore, patients with SFN can be counseled that progression and disability are likely to be modest in most cases. However, when patients do progress quickly, uncommon etiologies should be sought,” the editorialists wrote.
The study was supported by the Mayo Clinic Foundation, Mayo Clinic Center for Individualized Medicine, and Mayo Clinic Center of MS and Autoimmune Neurology. Dr. Klein has received teaching honorarium from Ackea pharmaceuticals for lectures on hereditary transthyretin amyloidosis and Fabry disease, consulted for Pfizer regarding tafamidis (all compensation for consulting activities is paid directly to Mayo Clinic), and participated in the clinical trials for inotersen and patisiran but received no personal compensation for his participation. Dr. Callaghan consults for DynaMed, performs medical legal consultations, including consultations for the Vaccine Injury Compensation Program, and receives research support from the American Academy of Neurology. Dr. Singleton has consulted for Regenacy.
A version of this article first appeared on Medscape.com.
The exact reason for the increase in isolated SFN “remains unclear,” said Christopher J. Klein, MD, of the Mayo Clinic in Rochester, Minn. However, “we noted during the study period the population has had increased BMI, which appears to be a risk factor for this disorder, with many (50%) developing either glucose impairment or frank diabetes during the study period even if not present at first small fiber neuropathy presentation, also with associated higher triglyceride levels,” he explained.
The study was published online October 27 in Neurology.
Significant upward trend
Investigators reviewed the records of all 94 adults diagnosed with pure SFN (no large fiber involvement) between 1998 and 2017 in Olmsted and adjacent counties in Minnesota – and compared them with 282 adults of similar age and gender who did not have neuropathy.
The incidence of SFN over the entire study period was 1.3 per 100,000 per year and the prevalence was 13.3 per 100,000.
There was a “significant upward trend” in SFN incidence over the study period that could not be attributed to the availability of intraepidermal nerve fiber density testing, the authors reported.
The median age of onset of SFN was 54 years and two-thirds were women (67%).
Diabetes, obesity, and hypertriglyceridemia were significantly more common in patients with SFN compared with matched controls. These metabolic risk factors are also associated with peripheral neuropathy regardless of fiber type.
Autonomic symptoms were common and generally mild, affecting 85% of patients with SFN, and included male erectile dysfunction, constipation, light-headedness and palpitations, urinary symptoms, diarrhea, dry eyes and mouth, sweat abnormalities, and gastroparesis.
Insomnia and use of opioid pain medication were more common in those with SFN than matched controls.
More than one-third (36%) of patients with SFN developed large fiber neuropathy an average of 5.3 years after developing SFN.
During an average follow-up of 6.1 years, adults with SFN were significantly more likely to suffer myocardial infarction (46% vs. 27%; odds ratio, 2.0; 95% CI, 1.8-4.9), congestive heart failure (27% vs. 12%; OR, 2.6; 95% CI, 1.4-4.8), peripheral vascular disease (22% vs. 6%; OR, 4.0; 95% CI, 1.9-8.1), stroke (24% vs. 10%; OR, 2.8; 95% CI, 1.5-5.3), diabetes (51% vs. 22%; OR, 4.6; 95% CI, 2.8-7.6) and rheumatologic disease (30% vs. 7%; OR, 5.3; 95% CI, 2.8-10.4).
For 70% of patients, no cause for SFN could be determined. Diabetes (15%) was the most common cause identified. Other less common causes included Sjögren syndrome, lupus, amyloidosis, and Fabry disease.
“It is important to quantitatively diagnose patients with SFN as many non-neurological musculoskeletal causes can mimic the disorder,” said Dr. Klein.
“If rates of progression are rapid, sinister causes such as out-of-control diabetes, hereditary [transthyretin] TTR amyloidosis, and Fabry disease can be responsible. For other patients, rates of progression are slow and generally do not lead to significant neurologic impairments,” he added.
“However,” he said, “internal medicine follow-up is important for all as this disorder associates with development with higher risk of cardiovascular disease, including commonly heart attacks.”
Of note, although mean age at death was not significantly different in patients with SFN than controls (70 vs. 73 years), there was a significantly higher number of deaths in patients with SFN (n = 18; 19%) than in matched controls (n = 35; 12%) from the time of symptom onset, the researchers reported.
Important research
This “important” study sheds light on the comorbidities and longitudinal consequences of SFN, wrote Brian Callaghan, MD, with the University of Michigan, Ann Arbor, and J. Robinson Singleton, MD, with the University of Utah, Salt Lake City, in an accompanying editorial in Neurology.
The study demonstrates clearly that SFN has “metabolic risk factors similar to those seen for sensory predominant peripheral neuropathies affecting a broader range of fiber types. As a result, therapies that address metabolic risk factors are likely to help prevent or treat both conditions,” they wrote.
Dr. Callaghan and Dr. Singleton added that a key strength of the study is the detailed follow-up that examines SFN progression over time. “The authors found that patients with SFN do not report high disability and that progression tends to be slow. Therefore, patients with SFN can be counseled that progression and disability are likely to be modest in most cases. However, when patients do progress quickly, uncommon etiologies should be sought,” the editorialists wrote.
The study was supported by the Mayo Clinic Foundation, Mayo Clinic Center for Individualized Medicine, and Mayo Clinic Center of MS and Autoimmune Neurology. Dr. Klein has received teaching honorarium from Ackea pharmaceuticals for lectures on hereditary transthyretin amyloidosis and Fabry disease, consulted for Pfizer regarding tafamidis (all compensation for consulting activities is paid directly to Mayo Clinic), and participated in the clinical trials for inotersen and patisiran but received no personal compensation for his participation. Dr. Callaghan consults for DynaMed, performs medical legal consultations, including consultations for the Vaccine Injury Compensation Program, and receives research support from the American Academy of Neurology. Dr. Singleton has consulted for Regenacy.
A version of this article first appeared on Medscape.com.
FROM NEUROLOGY
Latest national suicide data released
including pandemic-related job loss, financial strain, and deteriorating mental health, according to new federal statistics.
The number of annual suicides in the United States increased steadily from 2003 through 2018, followed by a 2% decline between 2018 and 2019. There was concern that deaths due to suicide would increase in 2020, but this doesn’t appear to be the case.
The provisional numbers show 45,855 deaths by suicide in the United States in 2020 – 3% lower than in 2019 (47,511), and 5% below the 2018 peak of 48,344 suicides, report Sally Curtin, MA, and colleagues with the National Center for Health Statistics, part of the U.S. Centers for Disease Control and Prevention.
The data were published online Nov. 3 in the National Vital Statistics System (NVSS) Vital Statistics Rapid Release.
On a monthly basis, the number of suicides was lower in 2020 than in 2019 in March through October and December – with the largest drop happening in April 2020 at a time when deaths from COVID-19 were peaking, the authors note. In April 2020, suicide deaths were 14% lower than in April 2019 (3,468 vs. 4,029).
The provisional age-adjusted suicide rate was 3% lower in 2020 (13.5 per 100,000) than in 2019 (13.9 per 100,000). It was 2% lower among men (21.9 compared with 22.4), and 8% lower for women (5.5 compared with 6.0).
Suicide rates among younger adults aged 10 to 34 years rose slightly between 2019 and 2020 but was only significant in those 25 to 34, with a 5% increase between 2019 and 2020.
Individuals aged 35 to 74 years had significant declines in suicide with the largest drop in those aged 45 to 54 years and 55 to 64 years.
Women in all race and Hispanic-origin groups showed declines in suicide rates between 2019 and 2020, but the decline was significant only among non-Hispanic white women (10%).
Suicide rates declined for non-Hispanic white and non-Hispanic Asian men but increased among non-Hispanic black, non-Hispanic American Indian or Alaska Native, and Hispanic men.
This analysis is based on more than 99% of expected death records. Based on previous patterns between provisional and final data, these provisional findings are expected to be consistent with final 2020 data, the authors say.
The study had no commercial funding. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
including pandemic-related job loss, financial strain, and deteriorating mental health, according to new federal statistics.
The number of annual suicides in the United States increased steadily from 2003 through 2018, followed by a 2% decline between 2018 and 2019. There was concern that deaths due to suicide would increase in 2020, but this doesn’t appear to be the case.
The provisional numbers show 45,855 deaths by suicide in the United States in 2020 – 3% lower than in 2019 (47,511), and 5% below the 2018 peak of 48,344 suicides, report Sally Curtin, MA, and colleagues with the National Center for Health Statistics, part of the U.S. Centers for Disease Control and Prevention.
The data were published online Nov. 3 in the National Vital Statistics System (NVSS) Vital Statistics Rapid Release.
On a monthly basis, the number of suicides was lower in 2020 than in 2019 in March through October and December – with the largest drop happening in April 2020 at a time when deaths from COVID-19 were peaking, the authors note. In April 2020, suicide deaths were 14% lower than in April 2019 (3,468 vs. 4,029).
The provisional age-adjusted suicide rate was 3% lower in 2020 (13.5 per 100,000) than in 2019 (13.9 per 100,000). It was 2% lower among men (21.9 compared with 22.4), and 8% lower for women (5.5 compared with 6.0).
Suicide rates among younger adults aged 10 to 34 years rose slightly between 2019 and 2020 but was only significant in those 25 to 34, with a 5% increase between 2019 and 2020.
Individuals aged 35 to 74 years had significant declines in suicide with the largest drop in those aged 45 to 54 years and 55 to 64 years.
Women in all race and Hispanic-origin groups showed declines in suicide rates between 2019 and 2020, but the decline was significant only among non-Hispanic white women (10%).
Suicide rates declined for non-Hispanic white and non-Hispanic Asian men but increased among non-Hispanic black, non-Hispanic American Indian or Alaska Native, and Hispanic men.
This analysis is based on more than 99% of expected death records. Based on previous patterns between provisional and final data, these provisional findings are expected to be consistent with final 2020 data, the authors say.
The study had no commercial funding. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
including pandemic-related job loss, financial strain, and deteriorating mental health, according to new federal statistics.
The number of annual suicides in the United States increased steadily from 2003 through 2018, followed by a 2% decline between 2018 and 2019. There was concern that deaths due to suicide would increase in 2020, but this doesn’t appear to be the case.
The provisional numbers show 45,855 deaths by suicide in the United States in 2020 – 3% lower than in 2019 (47,511), and 5% below the 2018 peak of 48,344 suicides, report Sally Curtin, MA, and colleagues with the National Center for Health Statistics, part of the U.S. Centers for Disease Control and Prevention.
The data were published online Nov. 3 in the National Vital Statistics System (NVSS) Vital Statistics Rapid Release.
On a monthly basis, the number of suicides was lower in 2020 than in 2019 in March through October and December – with the largest drop happening in April 2020 at a time when deaths from COVID-19 were peaking, the authors note. In April 2020, suicide deaths were 14% lower than in April 2019 (3,468 vs. 4,029).
The provisional age-adjusted suicide rate was 3% lower in 2020 (13.5 per 100,000) than in 2019 (13.9 per 100,000). It was 2% lower among men (21.9 compared with 22.4), and 8% lower for women (5.5 compared with 6.0).
Suicide rates among younger adults aged 10 to 34 years rose slightly between 2019 and 2020 but was only significant in those 25 to 34, with a 5% increase between 2019 and 2020.
Individuals aged 35 to 74 years had significant declines in suicide with the largest drop in those aged 45 to 54 years and 55 to 64 years.
Women in all race and Hispanic-origin groups showed declines in suicide rates between 2019 and 2020, but the decline was significant only among non-Hispanic white women (10%).
Suicide rates declined for non-Hispanic white and non-Hispanic Asian men but increased among non-Hispanic black, non-Hispanic American Indian or Alaska Native, and Hispanic men.
This analysis is based on more than 99% of expected death records. Based on previous patterns between provisional and final data, these provisional findings are expected to be consistent with final 2020 data, the authors say.
The study had no commercial funding. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FDA class I recall of CardioSave hybrid/rescue IABPs
Datascope/Getinge/Maquet is recalling CardioSave Hybrid and Rescue intra-aortic balloon pumps (IABPs) because some battery packs may have a shortened run time and fail unexpectedly, according to a medical device recall notice posted on the U.S. Food and Drug Administration website.
The FDA has identified this as a class I recall, the most serious type of recall, because of the risk for serious injury or death.
The recalled IABPs have substandard batteries that do not meet performance specifications and were mistakenly released to a limited number of customers.
If a patient requires life-supporting therapy with an IABP and the device does not work or stops working during use because of battery failure, the patient will be at risk for serious injury, including death, the FDA cautions.
Both IABP monitors display battery life and have low battery alarms when alternative power sources are needed.
Datascope/Getting/Maquet has received six complaints but no reports of injury or death related to this issue.
“However, there is a potential for underreporting since the end user reporting a failed battery or short battery run time cannot be aware that they originally received a substandard battery,” the FDA said.
The recall involves 137 battery packs distributed in the United States between Sept. 23, 2017, and Aug. 17, 2021. Product codes and lot numbers are available in the recall notice.
The company sent an urgent medical device removal letter to customers requesting that they check inventory to determine if there are any CardioSave LiIon battery packs with part number/reference number 0146-00-0097 and with serial numbers listed in the letter.
Customers are asked to replace any affected battery with an unaffected battery and remove the affected product from areas of use.
The company will issue credit or a replacement battery at no cost to the facility upon receipt of the response form attached to the letter.
Distributors who shipped any affected product to customers are asked to forward the device removal letter to customers.
All customers, regardless of whether or not they have defective batteries, are asked to complete and sign the response form to acknowledge that they received the notification and disposed of the affected batteries.
Completed forms can be scanned and emailed to Datascope/Getinge/Maquet at Li-Ionbattery.Datascope@getinge.com or by FAX to 1-877-446-3360.
Customers who have questions about this recall should contact their Datascope/Getinge/Maquet sales representative or, for technical questions, customer service (1-888-943-8872, option 2), Monday through Friday, 8:00 a.m. to 6:00 p.m. ET.
Any adverse events or suspected adverse events related to the recalled CardioSave Hybrid/Rescue IABPs should be reported to the FDA through MedWatch, its adverse event reporting program.
A version of this article first appeared on Medscape.com.
Datascope/Getinge/Maquet is recalling CardioSave Hybrid and Rescue intra-aortic balloon pumps (IABPs) because some battery packs may have a shortened run time and fail unexpectedly, according to a medical device recall notice posted on the U.S. Food and Drug Administration website.
The FDA has identified this as a class I recall, the most serious type of recall, because of the risk for serious injury or death.
The recalled IABPs have substandard batteries that do not meet performance specifications and were mistakenly released to a limited number of customers.
If a patient requires life-supporting therapy with an IABP and the device does not work or stops working during use because of battery failure, the patient will be at risk for serious injury, including death, the FDA cautions.
Both IABP monitors display battery life and have low battery alarms when alternative power sources are needed.
Datascope/Getting/Maquet has received six complaints but no reports of injury or death related to this issue.
“However, there is a potential for underreporting since the end user reporting a failed battery or short battery run time cannot be aware that they originally received a substandard battery,” the FDA said.
The recall involves 137 battery packs distributed in the United States between Sept. 23, 2017, and Aug. 17, 2021. Product codes and lot numbers are available in the recall notice.
The company sent an urgent medical device removal letter to customers requesting that they check inventory to determine if there are any CardioSave LiIon battery packs with part number/reference number 0146-00-0097 and with serial numbers listed in the letter.
Customers are asked to replace any affected battery with an unaffected battery and remove the affected product from areas of use.
The company will issue credit or a replacement battery at no cost to the facility upon receipt of the response form attached to the letter.
Distributors who shipped any affected product to customers are asked to forward the device removal letter to customers.
All customers, regardless of whether or not they have defective batteries, are asked to complete and sign the response form to acknowledge that they received the notification and disposed of the affected batteries.
Completed forms can be scanned and emailed to Datascope/Getinge/Maquet at Li-Ionbattery.Datascope@getinge.com or by FAX to 1-877-446-3360.
Customers who have questions about this recall should contact their Datascope/Getinge/Maquet sales representative or, for technical questions, customer service (1-888-943-8872, option 2), Monday through Friday, 8:00 a.m. to 6:00 p.m. ET.
Any adverse events or suspected adverse events related to the recalled CardioSave Hybrid/Rescue IABPs should be reported to the FDA through MedWatch, its adverse event reporting program.
A version of this article first appeared on Medscape.com.
Datascope/Getinge/Maquet is recalling CardioSave Hybrid and Rescue intra-aortic balloon pumps (IABPs) because some battery packs may have a shortened run time and fail unexpectedly, according to a medical device recall notice posted on the U.S. Food and Drug Administration website.
The FDA has identified this as a class I recall, the most serious type of recall, because of the risk for serious injury or death.
The recalled IABPs have substandard batteries that do not meet performance specifications and were mistakenly released to a limited number of customers.
If a patient requires life-supporting therapy with an IABP and the device does not work or stops working during use because of battery failure, the patient will be at risk for serious injury, including death, the FDA cautions.
Both IABP monitors display battery life and have low battery alarms when alternative power sources are needed.
Datascope/Getting/Maquet has received six complaints but no reports of injury or death related to this issue.
“However, there is a potential for underreporting since the end user reporting a failed battery or short battery run time cannot be aware that they originally received a substandard battery,” the FDA said.
The recall involves 137 battery packs distributed in the United States between Sept. 23, 2017, and Aug. 17, 2021. Product codes and lot numbers are available in the recall notice.
The company sent an urgent medical device removal letter to customers requesting that they check inventory to determine if there are any CardioSave LiIon battery packs with part number/reference number 0146-00-0097 and with serial numbers listed in the letter.
Customers are asked to replace any affected battery with an unaffected battery and remove the affected product from areas of use.
The company will issue credit or a replacement battery at no cost to the facility upon receipt of the response form attached to the letter.
Distributors who shipped any affected product to customers are asked to forward the device removal letter to customers.
All customers, regardless of whether or not they have defective batteries, are asked to complete and sign the response form to acknowledge that they received the notification and disposed of the affected batteries.
Completed forms can be scanned and emailed to Datascope/Getinge/Maquet at Li-Ionbattery.Datascope@getinge.com or by FAX to 1-877-446-3360.
Customers who have questions about this recall should contact their Datascope/Getinge/Maquet sales representative or, for technical questions, customer service (1-888-943-8872, option 2), Monday through Friday, 8:00 a.m. to 6:00 p.m. ET.
Any adverse events or suspected adverse events related to the recalled CardioSave Hybrid/Rescue IABPs should be reported to the FDA through MedWatch, its adverse event reporting program.
A version of this article first appeared on Medscape.com.
Open notes: Big benefits, few harms in psychiatry, experts say
There are multiple benefits and few harms from sharing clinical notes in patients with mental illness, results of a poll of international experts show.
As of April 5, 2021, new federal rules in the United States mandate that all patients are offered online access to their electronic health record.
“Given that sharing notes in psychiatry is likely to be more complicated than in some other specialties, we were unsure whether experts would consider the practice more harmful than beneficial,” Charlotte Blease, PhD, of Beth Israel Deaconess Medical Center in Boston, told this news organization.
“However, the results of our poll suggest clinicians’ anxieties about sharing mental health notes with patients may be misplaced. We found clear consensus among experts that the benefits of online access to clinical notes could outweigh the risks,” Dr. Blease said in a news release.
The study was published online in PLOS ONE.
Empowering patients
Investigators used an online Delphi poll, an established methodology used to investigate emerging health care policy – including in psychiatry – to solicit the views of an international panel of experts on the mental health effects of sharing clinical notes.
The panel included clinicians, chief medical information officers, patient advocates, and informatics experts with extensive experience and research knowledge about patient access to mental health notes.
There was consensus among the panel that offering online access to mental health notes could enhance patients’ understanding about their diagnosis, care plan, and rationale for treatments.
There was also consensus that access to clinical notes could enhance patient recall about what was communicated and improve mental health patients’ sense of control over their health care.
The panel also agreed that blocking mental health notes could lead to greater harms including increased feelings of stigmatization.
Confirmatory findings
The poll results support an earlier study by Dr. Blease and colleagues that evaluated the experiences of patients in accessing their online clinical notes.
Among these patients with major depressive disorder, schizophrenia, schizoaffective disorder, or bipolar-related disorder, “access helped to clarify why medications had been prescribed, improved understanding about side effects, and 20% of patients reported doing a better job taking their meds as prescribed,” said Dr. Blease.
However, the expert panel in the Delphi poll predicted that with “open notes” some patients might demand changes to their clinical notes, and that mental health clinicians might be less detailed/accurate in documenting negative aspects of the patient relationship, details about patients’ personalities, or symptoms of paranoia in patients.
“If some patients feel more judged or offended by what they read, this may undermine the therapeutic relationship. ,” she added.
“In some clinical cases where there is more focus on emergency care than in forming a therapeutic relationship, for example emergency department visits, we know almost nothing about the risks and benefits associated with OpenNotes,” senior author John Torous, MD, with Beth Israel Deaconess Medical Center and Harvard Medical School, said in an interview.
“One thing is clear,” Dr. Blease said. “Patient access to their online medical records is now mainstream, and we need more clinician education on how to write notes that patients will read, and more guidance among patients on the benefits and risks of accessing their notes.”
Support for this research was provided by a J. F. Keane Scholar Award and a Swedish Research Council on Health, Working Life, and Welfare grant. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
There are multiple benefits and few harms from sharing clinical notes in patients with mental illness, results of a poll of international experts show.
As of April 5, 2021, new federal rules in the United States mandate that all patients are offered online access to their electronic health record.
“Given that sharing notes in psychiatry is likely to be more complicated than in some other specialties, we were unsure whether experts would consider the practice more harmful than beneficial,” Charlotte Blease, PhD, of Beth Israel Deaconess Medical Center in Boston, told this news organization.
“However, the results of our poll suggest clinicians’ anxieties about sharing mental health notes with patients may be misplaced. We found clear consensus among experts that the benefits of online access to clinical notes could outweigh the risks,” Dr. Blease said in a news release.
The study was published online in PLOS ONE.
Empowering patients
Investigators used an online Delphi poll, an established methodology used to investigate emerging health care policy – including in psychiatry – to solicit the views of an international panel of experts on the mental health effects of sharing clinical notes.
The panel included clinicians, chief medical information officers, patient advocates, and informatics experts with extensive experience and research knowledge about patient access to mental health notes.
There was consensus among the panel that offering online access to mental health notes could enhance patients’ understanding about their diagnosis, care plan, and rationale for treatments.
There was also consensus that access to clinical notes could enhance patient recall about what was communicated and improve mental health patients’ sense of control over their health care.
The panel also agreed that blocking mental health notes could lead to greater harms including increased feelings of stigmatization.
Confirmatory findings
The poll results support an earlier study by Dr. Blease and colleagues that evaluated the experiences of patients in accessing their online clinical notes.
Among these patients with major depressive disorder, schizophrenia, schizoaffective disorder, or bipolar-related disorder, “access helped to clarify why medications had been prescribed, improved understanding about side effects, and 20% of patients reported doing a better job taking their meds as prescribed,” said Dr. Blease.
However, the expert panel in the Delphi poll predicted that with “open notes” some patients might demand changes to their clinical notes, and that mental health clinicians might be less detailed/accurate in documenting negative aspects of the patient relationship, details about patients’ personalities, or symptoms of paranoia in patients.
“If some patients feel more judged or offended by what they read, this may undermine the therapeutic relationship. ,” she added.
“In some clinical cases where there is more focus on emergency care than in forming a therapeutic relationship, for example emergency department visits, we know almost nothing about the risks and benefits associated with OpenNotes,” senior author John Torous, MD, with Beth Israel Deaconess Medical Center and Harvard Medical School, said in an interview.
“One thing is clear,” Dr. Blease said. “Patient access to their online medical records is now mainstream, and we need more clinician education on how to write notes that patients will read, and more guidance among patients on the benefits and risks of accessing their notes.”
Support for this research was provided by a J. F. Keane Scholar Award and a Swedish Research Council on Health, Working Life, and Welfare grant. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
There are multiple benefits and few harms from sharing clinical notes in patients with mental illness, results of a poll of international experts show.
As of April 5, 2021, new federal rules in the United States mandate that all patients are offered online access to their electronic health record.
“Given that sharing notes in psychiatry is likely to be more complicated than in some other specialties, we were unsure whether experts would consider the practice more harmful than beneficial,” Charlotte Blease, PhD, of Beth Israel Deaconess Medical Center in Boston, told this news organization.
“However, the results of our poll suggest clinicians’ anxieties about sharing mental health notes with patients may be misplaced. We found clear consensus among experts that the benefits of online access to clinical notes could outweigh the risks,” Dr. Blease said in a news release.
The study was published online in PLOS ONE.
Empowering patients
Investigators used an online Delphi poll, an established methodology used to investigate emerging health care policy – including in psychiatry – to solicit the views of an international panel of experts on the mental health effects of sharing clinical notes.
The panel included clinicians, chief medical information officers, patient advocates, and informatics experts with extensive experience and research knowledge about patient access to mental health notes.
There was consensus among the panel that offering online access to mental health notes could enhance patients’ understanding about their diagnosis, care plan, and rationale for treatments.
There was also consensus that access to clinical notes could enhance patient recall about what was communicated and improve mental health patients’ sense of control over their health care.
The panel also agreed that blocking mental health notes could lead to greater harms including increased feelings of stigmatization.
Confirmatory findings
The poll results support an earlier study by Dr. Blease and colleagues that evaluated the experiences of patients in accessing their online clinical notes.
Among these patients with major depressive disorder, schizophrenia, schizoaffective disorder, or bipolar-related disorder, “access helped to clarify why medications had been prescribed, improved understanding about side effects, and 20% of patients reported doing a better job taking their meds as prescribed,” said Dr. Blease.
However, the expert panel in the Delphi poll predicted that with “open notes” some patients might demand changes to their clinical notes, and that mental health clinicians might be less detailed/accurate in documenting negative aspects of the patient relationship, details about patients’ personalities, or symptoms of paranoia in patients.
“If some patients feel more judged or offended by what they read, this may undermine the therapeutic relationship. ,” she added.
“In some clinical cases where there is more focus on emergency care than in forming a therapeutic relationship, for example emergency department visits, we know almost nothing about the risks and benefits associated with OpenNotes,” senior author John Torous, MD, with Beth Israel Deaconess Medical Center and Harvard Medical School, said in an interview.
“One thing is clear,” Dr. Blease said. “Patient access to their online medical records is now mainstream, and we need more clinician education on how to write notes that patients will read, and more guidance among patients on the benefits and risks of accessing their notes.”
Support for this research was provided by a J. F. Keane Scholar Award and a Swedish Research Council on Health, Working Life, and Welfare grant. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.