Neurology Reviews

Insomnia in childhood persists into adulthood and may raise the risk for internalizing disorders in young adults, new research indicates. However, insomnia symptoms in childhood that remit in the transition to adolescence do not confer increased risk of mood or anxiety disorders later on, the study found.

“As insomnia symptoms may precipitate or maintain internalizing disorders, our findings further reinforce the need for early sleep interventions to prevent future mental health disorders,” said lead investigator Julio Fernandez-Mendoza, PhD, associate professor at Penn State University, Hershey.

He presented his research at Virtual SLEEP 2021, the 35th annual meeting of the Associated Professional Sleep Societies.
 

Results ‘very clear’

The findings are based on data from the Penn State Child Cohort, a longitudinal, population-based sample of 700 children with a median age of 9 years, including 421 who were followed up 8 years later as adolescents (median age, 16 years) and 502 who were followed up 15 years later as young adults (median age, 24 years).

The data are “very clear that the risk of having internalizing disorders in young adulthood associated with having persistent insomnia symptoms, since childhood through adolescence into young adulthood,” Dr. Fernandez-Mendoza said in his presentation.

A persistent developmental trajectory was associated with a threefold increased risk of adult internalizing disorder (hazard ratio, 3.19).

The risk of having an internalizing disorder in young adulthood associated with newly developing (incident) insomnia symptoms is about twofold higher (HR, 1.94), whereas the risk associated with the waxing and waning pattern of insomnia is 1.5-fold (HR, 1.53) higher and only marginally significant, he reported.

An equally important finding, said Dr. Fernandez-Mendoza, is that those who had remitted insomnia symptoms in the transition to adolescence and throughout young adulthood were not at increased risk of having an internalizing disorder in young adulthood.

“Insomnia symptoms in a persistent manner associated with long-term adverse mental health outcomes, but remission of those insomnia symptoms associated with a good prognosis,” he said.

It’s also important to note, he said, that about 40% of children do not outgrow their insomnia symptoms in the transition to adolescence and are at risk of developing mental health disorders later on during early adulthood.

Reached for comment, Nitun Verma, MD, a spokesperson for the American Academy of Sleep Medicine, said: “There is a connection with mood and anxiety disorders with sleep, especially insomnia. This is a good reminder that reviewing someone’s sleep habits should always be a part of assessing someone’s mental health.”

A version of this article first appeared on Medscape.com.

Insomnia in childhood persists into adulthood and may raise the risk for internalizing disorders in young adults, new research indicates. However, insomnia symptoms in childhood that remit in the transition to adolescence do not confer increased risk of mood or anxiety disorders later on, the study found.

“As insomnia symptoms may precipitate or maintain internalizing disorders, our findings further reinforce the need for early sleep interventions to prevent future mental health disorders,” said lead investigator Julio Fernandez-Mendoza, PhD, associate professor at Penn State University, Hershey.

He presented his research at Virtual SLEEP 2021, the 35th annual meeting of the Associated Professional Sleep Societies.
 

Results ‘very clear’

The findings are based on data from the Penn State Child Cohort, a longitudinal, population-based sample of 700 children with a median age of 9 years, including 421 who were followed up 8 years later as adolescents (median age, 16 years) and 502 who were followed up 15 years later as young adults (median age, 24 years).

The data are “very clear that the risk of having internalizing disorders in young adulthood associated with having persistent insomnia symptoms, since childhood through adolescence into young adulthood,” Dr. Fernandez-Mendoza said in his presentation.

A persistent developmental trajectory was associated with a threefold increased risk of adult internalizing disorder (hazard ratio, 3.19).

The risk of having an internalizing disorder in young adulthood associated with newly developing (incident) insomnia symptoms is about twofold higher (HR, 1.94), whereas the risk associated with the waxing and waning pattern of insomnia is 1.5-fold (HR, 1.53) higher and only marginally significant, he reported.

An equally important finding, said Dr. Fernandez-Mendoza, is that those who had remitted insomnia symptoms in the transition to adolescence and throughout young adulthood were not at increased risk of having an internalizing disorder in young adulthood.

“Insomnia symptoms in a persistent manner associated with long-term adverse mental health outcomes, but remission of those insomnia symptoms associated with a good prognosis,” he said.

It’s also important to note, he said, that about 40% of children do not outgrow their insomnia symptoms in the transition to adolescence and are at risk of developing mental health disorders later on during early adulthood.

Reached for comment, Nitun Verma, MD, a spokesperson for the American Academy of Sleep Medicine, said: “There is a connection with mood and anxiety disorders with sleep, especially insomnia. This is a good reminder that reviewing someone’s sleep habits should always be a part of assessing someone’s mental health.”

A version of this article first appeared on Medscape.com.

Insomnia in childhood persists into adulthood and may raise the risk for internalizing disorders in young adults, new research indicates. However, insomnia symptoms in childhood that remit in the transition to adolescence do not confer increased risk of mood or anxiety disorders later on, the study found.

“As insomnia symptoms may precipitate or maintain internalizing disorders, our findings further reinforce the need for early sleep interventions to prevent future mental health disorders,” said lead investigator Julio Fernandez-Mendoza, PhD, associate professor at Penn State University, Hershey.

He presented his research at Virtual SLEEP 2021, the 35th annual meeting of the Associated Professional Sleep Societies.
 

Results ‘very clear’

The findings are based on data from the Penn State Child Cohort, a longitudinal, population-based sample of 700 children with a median age of 9 years, including 421 who were followed up 8 years later as adolescents (median age, 16 years) and 502 who were followed up 15 years later as young adults (median age, 24 years).

The data are “very clear that the risk of having internalizing disorders in young adulthood associated with having persistent insomnia symptoms, since childhood through adolescence into young adulthood,” Dr. Fernandez-Mendoza said in his presentation.

A persistent developmental trajectory was associated with a threefold increased risk of adult internalizing disorder (hazard ratio, 3.19).

The risk of having an internalizing disorder in young adulthood associated with newly developing (incident) insomnia symptoms is about twofold higher (HR, 1.94), whereas the risk associated with the waxing and waning pattern of insomnia is 1.5-fold (HR, 1.53) higher and only marginally significant, he reported.

An equally important finding, said Dr. Fernandez-Mendoza, is that those who had remitted insomnia symptoms in the transition to adolescence and throughout young adulthood were not at increased risk of having an internalizing disorder in young adulthood.

“Insomnia symptoms in a persistent manner associated with long-term adverse mental health outcomes, but remission of those insomnia symptoms associated with a good prognosis,” he said.

It’s also important to note, he said, that about 40% of children do not outgrow their insomnia symptoms in the transition to adolescence and are at risk of developing mental health disorders later on during early adulthood.

Reached for comment, Nitun Verma, MD, a spokesperson for the American Academy of Sleep Medicine, said: “There is a connection with mood and anxiety disorders with sleep, especially insomnia. This is a good reminder that reviewing someone’s sleep habits should always be a part of assessing someone’s mental health.”

A version of this article first appeared on Medscape.com.

An in vitro study that used mouse endothelial cells to simulate the blood-brain barrier (BBB) suggests that specific proteins may be involved in destabilization of the protective barrier during a cortical spreading depression (CSD) event.

CSD has been linked to migraine aura, but a connection to pain symptoms is uncertain. “There’s just a lack of knowledge. We don’t understand migraine pathophysiology,” said Michael G. Harrington, MBChB, who was asked to comment on the study.

“The evidence for altered transport across the barrier in cortical spreading depression and the associated aura of migraine is pretty strong. The evidence for regular migraine, not so. In fact, there’s really no strong evidence for leakage in those people, and so it is still unresolved whether this initial cortical spreading depression that occurs in aura then triggers migraine afterwards, because it’s occurring during the aura. And in people who do not have the aura, is there a silent cortical spreading depression phenomenon with some leakage that triggers the migraine? That question is definitely not answered,” said Dr. Harrington, a research professor of neurology at the University of Southern California, Los Angeles.

Leakage of the BBB might allow passage of nociceptive compounds that could trigger migraine. Loss of BBB integrity has also been seen in other central nervous system pain disorders, suggesting that alterations to BBB functioning could have broader implications.

“In this model that we’re using, we’re seeing loss of overall barrier integrity, which lends itself to a whole cascade of further pathological possibilities,” Jared Wahl, a PhD candidate at the University of Arizona, Tucson, said in an interview. He presented the research at the American Headache Society’s 2021 annual meeting.

A leaky BBB could allow infiltration of a range of substances, but the potential for such a mechanism in migraine pathology is not well understood.

The researchers specifically investigated the potential role of claudin-5 in the tight junction (TJ) region of the BBB. The decision was made in part because the proteins involved in the BBB are difficult to study, and there is some familiarity with claudin-5, according to Mr. Wahl. ”Of all the proteins that are out there, for claudin-5 (there are) somewhat better techniques and products available to work with, and there’s been some previous research done to show that it’s implicated in blood brain barrier pathology. So it seemed like a good candidate to start with investigating this whole possible pathophysiological link between barrier disruption and migration of pronociceptive substances into the CNS during migraine attacks,” he said. The claudin proteins are also the major components of the tight junctions that seal off gaps between endothelial cells along the BBB.
 

Dynamic changes seen in the in vitro model

To simulate a CSD event, the researchers pulsed cultured cells for 5 minutes with astrocyte-conditioned media, artificial cerebrospinal fluid, KCl, glutamate, altered pH, or adenosine triphosphate (ATP). They used trans endothelial electrical resistance (TEER) to quickly and qualitatively screen for loss of barrier integrity, which is characterized by loss of electrical resistance. To quantify the magnitude of a breach, the researchers applied carbon-14 (C14)–labeled sucrose to one side of the barrier, and determined the amount of labeled sucrose transmitted to the other side of the barrier.

ATP and pH pulses that were outside normal physiological limits led to permeability. The team then used immunocytochemistry assays to visualize the condition of the model BBB, and found discontinuity of the tight junction membranes. Imaging of claudin-5 showed organizational changes within the tight junction, but there was no change in expression level, suggesting that the alterations were due to dynamic reorganization, according to Mr. Wahl.

Transient openings could allow passage of molecules such as bradykinin, calcitonin gene-related peptide (CGRP), and substance P, which could go on to affect the trigeminal nerve complex and trigger a migraine. “That’s sort of the crux of a lot of this migraine research, is gluing this physiological (mechanism) to how it is actually activating the CNS. And this is sort of where we’re going with it at the moment,” said Mr. Wahl.
 

Next steps

The researchers next plan to generate a cell line with claudin-5 linked to green fluorescent protein, then use confocal microscopy to image claudin-5 in real time as the BBB model responds to a simulated CSD.

Another important step will be to link physiological findings like those presented by Mr. Wahl to migraine-specific mechanisms. The results from this model will need to be expanded to include more than endothelial cells, especially astrocytes, pericytes, and neurons, as well as organoids, brain slices, or in vivo animal models, according to Dr. Harrington. “I think you could try and block the changes in occludin [another protein in the tight junction] or claudin-5 to see if, under the same provocation, that prevented the changes in a migraine model. That would be a direct way of connecting from CSD to migraine,” said Dr. Harrington.

If BBB disruption is confirmed to play an important role in migraine, and claudin-5 or other specific proteins are confirmed to be the cause, it could have clinical implications. A drug that could prevent those changes in the proteins and prevent a leak in the BBB could be a migraine preventative. “That could help prevent things like nociceptive substances migrating into the CNS, and could possibly be a well-tolerated drug target that doesn’t have the side effects or the overuse problems that a lot of stuff on the market has today,” said Mr. Wahl.

An in vitro study that used mouse endothelial cells to simulate the blood-brain barrier (BBB) suggests that specific proteins may be involved in destabilization of the protective barrier during a cortical spreading depression (CSD) event.

CSD has been linked to migraine aura, but a connection to pain symptoms is uncertain. “There’s just a lack of knowledge. We don’t understand migraine pathophysiology,” said Michael G. Harrington, MBChB, who was asked to comment on the study.

“The evidence for altered transport across the barrier in cortical spreading depression and the associated aura of migraine is pretty strong. The evidence for regular migraine, not so. In fact, there’s really no strong evidence for leakage in those people, and so it is still unresolved whether this initial cortical spreading depression that occurs in aura then triggers migraine afterwards, because it’s occurring during the aura. And in people who do not have the aura, is there a silent cortical spreading depression phenomenon with some leakage that triggers the migraine? That question is definitely not answered,” said Dr. Harrington, a research professor of neurology at the University of Southern California, Los Angeles.

Leakage of the BBB might allow passage of nociceptive compounds that could trigger migraine. Loss of BBB integrity has also been seen in other central nervous system pain disorders, suggesting that alterations to BBB functioning could have broader implications.

“In this model that we’re using, we’re seeing loss of overall barrier integrity, which lends itself to a whole cascade of further pathological possibilities,” Jared Wahl, a PhD candidate at the University of Arizona, Tucson, said in an interview. He presented the research at the American Headache Society’s 2021 annual meeting.

A leaky BBB could allow infiltration of a range of substances, but the potential for such a mechanism in migraine pathology is not well understood.

The researchers specifically investigated the potential role of claudin-5 in the tight junction (TJ) region of the BBB. The decision was made in part because the proteins involved in the BBB are difficult to study, and there is some familiarity with claudin-5, according to Mr. Wahl. ”Of all the proteins that are out there, for claudin-5 (there are) somewhat better techniques and products available to work with, and there’s been some previous research done to show that it’s implicated in blood brain barrier pathology. So it seemed like a good candidate to start with investigating this whole possible pathophysiological link between barrier disruption and migration of pronociceptive substances into the CNS during migraine attacks,” he said. The claudin proteins are also the major components of the tight junctions that seal off gaps between endothelial cells along the BBB.
 

Dynamic changes seen in the in vitro model

To simulate a CSD event, the researchers pulsed cultured cells for 5 minutes with astrocyte-conditioned media, artificial cerebrospinal fluid, KCl, glutamate, altered pH, or adenosine triphosphate (ATP). They used trans endothelial electrical resistance (TEER) to quickly and qualitatively screen for loss of barrier integrity, which is characterized by loss of electrical resistance. To quantify the magnitude of a breach, the researchers applied carbon-14 (C14)–labeled sucrose to one side of the barrier, and determined the amount of labeled sucrose transmitted to the other side of the barrier.

ATP and pH pulses that were outside normal physiological limits led to permeability. The team then used immunocytochemistry assays to visualize the condition of the model BBB, and found discontinuity of the tight junction membranes. Imaging of claudin-5 showed organizational changes within the tight junction, but there was no change in expression level, suggesting that the alterations were due to dynamic reorganization, according to Mr. Wahl.

Transient openings could allow passage of molecules such as bradykinin, calcitonin gene-related peptide (CGRP), and substance P, which could go on to affect the trigeminal nerve complex and trigger a migraine. “That’s sort of the crux of a lot of this migraine research, is gluing this physiological (mechanism) to how it is actually activating the CNS. And this is sort of where we’re going with it at the moment,” said Mr. Wahl.
 

Next steps

The researchers next plan to generate a cell line with claudin-5 linked to green fluorescent protein, then use confocal microscopy to image claudin-5 in real time as the BBB model responds to a simulated CSD.

Another important step will be to link physiological findings like those presented by Mr. Wahl to migraine-specific mechanisms. The results from this model will need to be expanded to include more than endothelial cells, especially astrocytes, pericytes, and neurons, as well as organoids, brain slices, or in vivo animal models, according to Dr. Harrington. “I think you could try and block the changes in occludin [another protein in the tight junction] or claudin-5 to see if, under the same provocation, that prevented the changes in a migraine model. That would be a direct way of connecting from CSD to migraine,” said Dr. Harrington.

If BBB disruption is confirmed to play an important role in migraine, and claudin-5 or other specific proteins are confirmed to be the cause, it could have clinical implications. A drug that could prevent those changes in the proteins and prevent a leak in the BBB could be a migraine preventative. “That could help prevent things like nociceptive substances migrating into the CNS, and could possibly be a well-tolerated drug target that doesn’t have the side effects or the overuse problems that a lot of stuff on the market has today,” said Mr. Wahl.

An in vitro study that used mouse endothelial cells to simulate the blood-brain barrier (BBB) suggests that specific proteins may be involved in destabilization of the protective barrier during a cortical spreading depression (CSD) event.

CSD has been linked to migraine aura, but a connection to pain symptoms is uncertain. “There’s just a lack of knowledge. We don’t understand migraine pathophysiology,” said Michael G. Harrington, MBChB, who was asked to comment on the study.

“The evidence for altered transport across the barrier in cortical spreading depression and the associated aura of migraine is pretty strong. The evidence for regular migraine, not so. In fact, there’s really no strong evidence for leakage in those people, and so it is still unresolved whether this initial cortical spreading depression that occurs in aura then triggers migraine afterwards, because it’s occurring during the aura. And in people who do not have the aura, is there a silent cortical spreading depression phenomenon with some leakage that triggers the migraine? That question is definitely not answered,” said Dr. Harrington, a research professor of neurology at the University of Southern California, Los Angeles.

Leakage of the BBB might allow passage of nociceptive compounds that could trigger migraine. Loss of BBB integrity has also been seen in other central nervous system pain disorders, suggesting that alterations to BBB functioning could have broader implications.

“In this model that we’re using, we’re seeing loss of overall barrier integrity, which lends itself to a whole cascade of further pathological possibilities,” Jared Wahl, a PhD candidate at the University of Arizona, Tucson, said in an interview. He presented the research at the American Headache Society’s 2021 annual meeting.

A leaky BBB could allow infiltration of a range of substances, but the potential for such a mechanism in migraine pathology is not well understood.

The researchers specifically investigated the potential role of claudin-5 in the tight junction (TJ) region of the BBB. The decision was made in part because the proteins involved in the BBB are difficult to study, and there is some familiarity with claudin-5, according to Mr. Wahl. ”Of all the proteins that are out there, for claudin-5 (there are) somewhat better techniques and products available to work with, and there’s been some previous research done to show that it’s implicated in blood brain barrier pathology. So it seemed like a good candidate to start with investigating this whole possible pathophysiological link between barrier disruption and migration of pronociceptive substances into the CNS during migraine attacks,” he said. The claudin proteins are also the major components of the tight junctions that seal off gaps between endothelial cells along the BBB.
 

Dynamic changes seen in the in vitro model

To simulate a CSD event, the researchers pulsed cultured cells for 5 minutes with astrocyte-conditioned media, artificial cerebrospinal fluid, KCl, glutamate, altered pH, or adenosine triphosphate (ATP). They used trans endothelial electrical resistance (TEER) to quickly and qualitatively screen for loss of barrier integrity, which is characterized by loss of electrical resistance. To quantify the magnitude of a breach, the researchers applied carbon-14 (C14)–labeled sucrose to one side of the barrier, and determined the amount of labeled sucrose transmitted to the other side of the barrier.

ATP and pH pulses that were outside normal physiological limits led to permeability. The team then used immunocytochemistry assays to visualize the condition of the model BBB, and found discontinuity of the tight junction membranes. Imaging of claudin-5 showed organizational changes within the tight junction, but there was no change in expression level, suggesting that the alterations were due to dynamic reorganization, according to Mr. Wahl.

Transient openings could allow passage of molecules such as bradykinin, calcitonin gene-related peptide (CGRP), and substance P, which could go on to affect the trigeminal nerve complex and trigger a migraine. “That’s sort of the crux of a lot of this migraine research, is gluing this physiological (mechanism) to how it is actually activating the CNS. And this is sort of where we’re going with it at the moment,” said Mr. Wahl.
 

Next steps

The researchers next plan to generate a cell line with claudin-5 linked to green fluorescent protein, then use confocal microscopy to image claudin-5 in real time as the BBB model responds to a simulated CSD.

Another important step will be to link physiological findings like those presented by Mr. Wahl to migraine-specific mechanisms. The results from this model will need to be expanded to include more than endothelial cells, especially astrocytes, pericytes, and neurons, as well as organoids, brain slices, or in vivo animal models, according to Dr. Harrington. “I think you could try and block the changes in occludin [another protein in the tight junction] or claudin-5 to see if, under the same provocation, that prevented the changes in a migraine model. That would be a direct way of connecting from CSD to migraine,” said Dr. Harrington.

If BBB disruption is confirmed to play an important role in migraine, and claudin-5 or other specific proteins are confirmed to be the cause, it could have clinical implications. A drug that could prevent those changes in the proteins and prevent a leak in the BBB could be a migraine preventative. “That could help prevent things like nociceptive substances migrating into the CNS, and could possibly be a well-tolerated drug target that doesn’t have the side effects or the overuse problems that a lot of stuff on the market has today,” said Mr. Wahl.

The migraine medication erenumab appears to pose no increased risk of hypertension, easing earlier concerns that this may be one of the drug’s adverse events, an analysis of postmarketing data shows. Nevertheless, investigators noted that more research is needed to confirm that this is the case.

While randomized clinical trials have shown no increased risk of hypertension related to the drug, it has been reported in postmarketing data. However, many of these events occurred in patients with previously documented hypertension or risk factors for the disorder, the investigators noted.

The rate of hypertension adverse events in postmarketing data was 0.144 per 100 person-years. Most such reports described only one instance of elevated blood pressure. In April 2020, the prescribing information for the drug was updated to include a mention of the risk of hypertension.

“Given the limitations of postmarketing reports, including incomplete information, lack of a control arm, and others, additional data are certainly needed to fully characterize the nature, the timing, and the extent to which hypertension is a risk associated with erenumab, and indeed other [calcitonin-gene-related peptide (CGRP)] pathway antagonists,” said study investigator David W. Dodick, MD, professor of neurology at the Mayo Clinic College of Medicine, Phoenix.

The findings were presented at the American Headache Society’s 2021 annual meeting.
 

No increased risk over time

A monoclonal antibody and CGRP antagonist, erenumab is approved in the United States for migraine prevention in adults. CGRP medications are vasodilators, and, therefore, migraine treatments that target this pathway could theoretically have hypertensive effects.

To assess the risk of hypertension in migraine patients treated with erenumab, investigators examined clinical trial and postmarketing data. The analysis included cases with limited information and patients with a different etiology for the development of hypertension.

Using Amgen Clinical Trial data, the researchers performed a pooled safety analysis of four placebo-controlled, double-blind phase 2 or 3 studies of the drug. Participants had episodic or chronic migraine and were between ages 18 and 60 years or age 65 years. The doses studied were 70 mg and 140 mg.

In these studies, blood pressure data for each patient were based on an average of at least two measurements taken after patients were in rested state for at least 5 minutes. The position used for blood pressure measurement for each patient was consistent throughout the study.

The investigators also analyzed postmarketing reports of hypertension from May 17, 2018, to Jan. 31, 2020, identified in Amgen Global Safety data.

The pooled studies included 1,043 participants receiving placebo, 893 receiving 70 mg of erenumab, and 507 receiving 140 mg of the drug. During the treatment phase, the incidence of hypertension was 0.9% among controls, 0.8% in the 70-mg group, and 0.2% in the 140-mg group. The proportion of patients who started a new antihypertensive medication was 1.2% in controls, 0.8% in the 70-mg group, and 0.2% in the 140-mg group.

In a long-term, open-label study, patients with episodic migraine received erenumab treatment for up to 5 years. The incidence of hypertension did not increase with time in this population.

The postmarketing data encompassed 245,682 person-years of erenumab exposure. The researchers identified 362 hypertension events (355 cases). The rate of these events was 0.144 per 100 person-years. The exposure-adjusted incidence of hypertension was 1.9 per 100 patient-years for erenumab.

Of the 362 hypertensive events, 158 (43.6%) were in patients with a medical history of hypertension or risk factors for hypertension. Information about the time to onset of hypertension was available for 121 (33.4%) adverse events.

Of this group, 56 (46.2%) occurred within 1 week of erenumab initiation, including 43 (35.5%) that occurred within 1 day. This rapid time to hypertension onset “is inconsistent with the pharmacokinetic profile of once-monthly erenumab 70 mg or 140 mg, which has a peak serum concentration in approximately 6 days,” said Dr. Dodick.
 

Hypertension ‘not a barrier’ to treatment

Commenting on the findings, Richard B. Lipton, MD, Edwin S. Lowe professor and vice chair of neurology at Albert Einstein College of Medicine, New York, noted that in theory blocking CGRP could increase blood pressure. However, he noted that the data and clinical experience do not suggest erenumab poses a serious risk.

“I have rarely seen new-onset hypertension with erenumab in the patients treated at our medical center. The few cases I have seen were in older adults with pre-existing hypertension,” he said.

The investigators’ review of clinical trial data together with global safety databases was a strength of their study, said Dr. Lipton. In clinical trials, patients are monitored carefully, and a placebo control group aids in the determination of background rates.

“In the trials, the incidence of new-onset hypertension or hypertension exacerbation was 0.9%, while the placebo rate was 0.2%,” said Dr. Lipton. “The absolute increase in the risk of hypertension was 0.6% or six cases per thousand: A low rate.” But clinical trials enroll carefully selected patients who do not represent the broad group of people treated with erenumab in clinical practice, he added.

The global safety data are more representative of patients who receive erenumab in real-world settings. The weaknesses of these data, though, are the lack of a control group and the incomplete ascertainment of data associated with spontaneous reporting.

Yet both types of studies, with their complementary strengths and weaknesses, indicated low rates of hypertension.

“The low incidence of hypertension, in my view, is not a barrier to the use of erenumab, though checking blood pressure after starting any new migraine therapy is prudent,” Dr. Lipton concluded.

The study was funded by Amgen. Dr. Dodick had no relevant disclosures. Dr. Lipton has consulted for and conducted studies funded by Amgen and by other companies that manufacture CGRP drugs. He has stock options in Biohaven.

A version of this article first appeared on Medscape.com.

The migraine medication erenumab appears to pose no increased risk of hypertension, easing earlier concerns that this may be one of the drug’s adverse events, an analysis of postmarketing data shows. Nevertheless, investigators noted that more research is needed to confirm that this is the case.

While randomized clinical trials have shown no increased risk of hypertension related to the drug, it has been reported in postmarketing data. However, many of these events occurred in patients with previously documented hypertension or risk factors for the disorder, the investigators noted.

The rate of hypertension adverse events in postmarketing data was 0.144 per 100 person-years. Most such reports described only one instance of elevated blood pressure. In April 2020, the prescribing information for the drug was updated to include a mention of the risk of hypertension.

“Given the limitations of postmarketing reports, including incomplete information, lack of a control arm, and others, additional data are certainly needed to fully characterize the nature, the timing, and the extent to which hypertension is a risk associated with erenumab, and indeed other [calcitonin-gene-related peptide (CGRP)] pathway antagonists,” said study investigator David W. Dodick, MD, professor of neurology at the Mayo Clinic College of Medicine, Phoenix.

The findings were presented at the American Headache Society’s 2021 annual meeting.
 

No increased risk over time

A monoclonal antibody and CGRP antagonist, erenumab is approved in the United States for migraine prevention in adults. CGRP medications are vasodilators, and, therefore, migraine treatments that target this pathway could theoretically have hypertensive effects.

To assess the risk of hypertension in migraine patients treated with erenumab, investigators examined clinical trial and postmarketing data. The analysis included cases with limited information and patients with a different etiology for the development of hypertension.

Using Amgen Clinical Trial data, the researchers performed a pooled safety analysis of four placebo-controlled, double-blind phase 2 or 3 studies of the drug. Participants had episodic or chronic migraine and were between ages 18 and 60 years or age 65 years. The doses studied were 70 mg and 140 mg.

In these studies, blood pressure data for each patient were based on an average of at least two measurements taken after patients were in rested state for at least 5 minutes. The position used for blood pressure measurement for each patient was consistent throughout the study.

The investigators also analyzed postmarketing reports of hypertension from May 17, 2018, to Jan. 31, 2020, identified in Amgen Global Safety data.

The pooled studies included 1,043 participants receiving placebo, 893 receiving 70 mg of erenumab, and 507 receiving 140 mg of the drug. During the treatment phase, the incidence of hypertension was 0.9% among controls, 0.8% in the 70-mg group, and 0.2% in the 140-mg group. The proportion of patients who started a new antihypertensive medication was 1.2% in controls, 0.8% in the 70-mg group, and 0.2% in the 140-mg group.

In a long-term, open-label study, patients with episodic migraine received erenumab treatment for up to 5 years. The incidence of hypertension did not increase with time in this population.

The postmarketing data encompassed 245,682 person-years of erenumab exposure. The researchers identified 362 hypertension events (355 cases). The rate of these events was 0.144 per 100 person-years. The exposure-adjusted incidence of hypertension was 1.9 per 100 patient-years for erenumab.

Of the 362 hypertensive events, 158 (43.6%) were in patients with a medical history of hypertension or risk factors for hypertension. Information about the time to onset of hypertension was available for 121 (33.4%) adverse events.

Of this group, 56 (46.2%) occurred within 1 week of erenumab initiation, including 43 (35.5%) that occurred within 1 day. This rapid time to hypertension onset “is inconsistent with the pharmacokinetic profile of once-monthly erenumab 70 mg or 140 mg, which has a peak serum concentration in approximately 6 days,” said Dr. Dodick.
 

Hypertension ‘not a barrier’ to treatment

Commenting on the findings, Richard B. Lipton, MD, Edwin S. Lowe professor and vice chair of neurology at Albert Einstein College of Medicine, New York, noted that in theory blocking CGRP could increase blood pressure. However, he noted that the data and clinical experience do not suggest erenumab poses a serious risk.

“I have rarely seen new-onset hypertension with erenumab in the patients treated at our medical center. The few cases I have seen were in older adults with pre-existing hypertension,” he said.

The investigators’ review of clinical trial data together with global safety databases was a strength of their study, said Dr. Lipton. In clinical trials, patients are monitored carefully, and a placebo control group aids in the determination of background rates.

“In the trials, the incidence of new-onset hypertension or hypertension exacerbation was 0.9%, while the placebo rate was 0.2%,” said Dr. Lipton. “The absolute increase in the risk of hypertension was 0.6% or six cases per thousand: A low rate.” But clinical trials enroll carefully selected patients who do not represent the broad group of people treated with erenumab in clinical practice, he added.

The global safety data are more representative of patients who receive erenumab in real-world settings. The weaknesses of these data, though, are the lack of a control group and the incomplete ascertainment of data associated with spontaneous reporting.

Yet both types of studies, with their complementary strengths and weaknesses, indicated low rates of hypertension.

“The low incidence of hypertension, in my view, is not a barrier to the use of erenumab, though checking blood pressure after starting any new migraine therapy is prudent,” Dr. Lipton concluded.

The study was funded by Amgen. Dr. Dodick had no relevant disclosures. Dr. Lipton has consulted for and conducted studies funded by Amgen and by other companies that manufacture CGRP drugs. He has stock options in Biohaven.

A version of this article first appeared on Medscape.com.

The migraine medication erenumab appears to pose no increased risk of hypertension, easing earlier concerns that this may be one of the drug’s adverse events, an analysis of postmarketing data shows. Nevertheless, investigators noted that more research is needed to confirm that this is the case.

While randomized clinical trials have shown no increased risk of hypertension related to the drug, it has been reported in postmarketing data. However, many of these events occurred in patients with previously documented hypertension or risk factors for the disorder, the investigators noted.

The rate of hypertension adverse events in postmarketing data was 0.144 per 100 person-years. Most such reports described only one instance of elevated blood pressure. In April 2020, the prescribing information for the drug was updated to include a mention of the risk of hypertension.

“Given the limitations of postmarketing reports, including incomplete information, lack of a control arm, and others, additional data are certainly needed to fully characterize the nature, the timing, and the extent to which hypertension is a risk associated with erenumab, and indeed other [calcitonin-gene-related peptide (CGRP)] pathway antagonists,” said study investigator David W. Dodick, MD, professor of neurology at the Mayo Clinic College of Medicine, Phoenix.

The findings were presented at the American Headache Society’s 2021 annual meeting.
 

No increased risk over time

A monoclonal antibody and CGRP antagonist, erenumab is approved in the United States for migraine prevention in adults. CGRP medications are vasodilators, and, therefore, migraine treatments that target this pathway could theoretically have hypertensive effects.

To assess the risk of hypertension in migraine patients treated with erenumab, investigators examined clinical trial and postmarketing data. The analysis included cases with limited information and patients with a different etiology for the development of hypertension.

Using Amgen Clinical Trial data, the researchers performed a pooled safety analysis of four placebo-controlled, double-blind phase 2 or 3 studies of the drug. Participants had episodic or chronic migraine and were between ages 18 and 60 years or age 65 years. The doses studied were 70 mg and 140 mg.

In these studies, blood pressure data for each patient were based on an average of at least two measurements taken after patients were in rested state for at least 5 minutes. The position used for blood pressure measurement for each patient was consistent throughout the study.

The investigators also analyzed postmarketing reports of hypertension from May 17, 2018, to Jan. 31, 2020, identified in Amgen Global Safety data.

The pooled studies included 1,043 participants receiving placebo, 893 receiving 70 mg of erenumab, and 507 receiving 140 mg of the drug. During the treatment phase, the incidence of hypertension was 0.9% among controls, 0.8% in the 70-mg group, and 0.2% in the 140-mg group. The proportion of patients who started a new antihypertensive medication was 1.2% in controls, 0.8% in the 70-mg group, and 0.2% in the 140-mg group.

In a long-term, open-label study, patients with episodic migraine received erenumab treatment for up to 5 years. The incidence of hypertension did not increase with time in this population.

The postmarketing data encompassed 245,682 person-years of erenumab exposure. The researchers identified 362 hypertension events (355 cases). The rate of these events was 0.144 per 100 person-years. The exposure-adjusted incidence of hypertension was 1.9 per 100 patient-years for erenumab.

Of the 362 hypertensive events, 158 (43.6%) were in patients with a medical history of hypertension or risk factors for hypertension. Information about the time to onset of hypertension was available for 121 (33.4%) adverse events.

Of this group, 56 (46.2%) occurred within 1 week of erenumab initiation, including 43 (35.5%) that occurred within 1 day. This rapid time to hypertension onset “is inconsistent with the pharmacokinetic profile of once-monthly erenumab 70 mg or 140 mg, which has a peak serum concentration in approximately 6 days,” said Dr. Dodick.
 

Hypertension ‘not a barrier’ to treatment

Commenting on the findings, Richard B. Lipton, MD, Edwin S. Lowe professor and vice chair of neurology at Albert Einstein College of Medicine, New York, noted that in theory blocking CGRP could increase blood pressure. However, he noted that the data and clinical experience do not suggest erenumab poses a serious risk.

“I have rarely seen new-onset hypertension with erenumab in the patients treated at our medical center. The few cases I have seen were in older adults with pre-existing hypertension,” he said.

The investigators’ review of clinical trial data together with global safety databases was a strength of their study, said Dr. Lipton. In clinical trials, patients are monitored carefully, and a placebo control group aids in the determination of background rates.

“In the trials, the incidence of new-onset hypertension or hypertension exacerbation was 0.9%, while the placebo rate was 0.2%,” said Dr. Lipton. “The absolute increase in the risk of hypertension was 0.6% or six cases per thousand: A low rate.” But clinical trials enroll carefully selected patients who do not represent the broad group of people treated with erenumab in clinical practice, he added.

The global safety data are more representative of patients who receive erenumab in real-world settings. The weaknesses of these data, though, are the lack of a control group and the incomplete ascertainment of data associated with spontaneous reporting.

Yet both types of studies, with their complementary strengths and weaknesses, indicated low rates of hypertension.

“The low incidence of hypertension, in my view, is not a barrier to the use of erenumab, though checking blood pressure after starting any new migraine therapy is prudent,” Dr. Lipton concluded.

The study was funded by Amgen. Dr. Dodick had no relevant disclosures. Dr. Lipton has consulted for and conducted studies funded by Amgen and by other companies that manufacture CGRP drugs. He has stock options in Biohaven.

A version of this article first appeared on Medscape.com.

Managing depression and anxiety in Parkinson’s disease should start with a review of medications and involve multidisciplinary care, according to a recent summary of evidence.

“Depression and anxiety have a complex relationship with the disease and while the exact mechanism for this association is unknown, both disturbances occur with increased prevalence across the disease course and when present earlier in life, increase the risk of PD by about twofold,” wrote Gregory M. Pontone, MD, of Johns Hopkins University, Baltimore, and colleagues.

Randomized trials to guide treatment of anxiety and depression in patients with Parkinson’s disease (PD) are limited, the researchers noted. However, data from a longitudinal study showed that PD patients whose depression remitted spontaneously or responded to treatment were able to attain a level of function similar to that of never-depressed PD patients, Dr. Pontone and colleagues said.

The researchers offered a pair of treatment algorithms to help guide clinicians in managing depression and anxiety in PD. However, a caveat to keep in mind is that “the benefit of antidepressant medications, used for depression or anxiety, can be confounded when motor symptoms are not optimally treated,” the researchers emphasized.

For depression, the researchers advised starting with some lab work; “at a minimum we suggest checking a complete blood count, metabolic panel, TSH, B12, and folate,” they noted. They recommended an antidepressant, cognitive-behavioral therapy, or both, as a first-line treatment, such as monotherapy with selective norepinephrine reuptake inhibitors or selective serotonin reuptake inhibitors. They advised titrating the chosen monotherapy to a minimum effective dose over a 2- to 3-week period to assess response.

“We recommend continuing antidepressant therapy for at least 1 year based on literature in non-PD populations and anecdotal clinical experience. At 1 year, if not in remission, consider continuing treatment or augmenting to improve response,” the researchers said.

Based on the current DSM-5 criteria, up to one-third of PD patients have an unspecified anxiety disorder, the researchers said, and they recommended using anxiety rating scales to diagnose anxiety in PD. “Given the high prevalence of atypical anxiety syndromes in PD and their potential association with both motor and nonmotor symptoms of the disease, working with the neurologist to achieve optimal control of PD is an essential first step to alleviating anxiety,” they emphasized.

The researchers also advised addressing comorbidities, including cardiovascular disease, chronic pain, diabetes, gastrointestinal issues, hyperthyroidism, and lung disease, all of which can be associated with anxiety. Once comorbidities are addressed, they advised caution given the lack of evidence for efficacy of both pharmacologic and nonpharmacologic anxiety treatments for PD patients. However, first-tier treatment for anxiety could include monotherapy with serotonin-norepinephrine reuptake inhibitors or selective serotonin reuptake inhibitors, they said.

PD patients with depression and anxiety also may benefit from nonpharmacologic interventions, including exercise, mindfulness, relaxation therapy, and cognitive behavioral therapy the researchers said.

Although the algorithm may not differ significantly from current treatment protocols, it highlights aspects unique to PD patients, the researchers said. In particular, the algorithm shows “that interventions used for motor symptoms, for example, dopamine agonists, may be especially potent for mood in the PD population and that augmentation strategies, such as antipsychotics and lithium, may not be well tolerated given their outsized risk of adverse events in PD,” they said.

“While an article of this kind cannot hope to address the gap in knowledge on comparative efficacy between interventions, it can guide readers on the best strategies for implementation and risk mitigation in PD – essentially focusing more on effectiveness,” they concluded.

The study received no outside funding. Dr. Pontone disclosed serving as a consultant for Acadia Pharmaceuticals and Concert Pharmaceuticals.

Managing depression and anxiety in Parkinson’s disease should start with a review of medications and involve multidisciplinary care, according to a recent summary of evidence.

“Depression and anxiety have a complex relationship with the disease and while the exact mechanism for this association is unknown, both disturbances occur with increased prevalence across the disease course and when present earlier in life, increase the risk of PD by about twofold,” wrote Gregory M. Pontone, MD, of Johns Hopkins University, Baltimore, and colleagues.

Randomized trials to guide treatment of anxiety and depression in patients with Parkinson’s disease (PD) are limited, the researchers noted. However, data from a longitudinal study showed that PD patients whose depression remitted spontaneously or responded to treatment were able to attain a level of function similar to that of never-depressed PD patients, Dr. Pontone and colleagues said.

The researchers offered a pair of treatment algorithms to help guide clinicians in managing depression and anxiety in PD. However, a caveat to keep in mind is that “the benefit of antidepressant medications, used for depression or anxiety, can be confounded when motor symptoms are not optimally treated,” the researchers emphasized.

For depression, the researchers advised starting with some lab work; “at a minimum we suggest checking a complete blood count, metabolic panel, TSH, B12, and folate,” they noted. They recommended an antidepressant, cognitive-behavioral therapy, or both, as a first-line treatment, such as monotherapy with selective norepinephrine reuptake inhibitors or selective serotonin reuptake inhibitors. They advised titrating the chosen monotherapy to a minimum effective dose over a 2- to 3-week period to assess response.

“We recommend continuing antidepressant therapy for at least 1 year based on literature in non-PD populations and anecdotal clinical experience. At 1 year, if not in remission, consider continuing treatment or augmenting to improve response,” the researchers said.

Based on the current DSM-5 criteria, up to one-third of PD patients have an unspecified anxiety disorder, the researchers said, and they recommended using anxiety rating scales to diagnose anxiety in PD. “Given the high prevalence of atypical anxiety syndromes in PD and their potential association with both motor and nonmotor symptoms of the disease, working with the neurologist to achieve optimal control of PD is an essential first step to alleviating anxiety,” they emphasized.

The researchers also advised addressing comorbidities, including cardiovascular disease, chronic pain, diabetes, gastrointestinal issues, hyperthyroidism, and lung disease, all of which can be associated with anxiety. Once comorbidities are addressed, they advised caution given the lack of evidence for efficacy of both pharmacologic and nonpharmacologic anxiety treatments for PD patients. However, first-tier treatment for anxiety could include monotherapy with serotonin-norepinephrine reuptake inhibitors or selective serotonin reuptake inhibitors, they said.

PD patients with depression and anxiety also may benefit from nonpharmacologic interventions, including exercise, mindfulness, relaxation therapy, and cognitive behavioral therapy the researchers said.

Although the algorithm may not differ significantly from current treatment protocols, it highlights aspects unique to PD patients, the researchers said. In particular, the algorithm shows “that interventions used for motor symptoms, for example, dopamine agonists, may be especially potent for mood in the PD population and that augmentation strategies, such as antipsychotics and lithium, may not be well tolerated given their outsized risk of adverse events in PD,” they said.

“While an article of this kind cannot hope to address the gap in knowledge on comparative efficacy between interventions, it can guide readers on the best strategies for implementation and risk mitigation in PD – essentially focusing more on effectiveness,” they concluded.

The study received no outside funding. Dr. Pontone disclosed serving as a consultant for Acadia Pharmaceuticals and Concert Pharmaceuticals.

Managing depression and anxiety in Parkinson’s disease should start with a review of medications and involve multidisciplinary care, according to a recent summary of evidence.

“Depression and anxiety have a complex relationship with the disease and while the exact mechanism for this association is unknown, both disturbances occur with increased prevalence across the disease course and when present earlier in life, increase the risk of PD by about twofold,” wrote Gregory M. Pontone, MD, of Johns Hopkins University, Baltimore, and colleagues.

Randomized trials to guide treatment of anxiety and depression in patients with Parkinson’s disease (PD) are limited, the researchers noted. However, data from a longitudinal study showed that PD patients whose depression remitted spontaneously or responded to treatment were able to attain a level of function similar to that of never-depressed PD patients, Dr. Pontone and colleagues said.

The researchers offered a pair of treatment algorithms to help guide clinicians in managing depression and anxiety in PD. However, a caveat to keep in mind is that “the benefit of antidepressant medications, used for depression or anxiety, can be confounded when motor symptoms are not optimally treated,” the researchers emphasized.

For depression, the researchers advised starting with some lab work; “at a minimum we suggest checking a complete blood count, metabolic panel, TSH, B12, and folate,” they noted. They recommended an antidepressant, cognitive-behavioral therapy, or both, as a first-line treatment, such as monotherapy with selective norepinephrine reuptake inhibitors or selective serotonin reuptake inhibitors. They advised titrating the chosen monotherapy to a minimum effective dose over a 2- to 3-week period to assess response.

“We recommend continuing antidepressant therapy for at least 1 year based on literature in non-PD populations and anecdotal clinical experience. At 1 year, if not in remission, consider continuing treatment or augmenting to improve response,” the researchers said.

Based on the current DSM-5 criteria, up to one-third of PD patients have an unspecified anxiety disorder, the researchers said, and they recommended using anxiety rating scales to diagnose anxiety in PD. “Given the high prevalence of atypical anxiety syndromes in PD and their potential association with both motor and nonmotor symptoms of the disease, working with the neurologist to achieve optimal control of PD is an essential first step to alleviating anxiety,” they emphasized.

The researchers also advised addressing comorbidities, including cardiovascular disease, chronic pain, diabetes, gastrointestinal issues, hyperthyroidism, and lung disease, all of which can be associated with anxiety. Once comorbidities are addressed, they advised caution given the lack of evidence for efficacy of both pharmacologic and nonpharmacologic anxiety treatments for PD patients. However, first-tier treatment for anxiety could include monotherapy with serotonin-norepinephrine reuptake inhibitors or selective serotonin reuptake inhibitors, they said.

PD patients with depression and anxiety also may benefit from nonpharmacologic interventions, including exercise, mindfulness, relaxation therapy, and cognitive behavioral therapy the researchers said.

Although the algorithm may not differ significantly from current treatment protocols, it highlights aspects unique to PD patients, the researchers said. In particular, the algorithm shows “that interventions used for motor symptoms, for example, dopamine agonists, may be especially potent for mood in the PD population and that augmentation strategies, such as antipsychotics and lithium, may not be well tolerated given their outsized risk of adverse events in PD,” they said.

“While an article of this kind cannot hope to address the gap in knowledge on comparative efficacy between interventions, it can guide readers on the best strategies for implementation and risk mitigation in PD – essentially focusing more on effectiveness,” they concluded.

The study received no outside funding. Dr. Pontone disclosed serving as a consultant for Acadia Pharmaceuticals and Concert Pharmaceuticals.

Patients with obesity who underwent bariatric surgery had 46% lower odds of stroke 1 year later, similar odds of stroke 3 years later, and 22% lower odds of stroke 5 years later, compared with matched control patients, in new research.

purestock/Thinkstock

Michael D. Williams, MD, presented the study findings (abstract A002) at the annual meeting of the American Society for Metabolic & Bariatric Surgery.

The findings are “very good news,” even though the protection against stroke declined further out from the surgery, John D. Scott, MD, scientific program chair of the ASMBS meeting, told this news organization.

The investigators matched more than 56,000 patients with obesity who had bariatric surgery with an equal number of similar patients who did not have this surgery, from a large national insurance database, in what they believe is the largest study of this to date.

“Any intervention that decreases your risk of [cardiovascular] events is good news,” said Dr. Scott, a clinical professor of surgery at the University of South Carolina, Greenville, and metabolic and bariatric surgery director at Prisma Health in Greenville, S.C. “And having a 22%-45% chance of reduction in stroke risk is a very worthwhile intervention.”

Asked how this would change the way clinicians inform patients of what to expect from bariatric surgery, he said: “I would advise patients that studies like this show that surgery would not increase your risk of having a stroke.

“This is consistent with many studies that show that the risks of all macrovascular events decrease after the comorbidity reductions seen after surgery.”

According to Dr. Scott, “the next steps might include a prospective randomized trial of medical treatment versus surgery alone for [cardiovascular]/stroke outcomes, but this is unlikely.”

Similarly, Dr. Williams told this news organization that “I would tell [patients] that surgery is an effective and durable method for weight loss. It also can improve comorbid conditions, particularly diabetes and hypertension.”

Even with this study, “I’m not sure it’s appropriate to say that bariatric surgery will reduce the risk of stroke,” he cautioned.

“However, as we continue to investigate the effects of bariatric surgery, this study contributes to the greater body of knowledge that suggests that reduction in ischemic stroke risk is yet another benefit of bariatric surgery.”

The assigned discussant, Corrigan L. McBride, MD, MBA wanted to know if the lower odds ratio at 1 year might be because preoperative patient selection might eliminate patients at high risk of poor cardiovascular outcomes.

Dr. Williams, a resident at Rush Medical College, Chicago, replied that it is difficult to eliminate potential selection bias, despite best efforts, but this study shows that he can tell patients: “Having surgery is not going to increases your risk of stroke.”

“This is an important study,” Dr. McBride, professor and chief of minimally invasive surgery and bariatric surgery, University of Nebraska Medical Center, Omaha, told this news organization.

“It is the first large study to show a decreased [or no increased] risk of stroke 1, 3, and 5 years after bariatric surgery compared to matched patients, and it had enough data to look at stroke as a standalone endpoint,” Dr. McBride said. “It is important too, for patients and their physicians to understand that there is a lower chance of them having a stroke if they have surgery than if they do not.”
 

‘Important,’ ‘good news’ for stroke risk after bariatric surgery

The impact of bariatric surgery on remission of type 2 diabetes is well known, Dr. Williams noted, and other studies have reported how bariatric surgery affects the risk of major adverse cardiovascular events – a composite of stroke, myocardial infarction, coronary artery disease, and all-cause death – including a study presented in the same meeting session.

However, a very large sample size is needed to be able to demonstrate the effect of bariatric surgery on stroke, since stroke is a rare event.

The researchers analyzed data from the Mariner (PearlDiver.) all-payer insurance national claims database of patients in the United States.

They matched 56,514 patients with a body mass index over 35 kg/m² and comorbidities or a BMI of more than 40 who underwent sleeve gastrectomy or Roux-en-Y gastric bypass during 2010-2019 with 56,514 control patients who did not undergo bariatric surgery.

A year after bariatric surgery, patients in that group had a lower stroke rate than patients in the control group (0.6% vs. 1.2%), and they had close to 50% lower odds of having a stroke (odds ratio, 0.54; 95% CI, 0.47-0.61).

Three years after bariatric surgery, there were 44,948 patients in each group; the rate of stroke was 2.1% in the surgery group and 2.2% in the control group, and there was no significant difference in the odds of having a stroke (OR, 0.96; 95% CI, 0.91-1.00).

Five years after bariatric surgery, there were 27,619 patients in each group; the stroke rate was lower in the bariatric surgery group than in the control group (2.8% vs 3.6%), but reduced odds of stroke was not as great as after 1 year (OR, 0.78; 95% CI, 0.65-0.90).

Dr. Williams has no relevant financial disclosures. Dr. McBride and Dr. Scott disclosed that they are speakers/trainers/faculty advisers for Gore. Dr. Scott is also a consultant for C-SATS (part of Johnson & Johnson).

Patients with obesity who underwent bariatric surgery had 46% lower odds of stroke 1 year later, similar odds of stroke 3 years later, and 22% lower odds of stroke 5 years later, compared with matched control patients, in new research.

purestock/Thinkstock

Michael D. Williams, MD, presented the study findings (abstract A002) at the annual meeting of the American Society for Metabolic & Bariatric Surgery.

The findings are “very good news,” even though the protection against stroke declined further out from the surgery, John D. Scott, MD, scientific program chair of the ASMBS meeting, told this news organization.

The investigators matched more than 56,000 patients with obesity who had bariatric surgery with an equal number of similar patients who did not have this surgery, from a large national insurance database, in what they believe is the largest study of this to date.

“Any intervention that decreases your risk of [cardiovascular] events is good news,” said Dr. Scott, a clinical professor of surgery at the University of South Carolina, Greenville, and metabolic and bariatric surgery director at Prisma Health in Greenville, S.C. “And having a 22%-45% chance of reduction in stroke risk is a very worthwhile intervention.”

Asked how this would change the way clinicians inform patients of what to expect from bariatric surgery, he said: “I would advise patients that studies like this show that surgery would not increase your risk of having a stroke.

“This is consistent with many studies that show that the risks of all macrovascular events decrease after the comorbidity reductions seen after surgery.”

According to Dr. Scott, “the next steps might include a prospective randomized trial of medical treatment versus surgery alone for [cardiovascular]/stroke outcomes, but this is unlikely.”

Similarly, Dr. Williams told this news organization that “I would tell [patients] that surgery is an effective and durable method for weight loss. It also can improve comorbid conditions, particularly diabetes and hypertension.”

Even with this study, “I’m not sure it’s appropriate to say that bariatric surgery will reduce the risk of stroke,” he cautioned.

“However, as we continue to investigate the effects of bariatric surgery, this study contributes to the greater body of knowledge that suggests that reduction in ischemic stroke risk is yet another benefit of bariatric surgery.”

The assigned discussant, Corrigan L. McBride, MD, MBA wanted to know if the lower odds ratio at 1 year might be because preoperative patient selection might eliminate patients at high risk of poor cardiovascular outcomes.

Dr. Williams, a resident at Rush Medical College, Chicago, replied that it is difficult to eliminate potential selection bias, despite best efforts, but this study shows that he can tell patients: “Having surgery is not going to increases your risk of stroke.”

“This is an important study,” Dr. McBride, professor and chief of minimally invasive surgery and bariatric surgery, University of Nebraska Medical Center, Omaha, told this news organization.

“It is the first large study to show a decreased [or no increased] risk of stroke 1, 3, and 5 years after bariatric surgery compared to matched patients, and it had enough data to look at stroke as a standalone endpoint,” Dr. McBride said. “It is important too, for patients and their physicians to understand that there is a lower chance of them having a stroke if they have surgery than if they do not.”
 

‘Important,’ ‘good news’ for stroke risk after bariatric surgery

The impact of bariatric surgery on remission of type 2 diabetes is well known, Dr. Williams noted, and other studies have reported how bariatric surgery affects the risk of major adverse cardiovascular events – a composite of stroke, myocardial infarction, coronary artery disease, and all-cause death – including a study presented in the same meeting session.

However, a very large sample size is needed to be able to demonstrate the effect of bariatric surgery on stroke, since stroke is a rare event.

The researchers analyzed data from the Mariner (PearlDiver.) all-payer insurance national claims database of patients in the United States.

They matched 56,514 patients with a body mass index over 35 kg/m² and comorbidities or a BMI of more than 40 who underwent sleeve gastrectomy or Roux-en-Y gastric bypass during 2010-2019 with 56,514 control patients who did not undergo bariatric surgery.

A year after bariatric surgery, patients in that group had a lower stroke rate than patients in the control group (0.6% vs. 1.2%), and they had close to 50% lower odds of having a stroke (odds ratio, 0.54; 95% CI, 0.47-0.61).

Three years after bariatric surgery, there were 44,948 patients in each group; the rate of stroke was 2.1% in the surgery group and 2.2% in the control group, and there was no significant difference in the odds of having a stroke (OR, 0.96; 95% CI, 0.91-1.00).

Five years after bariatric surgery, there were 27,619 patients in each group; the stroke rate was lower in the bariatric surgery group than in the control group (2.8% vs 3.6%), but reduced odds of stroke was not as great as after 1 year (OR, 0.78; 95% CI, 0.65-0.90).

Dr. Williams has no relevant financial disclosures. Dr. McBride and Dr. Scott disclosed that they are speakers/trainers/faculty advisers for Gore. Dr. Scott is also a consultant for C-SATS (part of Johnson & Johnson).

Patients with obesity who underwent bariatric surgery had 46% lower odds of stroke 1 year later, similar odds of stroke 3 years later, and 22% lower odds of stroke 5 years later, compared with matched control patients, in new research.

purestock/Thinkstock

Michael D. Williams, MD, presented the study findings (abstract A002) at the annual meeting of the American Society for Metabolic & Bariatric Surgery.

The findings are “very good news,” even though the protection against stroke declined further out from the surgery, John D. Scott, MD, scientific program chair of the ASMBS meeting, told this news organization.

The investigators matched more than 56,000 patients with obesity who had bariatric surgery with an equal number of similar patients who did not have this surgery, from a large national insurance database, in what they believe is the largest study of this to date.

“Any intervention that decreases your risk of [cardiovascular] events is good news,” said Dr. Scott, a clinical professor of surgery at the University of South Carolina, Greenville, and metabolic and bariatric surgery director at Prisma Health in Greenville, S.C. “And having a 22%-45% chance of reduction in stroke risk is a very worthwhile intervention.”

Asked how this would change the way clinicians inform patients of what to expect from bariatric surgery, he said: “I would advise patients that studies like this show that surgery would not increase your risk of having a stroke.

“This is consistent with many studies that show that the risks of all macrovascular events decrease after the comorbidity reductions seen after surgery.”

According to Dr. Scott, “the next steps might include a prospective randomized trial of medical treatment versus surgery alone for [cardiovascular]/stroke outcomes, but this is unlikely.”

Similarly, Dr. Williams told this news organization that “I would tell [patients] that surgery is an effective and durable method for weight loss. It also can improve comorbid conditions, particularly diabetes and hypertension.”

Even with this study, “I’m not sure it’s appropriate to say that bariatric surgery will reduce the risk of stroke,” he cautioned.

“However, as we continue to investigate the effects of bariatric surgery, this study contributes to the greater body of knowledge that suggests that reduction in ischemic stroke risk is yet another benefit of bariatric surgery.”

The assigned discussant, Corrigan L. McBride, MD, MBA wanted to know if the lower odds ratio at 1 year might be because preoperative patient selection might eliminate patients at high risk of poor cardiovascular outcomes.

Dr. Williams, a resident at Rush Medical College, Chicago, replied that it is difficult to eliminate potential selection bias, despite best efforts, but this study shows that he can tell patients: “Having surgery is not going to increases your risk of stroke.”

“This is an important study,” Dr. McBride, professor and chief of minimally invasive surgery and bariatric surgery, University of Nebraska Medical Center, Omaha, told this news organization.

“It is the first large study to show a decreased [or no increased] risk of stroke 1, 3, and 5 years after bariatric surgery compared to matched patients, and it had enough data to look at stroke as a standalone endpoint,” Dr. McBride said. “It is important too, for patients and their physicians to understand that there is a lower chance of them having a stroke if they have surgery than if they do not.”
 

‘Important,’ ‘good news’ for stroke risk after bariatric surgery

The impact of bariatric surgery on remission of type 2 diabetes is well known, Dr. Williams noted, and other studies have reported how bariatric surgery affects the risk of major adverse cardiovascular events – a composite of stroke, myocardial infarction, coronary artery disease, and all-cause death – including a study presented in the same meeting session.

However, a very large sample size is needed to be able to demonstrate the effect of bariatric surgery on stroke, since stroke is a rare event.

The researchers analyzed data from the Mariner (PearlDiver.) all-payer insurance national claims database of patients in the United States.

They matched 56,514 patients with a body mass index over 35 kg/m² and comorbidities or a BMI of more than 40 who underwent sleeve gastrectomy or Roux-en-Y gastric bypass during 2010-2019 with 56,514 control patients who did not undergo bariatric surgery.

A year after bariatric surgery, patients in that group had a lower stroke rate than patients in the control group (0.6% vs. 1.2%), and they had close to 50% lower odds of having a stroke (odds ratio, 0.54; 95% CI, 0.47-0.61).

Three years after bariatric surgery, there were 44,948 patients in each group; the rate of stroke was 2.1% in the surgery group and 2.2% in the control group, and there was no significant difference in the odds of having a stroke (OR, 0.96; 95% CI, 0.91-1.00).

Five years after bariatric surgery, there were 27,619 patients in each group; the stroke rate was lower in the bariatric surgery group than in the control group (2.8% vs 3.6%), but reduced odds of stroke was not as great as after 1 year (OR, 0.78; 95% CI, 0.65-0.90).

Dr. Williams has no relevant financial disclosures. Dr. McBride and Dr. Scott disclosed that they are speakers/trainers/faculty advisers for Gore. Dr. Scott is also a consultant for C-SATS (part of Johnson & Johnson).

Prophylactic anticoagulation to prevent venous thromboembolism (VTE) was associated with reduced 60-day mortality in patients with COVID-19 who were ill enough to require hospitalization, a new report shows.

In a cohort study of more than 1,300 hospitalized patients with COVID-19 infection across 30 hospitals in Michigan, both prophylactic- and therapeutic-dose anticoagulation were associated with reduced in-hospital mortality; however, at 60 days, only prophylactic-dose anticoagulation remained associated with lower mortality.

And adherence was key; nonadherence, or missing 2 days or more of anticoagulation, was linked to more deaths at 60 days.

The findings, which were published online June 11 in JAMA Network Open, are final proof that a prophylactic anticoagulation strategy for the hospitalized COVID population is, indeed, the right one, Valerie M. Vaughn, MD, director of hospital medicine research at the University of Utah, Salt Lake City, said in an interview.

“We’ve probably always known that patients with COVID need prophylaxis for VTE, but we found that early on, unfortunately, that wasn’t being done,” Dr. Vaughn said.

“Now, we see that prophylactic rates have increased. We always knew to use anticoagulation prophylactically in patients who were hospitalized with infection because of their risk for VTE, so this study just drives home that proper adherence to an anticoagulation protocol improves mortality,” she said.

Dr. Vaughn was on the front lines when COVID-19 came to Michigan, where the research was conducted.

“We probably should have been anticoagulating from the get-go, but you have to remember that in the early days of COVID, the hospitals in Michigan were being overwhelmed. They didn’t have PPE. They were taking care of patients outside of their typical hospital beds or setting up field hospitals,” she said. “It was not quite as bad as New York, but at the University of Michigan, we set up four or five ICUs outside of our normal care.”

They also converted the top floor of their pediatric hospital into an ICU to take care of patients with COVID during the first surge, she added. “We didn’t know much about this disease, but faced with this influx of patients, many of whom were dying with blood clots, we had to do something.”  

Some hospitals began prophylactically anticoagulating their patients, but others hesitated before adopting the strategy. “But now we feel confident that prophylactic anticoagulation, done according to the right protocol, with no interruptions in the treatment, is beneficial,” Dr. Vaughn said.

The best medication choice is enoxaparin (Lovenox), which can be given once a day, as opposed to heparin, which needs to be given via injection three times a day, she said.

“Prophylactic dose anticoagulation is typically given by an injection under the skin, but a lot of times, I’ve had patients tell me they feel like a human pin cushion and have all these bruises from being stuck with needles every day, which I can totally relate to,” she said.

“It is important for us as clinicians to explain that we’re having to poke our patients because it is good for them and will help them fight COVID,” she added. “Also having the once-a-day option is going to be a lot better for adherence, and adherence to the protocol, not missing any days, is key to the better outcome.”

Dr. Vaughn and her team reviewed the charts of 1,351 patients (48% women, 49% Black, median age 64 [range 52-75]) who were hospitalized throughout Michigan during the first several months of the COVID-19 pandemic, from March to June 2020.

Only 18 patients (1.3%) had a confirmed VTE and 219 patients (16.2%) received treatment-dose anticoagulation.

The researchers noted that use of treatment-dose anticoagulation without imaging ranged from 0% to 29% across hospitals and increased significantly over time.

Of the 1,127 patients who received anticoagulation, 392 (34.8%) missed 2 days or more of prophylaxis.

In addition, there were varying rates of missed prophylaxis among the hospitals, from 11% to 61%, but these rates decreased markedly over time.

Missed doses were associated with a higher 60-day mortality (adjusted hazard ratio, 1.31; 95% confidence interval, 1.03-1.67), but not in-hospital mortality (aHR, 0.97; 95% CI, 0.91-1.03).

Compared with no anticoagulation, receiving any dose of anticoagulation was associated with lower in-hospital mortality.

However, only prophylactic-dose anticoagulation remained associated with lower mortality at 60 days. The adjusted hazard ratio for prophylactic-dose anticoagulation was 0.71 (95% CI, 0.51-0.90), compared with 0.92 (95% CI, 0.63-1.35) for treatment-dose anticoagulation.
 

Study boosts confidence

Despite its limitations, the study should make clinicians more confident that the use of prophylactic anticoagulation is warranted for hospitalized patients with COVID-19, write Andrew B. Dicks, MD, and Ido Weinberg, MD, from Massachusetts General Hospital, Boston, in an invited commentary.

“Practically, we still lack the granular data we need to help guide us in patient-by-patient decision-making – such as anticoagulation agent choice, dosage, and duration of therapy – especially as dictated by acuity of patient illness,” Dr. Dicks and Dr. Weinberg note.

“While we still await the data from randomized controlled trials to guide the optimal anticoagulation dose and duration, this study adds significant merit to the previously published recommendations from several different medical organizations regarding the use of prophylactic anticoagulation in hospitalized patients with COVID-19,” Dr. Dicks told this news organization.

The study was supported by Blue Cross and Blue Shield of Michigan and Blue Care Network as part of their Value Partnerships program. Dr. Vaughn has reported receiving speaking fees from Thermo Fisher Scientific. Dr. Dicks and Dr. Weinberg have reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Prophylactic anticoagulation to prevent venous thromboembolism (VTE) was associated with reduced 60-day mortality in patients with COVID-19 who were ill enough to require hospitalization, a new report shows.

In a cohort study of more than 1,300 hospitalized patients with COVID-19 infection across 30 hospitals in Michigan, both prophylactic- and therapeutic-dose anticoagulation were associated with reduced in-hospital mortality; however, at 60 days, only prophylactic-dose anticoagulation remained associated with lower mortality.

And adherence was key; nonadherence, or missing 2 days or more of anticoagulation, was linked to more deaths at 60 days.

The findings, which were published online June 11 in JAMA Network Open, are final proof that a prophylactic anticoagulation strategy for the hospitalized COVID population is, indeed, the right one, Valerie M. Vaughn, MD, director of hospital medicine research at the University of Utah, Salt Lake City, said in an interview.

“We’ve probably always known that patients with COVID need prophylaxis for VTE, but we found that early on, unfortunately, that wasn’t being done,” Dr. Vaughn said.

“Now, we see that prophylactic rates have increased. We always knew to use anticoagulation prophylactically in patients who were hospitalized with infection because of their risk for VTE, so this study just drives home that proper adherence to an anticoagulation protocol improves mortality,” she said.

Dr. Vaughn was on the front lines when COVID-19 came to Michigan, where the research was conducted.

“We probably should have been anticoagulating from the get-go, but you have to remember that in the early days of COVID, the hospitals in Michigan were being overwhelmed. They didn’t have PPE. They were taking care of patients outside of their typical hospital beds or setting up field hospitals,” she said. “It was not quite as bad as New York, but at the University of Michigan, we set up four or five ICUs outside of our normal care.”

They also converted the top floor of their pediatric hospital into an ICU to take care of patients with COVID during the first surge, she added. “We didn’t know much about this disease, but faced with this influx of patients, many of whom were dying with blood clots, we had to do something.”  

Some hospitals began prophylactically anticoagulating their patients, but others hesitated before adopting the strategy. “But now we feel confident that prophylactic anticoagulation, done according to the right protocol, with no interruptions in the treatment, is beneficial,” Dr. Vaughn said.

The best medication choice is enoxaparin (Lovenox), which can be given once a day, as opposed to heparin, which needs to be given via injection three times a day, she said.

“Prophylactic dose anticoagulation is typically given by an injection under the skin, but a lot of times, I’ve had patients tell me they feel like a human pin cushion and have all these bruises from being stuck with needles every day, which I can totally relate to,” she said.

“It is important for us as clinicians to explain that we’re having to poke our patients because it is good for them and will help them fight COVID,” she added. “Also having the once-a-day option is going to be a lot better for adherence, and adherence to the protocol, not missing any days, is key to the better outcome.”

Dr. Vaughn and her team reviewed the charts of 1,351 patients (48% women, 49% Black, median age 64 [range 52-75]) who were hospitalized throughout Michigan during the first several months of the COVID-19 pandemic, from March to June 2020.

Only 18 patients (1.3%) had a confirmed VTE and 219 patients (16.2%) received treatment-dose anticoagulation.

The researchers noted that use of treatment-dose anticoagulation without imaging ranged from 0% to 29% across hospitals and increased significantly over time.

Of the 1,127 patients who received anticoagulation, 392 (34.8%) missed 2 days or more of prophylaxis.

In addition, there were varying rates of missed prophylaxis among the hospitals, from 11% to 61%, but these rates decreased markedly over time.

Missed doses were associated with a higher 60-day mortality (adjusted hazard ratio, 1.31; 95% confidence interval, 1.03-1.67), but not in-hospital mortality (aHR, 0.97; 95% CI, 0.91-1.03).

Compared with no anticoagulation, receiving any dose of anticoagulation was associated with lower in-hospital mortality.

However, only prophylactic-dose anticoagulation remained associated with lower mortality at 60 days. The adjusted hazard ratio for prophylactic-dose anticoagulation was 0.71 (95% CI, 0.51-0.90), compared with 0.92 (95% CI, 0.63-1.35) for treatment-dose anticoagulation.
 

Study boosts confidence

Despite its limitations, the study should make clinicians more confident that the use of prophylactic anticoagulation is warranted for hospitalized patients with COVID-19, write Andrew B. Dicks, MD, and Ido Weinberg, MD, from Massachusetts General Hospital, Boston, in an invited commentary.

“Practically, we still lack the granular data we need to help guide us in patient-by-patient decision-making – such as anticoagulation agent choice, dosage, and duration of therapy – especially as dictated by acuity of patient illness,” Dr. Dicks and Dr. Weinberg note.

“While we still await the data from randomized controlled trials to guide the optimal anticoagulation dose and duration, this study adds significant merit to the previously published recommendations from several different medical organizations regarding the use of prophylactic anticoagulation in hospitalized patients with COVID-19,” Dr. Dicks told this news organization.

The study was supported by Blue Cross and Blue Shield of Michigan and Blue Care Network as part of their Value Partnerships program. Dr. Vaughn has reported receiving speaking fees from Thermo Fisher Scientific. Dr. Dicks and Dr. Weinberg have reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Prophylactic anticoagulation to prevent venous thromboembolism (VTE) was associated with reduced 60-day mortality in patients with COVID-19 who were ill enough to require hospitalization, a new report shows.

In a cohort study of more than 1,300 hospitalized patients with COVID-19 infection across 30 hospitals in Michigan, both prophylactic- and therapeutic-dose anticoagulation were associated with reduced in-hospital mortality; however, at 60 days, only prophylactic-dose anticoagulation remained associated with lower mortality.

And adherence was key; nonadherence, or missing 2 days or more of anticoagulation, was linked to more deaths at 60 days.

The findings, which were published online June 11 in JAMA Network Open, are final proof that a prophylactic anticoagulation strategy for the hospitalized COVID population is, indeed, the right one, Valerie M. Vaughn, MD, director of hospital medicine research at the University of Utah, Salt Lake City, said in an interview.

“We’ve probably always known that patients with COVID need prophylaxis for VTE, but we found that early on, unfortunately, that wasn’t being done,” Dr. Vaughn said.

“Now, we see that prophylactic rates have increased. We always knew to use anticoagulation prophylactically in patients who were hospitalized with infection because of their risk for VTE, so this study just drives home that proper adherence to an anticoagulation protocol improves mortality,” she said.

Dr. Vaughn was on the front lines when COVID-19 came to Michigan, where the research was conducted.

“We probably should have been anticoagulating from the get-go, but you have to remember that in the early days of COVID, the hospitals in Michigan were being overwhelmed. They didn’t have PPE. They were taking care of patients outside of their typical hospital beds or setting up field hospitals,” she said. “It was not quite as bad as New York, but at the University of Michigan, we set up four or five ICUs outside of our normal care.”

They also converted the top floor of their pediatric hospital into an ICU to take care of patients with COVID during the first surge, she added. “We didn’t know much about this disease, but faced with this influx of patients, many of whom were dying with blood clots, we had to do something.”  

Some hospitals began prophylactically anticoagulating their patients, but others hesitated before adopting the strategy. “But now we feel confident that prophylactic anticoagulation, done according to the right protocol, with no interruptions in the treatment, is beneficial,” Dr. Vaughn said.

The best medication choice is enoxaparin (Lovenox), which can be given once a day, as opposed to heparin, which needs to be given via injection three times a day, she said.

“Prophylactic dose anticoagulation is typically given by an injection under the skin, but a lot of times, I’ve had patients tell me they feel like a human pin cushion and have all these bruises from being stuck with needles every day, which I can totally relate to,” she said.

“It is important for us as clinicians to explain that we’re having to poke our patients because it is good for them and will help them fight COVID,” she added. “Also having the once-a-day option is going to be a lot better for adherence, and adherence to the protocol, not missing any days, is key to the better outcome.”

Dr. Vaughn and her team reviewed the charts of 1,351 patients (48% women, 49% Black, median age 64 [range 52-75]) who were hospitalized throughout Michigan during the first several months of the COVID-19 pandemic, from March to June 2020.

Only 18 patients (1.3%) had a confirmed VTE and 219 patients (16.2%) received treatment-dose anticoagulation.

The researchers noted that use of treatment-dose anticoagulation without imaging ranged from 0% to 29% across hospitals and increased significantly over time.

Of the 1,127 patients who received anticoagulation, 392 (34.8%) missed 2 days or more of prophylaxis.

In addition, there were varying rates of missed prophylaxis among the hospitals, from 11% to 61%, but these rates decreased markedly over time.

Missed doses were associated with a higher 60-day mortality (adjusted hazard ratio, 1.31; 95% confidence interval, 1.03-1.67), but not in-hospital mortality (aHR, 0.97; 95% CI, 0.91-1.03).

Compared with no anticoagulation, receiving any dose of anticoagulation was associated with lower in-hospital mortality.

However, only prophylactic-dose anticoagulation remained associated with lower mortality at 60 days. The adjusted hazard ratio for prophylactic-dose anticoagulation was 0.71 (95% CI, 0.51-0.90), compared with 0.92 (95% CI, 0.63-1.35) for treatment-dose anticoagulation.
 

Study boosts confidence

Despite its limitations, the study should make clinicians more confident that the use of prophylactic anticoagulation is warranted for hospitalized patients with COVID-19, write Andrew B. Dicks, MD, and Ido Weinberg, MD, from Massachusetts General Hospital, Boston, in an invited commentary.

“Practically, we still lack the granular data we need to help guide us in patient-by-patient decision-making – such as anticoagulation agent choice, dosage, and duration of therapy – especially as dictated by acuity of patient illness,” Dr. Dicks and Dr. Weinberg note.

“While we still await the data from randomized controlled trials to guide the optimal anticoagulation dose and duration, this study adds significant merit to the previously published recommendations from several different medical organizations regarding the use of prophylactic anticoagulation in hospitalized patients with COVID-19,” Dr. Dicks told this news organization.

The study was supported by Blue Cross and Blue Shield of Michigan and Blue Care Network as part of their Value Partnerships program. Dr. Vaughn has reported receiving speaking fees from Thermo Fisher Scientific. Dr. Dicks and Dr. Weinberg have reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Agents that reverse the effect of direct oral anticoagulants (DOACs) are highly effective in patients with severe bleeding, but mortality rates remain high despite their use, a meta-analysis shows.

Effective hemostasis was achieved in 78.5% of patients treated with a reversal agent, whereas failure to achieve hemostasis was associated with more than a threefold higher relative risk for death (relative risk, 3.63; 95% confidence interval, 2.56-5.16).

“This has implications in practice because it emphasizes the need for achieving effective hemostasis, if not with only one agent, trying other agents or treatment modalities, because it is a strong predictor of survival,” lead author Antonio Gómez-Outes, MD, PhD, said in an interview.

The bad news, he said, is that the mortality rate was still significant, at 17.7%, and approximately half of patients with DOAC-related severe intracranial bleeding survived with long-term moderate/severe disability.

“The lesson is to prevent these bleeding events because once they appear, even if you give an antidote, the outcome is poor, particularly for intracranial bleeding,” said Dr. Gómez-Outes, division of pharmacology and clinical drug evaluation, Spanish Agency for Medicines and Medical Devices, Madrid.

To put this in context, mortality rates were close to 50% after intracranial bleeding a decade ago when there were no antidotes or reversal agents, he observed. “So to some extent, patient care has improved, and the outcome has improved, but there is a long road to improve regarding disability.”

More than 100,000 DOAC-related major bleeding cases occur each year in the United States and European Union, Dr. Gómez-Outes said, and about half are severe enough to require hospitalization and potentially the use of a reversal agent. These include idarucizumab (Praxbind) for dabigatran reversal and prothombin complex concentrates (4CCC) or andexanet alpha (Andexxa) for reversal of direct factor Xa inhibitors like rivaroxaban, apixaban, and edoxaban.

As reported in the June 22 issue of the Journal of the American College of Cardiology, the meta-analysis comprised 4,735 patients (mean age, 77 years; 57% male) with severe DOAC-related bleeding who received 4PCC (n = 2,688), idarucizumab (n = 1,111), or andexanet (n = 936) in 60 studies between January 2010 and December 2020.

Atrial fibrillation (AFib) was the most common reason for use of a DOAC (82%), followed by venous thromboembolism (14%). Rivaroxaban was used in 36%, apixaban in 32%, dabigatran in 31%, and edoxaban in 1%.

The index bleeding event was intracranial hemorrhage (ICH) in 55%. Anticoagulation was restarted in 57% of patients an average of 11 days after admission.

Mortality rates were 20.2% in patients with ICH and 15.4% in those with extracranial bleeding. There were no differences in death rates by reversal agent used, type of study, risk for bias, or study sponsorship in meta-regression analysis.

Rebleeding occurred in 13.2% of patients; 82.0% of these events were described as an ICH, and 78.0% occurred after anticoagulation was restarted.

The overall rate of thromboembolism was 4.6%. The risk was particularly high with andexanet, at 10.7%, and relatively low with idarucizumab (3.8%) and 4PCC (4.3%), the authors note.

“Our meta-analysis suggests specific reversal with andexanet is not superior to unspecific reversal with 4PCC, and that’s good news because many centers, in many countries, have no access to specific antidotes that are more costly,” Dr. Gómez-Outes said. “4PCC is an effective and relatively safe drug, so it’s still a good option for these patients.”

Labeling for andexanet includes a warning for thromboembolic events, but in the absence of direct comparisons, the findings should be interpreted with caution, he added. Further insights are expected from an ongoing randomized trial of andexanet and standard of care in 900 patients who present with acute ICH less than 15 hours after taking an oral factor Xa inhibitor. The preliminary completion date is set for 2023.

“The meta-analysis raises awareness about the rates of mortality and thromboembolism after reversal agent administration, although understanding the implications of these data is challenging,” Christopher Granger, MD, and Sean P. Pokomey, MD, MBA, Duke University Medical Center, Durham, N.C., say in an accompanying editorial.

The fact that failure to achieve hemostasis was associated with death is expected and might be related to the way hemostasis was defined, rather than the actual failure of the hemostatic treatments, they suggest. “The prothrombotic effects of each agent, including andexanet, need to be better understood, as clinicians work toward including reversal agents into algorithms for bleeding management.”

Effective hemostasis was defined in the studies through various methods as: “Excellent/good” using the Sarode and ANNEXA-4 scales; “yes” in the International Society on Thrombosis and Hemostasis Scale; and with other scales and through clinical judgment.

Although the size of the meta-analysis dwarfs previous reviews, the editorialists and authors point out that 47 of the 60 studies were retrospective, only two had control groups, and 45 had a high risk for bias.

In general, there was also poor reporting of key clinical data, such as postbleeding anticoagulation management, and a limitation of the mortality analysis is that it was based in selected patients with effective hemostasis assessed within 48 hours, which may not capture early deaths, the authors note.

“The morbidity and mortality from ischemic strokes as a result of undertreatment of stroke prevention in patients with AFib continue to dwarf the bleeding related mortality among patients with AFib and on DOACs, and thus the number one priority is to treat nearly all patients with AFib with a DOAC,” Dr. Granger and Dr. Pokomey conclude. “The availability of reversal agents for DOACs should provide reassurance, with another tool in our armamentarium, to providers to prescribe OACs for stroke prevention.”

No funding/grant support was received to conduct the study. Coauthor Ramón Lecumberri has received personal fees from Boehringer Ingelheim and Bristol Myers Squibb outside the submitted work. All other authors report no relevant financial relationships. Dr. Granger has received research and consulting fees from Bristol Myers Squibb, Pfizer, Boehringer Ingelheim, Bayer, Janssen, Boston Scientific, Apple, AstraZeneca, Novartis, AbbVie, Biomed, CeleCor, GSK, Novartis, Medtronic, Merck, Novo Nordisk, Philips, Rho, and the U.S. Food and Drug Administration. Dr. Pokomey has received modest consulting support from Bristol Myers Squibb, Pfizer, Boston Scientific, Medtronic, Janssen, and Zoll; modest research support from Gilead, Boston Scientific, Bristol Myers Squibb, Pfizer, and Janssen; and significant research support from the FDA.

A version of this article first appeared on Medscape.com.

Agents that reverse the effect of direct oral anticoagulants (DOACs) are highly effective in patients with severe bleeding, but mortality rates remain high despite their use, a meta-analysis shows.

Effective hemostasis was achieved in 78.5% of patients treated with a reversal agent, whereas failure to achieve hemostasis was associated with more than a threefold higher relative risk for death (relative risk, 3.63; 95% confidence interval, 2.56-5.16).

“This has implications in practice because it emphasizes the need for achieving effective hemostasis, if not with only one agent, trying other agents or treatment modalities, because it is a strong predictor of survival,” lead author Antonio Gómez-Outes, MD, PhD, said in an interview.

The bad news, he said, is that the mortality rate was still significant, at 17.7%, and approximately half of patients with DOAC-related severe intracranial bleeding survived with long-term moderate/severe disability.

“The lesson is to prevent these bleeding events because once they appear, even if you give an antidote, the outcome is poor, particularly for intracranial bleeding,” said Dr. Gómez-Outes, division of pharmacology and clinical drug evaluation, Spanish Agency for Medicines and Medical Devices, Madrid.

To put this in context, mortality rates were close to 50% after intracranial bleeding a decade ago when there were no antidotes or reversal agents, he observed. “So to some extent, patient care has improved, and the outcome has improved, but there is a long road to improve regarding disability.”

More than 100,000 DOAC-related major bleeding cases occur each year in the United States and European Union, Dr. Gómez-Outes said, and about half are severe enough to require hospitalization and potentially the use of a reversal agent. These include idarucizumab (Praxbind) for dabigatran reversal and prothombin complex concentrates (4CCC) or andexanet alpha (Andexxa) for reversal of direct factor Xa inhibitors like rivaroxaban, apixaban, and edoxaban.

As reported in the June 22 issue of the Journal of the American College of Cardiology, the meta-analysis comprised 4,735 patients (mean age, 77 years; 57% male) with severe DOAC-related bleeding who received 4PCC (n = 2,688), idarucizumab (n = 1,111), or andexanet (n = 936) in 60 studies between January 2010 and December 2020.

Atrial fibrillation (AFib) was the most common reason for use of a DOAC (82%), followed by venous thromboembolism (14%). Rivaroxaban was used in 36%, apixaban in 32%, dabigatran in 31%, and edoxaban in 1%.

The index bleeding event was intracranial hemorrhage (ICH) in 55%. Anticoagulation was restarted in 57% of patients an average of 11 days after admission.

Mortality rates were 20.2% in patients with ICH and 15.4% in those with extracranial bleeding. There were no differences in death rates by reversal agent used, type of study, risk for bias, or study sponsorship in meta-regression analysis.

Rebleeding occurred in 13.2% of patients; 82.0% of these events were described as an ICH, and 78.0% occurred after anticoagulation was restarted.

The overall rate of thromboembolism was 4.6%. The risk was particularly high with andexanet, at 10.7%, and relatively low with idarucizumab (3.8%) and 4PCC (4.3%), the authors note.

“Our meta-analysis suggests specific reversal with andexanet is not superior to unspecific reversal with 4PCC, and that’s good news because many centers, in many countries, have no access to specific antidotes that are more costly,” Dr. Gómez-Outes said. “4PCC is an effective and relatively safe drug, so it’s still a good option for these patients.”

Labeling for andexanet includes a warning for thromboembolic events, but in the absence of direct comparisons, the findings should be interpreted with caution, he added. Further insights are expected from an ongoing randomized trial of andexanet and standard of care in 900 patients who present with acute ICH less than 15 hours after taking an oral factor Xa inhibitor. The preliminary completion date is set for 2023.

“The meta-analysis raises awareness about the rates of mortality and thromboembolism after reversal agent administration, although understanding the implications of these data is challenging,” Christopher Granger, MD, and Sean P. Pokomey, MD, MBA, Duke University Medical Center, Durham, N.C., say in an accompanying editorial.

The fact that failure to achieve hemostasis was associated with death is expected and might be related to the way hemostasis was defined, rather than the actual failure of the hemostatic treatments, they suggest. “The prothrombotic effects of each agent, including andexanet, need to be better understood, as clinicians work toward including reversal agents into algorithms for bleeding management.”

Effective hemostasis was defined in the studies through various methods as: “Excellent/good” using the Sarode and ANNEXA-4 scales; “yes” in the International Society on Thrombosis and Hemostasis Scale; and with other scales and through clinical judgment.

Although the size of the meta-analysis dwarfs previous reviews, the editorialists and authors point out that 47 of the 60 studies were retrospective, only two had control groups, and 45 had a high risk for bias.

In general, there was also poor reporting of key clinical data, such as postbleeding anticoagulation management, and a limitation of the mortality analysis is that it was based in selected patients with effective hemostasis assessed within 48 hours, which may not capture early deaths, the authors note.

“The morbidity and mortality from ischemic strokes as a result of undertreatment of stroke prevention in patients with AFib continue to dwarf the bleeding related mortality among patients with AFib and on DOACs, and thus the number one priority is to treat nearly all patients with AFib with a DOAC,” Dr. Granger and Dr. Pokomey conclude. “The availability of reversal agents for DOACs should provide reassurance, with another tool in our armamentarium, to providers to prescribe OACs for stroke prevention.”

No funding/grant support was received to conduct the study. Coauthor Ramón Lecumberri has received personal fees from Boehringer Ingelheim and Bristol Myers Squibb outside the submitted work. All other authors report no relevant financial relationships. Dr. Granger has received research and consulting fees from Bristol Myers Squibb, Pfizer, Boehringer Ingelheim, Bayer, Janssen, Boston Scientific, Apple, AstraZeneca, Novartis, AbbVie, Biomed, CeleCor, GSK, Novartis, Medtronic, Merck, Novo Nordisk, Philips, Rho, and the U.S. Food and Drug Administration. Dr. Pokomey has received modest consulting support from Bristol Myers Squibb, Pfizer, Boston Scientific, Medtronic, Janssen, and Zoll; modest research support from Gilead, Boston Scientific, Bristol Myers Squibb, Pfizer, and Janssen; and significant research support from the FDA.

A version of this article first appeared on Medscape.com.

Agents that reverse the effect of direct oral anticoagulants (DOACs) are highly effective in patients with severe bleeding, but mortality rates remain high despite their use, a meta-analysis shows.

Effective hemostasis was achieved in 78.5% of patients treated with a reversal agent, whereas failure to achieve hemostasis was associated with more than a threefold higher relative risk for death (relative risk, 3.63; 95% confidence interval, 2.56-5.16).

“This has implications in practice because it emphasizes the need for achieving effective hemostasis, if not with only one agent, trying other agents or treatment modalities, because it is a strong predictor of survival,” lead author Antonio Gómez-Outes, MD, PhD, said in an interview.

The bad news, he said, is that the mortality rate was still significant, at 17.7%, and approximately half of patients with DOAC-related severe intracranial bleeding survived with long-term moderate/severe disability.

“The lesson is to prevent these bleeding events because once they appear, even if you give an antidote, the outcome is poor, particularly for intracranial bleeding,” said Dr. Gómez-Outes, division of pharmacology and clinical drug evaluation, Spanish Agency for Medicines and Medical Devices, Madrid.

To put this in context, mortality rates were close to 50% after intracranial bleeding a decade ago when there were no antidotes or reversal agents, he observed. “So to some extent, patient care has improved, and the outcome has improved, but there is a long road to improve regarding disability.”

More than 100,000 DOAC-related major bleeding cases occur each year in the United States and European Union, Dr. Gómez-Outes said, and about half are severe enough to require hospitalization and potentially the use of a reversal agent. These include idarucizumab (Praxbind) for dabigatran reversal and prothombin complex concentrates (4CCC) or andexanet alpha (Andexxa) for reversal of direct factor Xa inhibitors like rivaroxaban, apixaban, and edoxaban.

As reported in the June 22 issue of the Journal of the American College of Cardiology, the meta-analysis comprised 4,735 patients (mean age, 77 years; 57% male) with severe DOAC-related bleeding who received 4PCC (n = 2,688), idarucizumab (n = 1,111), or andexanet (n = 936) in 60 studies between January 2010 and December 2020.

Atrial fibrillation (AFib) was the most common reason for use of a DOAC (82%), followed by venous thromboembolism (14%). Rivaroxaban was used in 36%, apixaban in 32%, dabigatran in 31%, and edoxaban in 1%.

The index bleeding event was intracranial hemorrhage (ICH) in 55%. Anticoagulation was restarted in 57% of patients an average of 11 days after admission.

Mortality rates were 20.2% in patients with ICH and 15.4% in those with extracranial bleeding. There were no differences in death rates by reversal agent used, type of study, risk for bias, or study sponsorship in meta-regression analysis.

Rebleeding occurred in 13.2% of patients; 82.0% of these events were described as an ICH, and 78.0% occurred after anticoagulation was restarted.

The overall rate of thromboembolism was 4.6%. The risk was particularly high with andexanet, at 10.7%, and relatively low with idarucizumab (3.8%) and 4PCC (4.3%), the authors note.

“Our meta-analysis suggests specific reversal with andexanet is not superior to unspecific reversal with 4PCC, and that’s good news because many centers, in many countries, have no access to specific antidotes that are more costly,” Dr. Gómez-Outes said. “4PCC is an effective and relatively safe drug, so it’s still a good option for these patients.”

Labeling for andexanet includes a warning for thromboembolic events, but in the absence of direct comparisons, the findings should be interpreted with caution, he added. Further insights are expected from an ongoing randomized trial of andexanet and standard of care in 900 patients who present with acute ICH less than 15 hours after taking an oral factor Xa inhibitor. The preliminary completion date is set for 2023.

“The meta-analysis raises awareness about the rates of mortality and thromboembolism after reversal agent administration, although understanding the implications of these data is challenging,” Christopher Granger, MD, and Sean P. Pokomey, MD, MBA, Duke University Medical Center, Durham, N.C., say in an accompanying editorial.

The fact that failure to achieve hemostasis was associated with death is expected and might be related to the way hemostasis was defined, rather than the actual failure of the hemostatic treatments, they suggest. “The prothrombotic effects of each agent, including andexanet, need to be better understood, as clinicians work toward including reversal agents into algorithms for bleeding management.”

Effective hemostasis was defined in the studies through various methods as: “Excellent/good” using the Sarode and ANNEXA-4 scales; “yes” in the International Society on Thrombosis and Hemostasis Scale; and with other scales and through clinical judgment.

Although the size of the meta-analysis dwarfs previous reviews, the editorialists and authors point out that 47 of the 60 studies were retrospective, only two had control groups, and 45 had a high risk for bias.

In general, there was also poor reporting of key clinical data, such as postbleeding anticoagulation management, and a limitation of the mortality analysis is that it was based in selected patients with effective hemostasis assessed within 48 hours, which may not capture early deaths, the authors note.

“The morbidity and mortality from ischemic strokes as a result of undertreatment of stroke prevention in patients with AFib continue to dwarf the bleeding related mortality among patients with AFib and on DOACs, and thus the number one priority is to treat nearly all patients with AFib with a DOAC,” Dr. Granger and Dr. Pokomey conclude. “The availability of reversal agents for DOACs should provide reassurance, with another tool in our armamentarium, to providers to prescribe OACs for stroke prevention.”

No funding/grant support was received to conduct the study. Coauthor Ramón Lecumberri has received personal fees from Boehringer Ingelheim and Bristol Myers Squibb outside the submitted work. All other authors report no relevant financial relationships. Dr. Granger has received research and consulting fees from Bristol Myers Squibb, Pfizer, Boehringer Ingelheim, Bayer, Janssen, Boston Scientific, Apple, AstraZeneca, Novartis, AbbVie, Biomed, CeleCor, GSK, Novartis, Medtronic, Merck, Novo Nordisk, Philips, Rho, and the U.S. Food and Drug Administration. Dr. Pokomey has received modest consulting support from Bristol Myers Squibb, Pfizer, Boston Scientific, Medtronic, Janssen, and Zoll; modest research support from Gilead, Boston Scientific, Bristol Myers Squibb, Pfizer, and Janssen; and significant research support from the FDA.

A version of this article first appeared on Medscape.com.

Gerald E. Harmon, MD, a family physician in South Carolina whose patients sometimes leave produce in the back of his pickup truck, has practiced medicine during military deployments and during 15-hour shifts in the COVID-19 pandemic.

He has encountered “all manner of unexpected situations” and feels “more than prepared” to serve as president of the American Medical Association, he said.

At the same time, “I still find myself a little nervous about it,” Dr. Harmon said in an interview the day after he was sworn in as president. “I would be less than candid if I didn’t tell you that. I don’t mean intimidated. ... It’s almost like before an athletic event.”

Dr. Harmon was sworn in June 15 as the 176th president of the AMA during the virtual Special Meeting of the AMA House of Delegates. He follows Susan R. Bailey, MD, an allergist from Fort Worth, Tex., in leading the organization, which has more than 270,000 members.
 

Advancing health equity

During his inaugural address, Dr. Harmon discussed the pandemic and the AMA’s plan to advance health equity.

COVID-19 “has revealed enormous gaps in how we care for people and communities in America, demonstrated in the disproportionate impact of this pandemic on communities of color and in the weaknesses of our underfunded and underresourced public health infrastructure,” Dr. Harmon said.

He described medical professionals as being “at war against seemingly formidable adversaries,” including the pandemic, the effects of prolonged isolation on emotional and behavioral health, and political and racial tension. There is an “immense battle to rid our health system – and society – of health disparities and racism,” he said. “As we face these battles, we must remember that our actions as physicians and as leaders will have far-reaching consequences.”

Other challenges before the AMA include vaccinating patients, recovering from the ongoing pandemic, removing unnecessary obstacles to care, ending an epidemic of drug overdoses, improving outcomes for patients with chronic disease, incorporating technology in ways that benefit doctors and patients, and preparing future physicians, Dr. Harmon noted.

“We are going to embed the principles of equity and racial justice within the AMA and throughout our health system,” added Dr. Harmon, who has been an AMA board member since 2013 and served as board chair from 2017 to 2018. He highlighted the AMA’s strategic plan, released in May 2021, to advance health equity and justice and improve the quality of care for people who have been marginalized.

“Meaningful progress won’t happen until we, as doctors, recognize how profoundly systemic racism influences the health of our patients, and until we commit to taking action within our own spheres of influence,” Dr. Harmon said. “As a family doctor in a very diverse state, I have treated people from all backgrounds, and have seen inequities up close, inequities that understandably lead to distrust.”

Commenting in an interview on JAMA’s controversial tweet and podcast related to structural racism from earlier this year that have been deleted and removed from JAMA’s website, Dr. Harmon said, JAMA maintains editorial independence from the AMA, but that direction from a journal oversight committee could lead to changes at the journal that could help prevent similar incidents.

“We’ll support whatever the journal oversight committee suggests,” Dr. Harmon said.

“We had public statements about [the podcast]. I do think that we’ll be able to move very quickly in a stronger direction to address the issue of systemic racism,” Dr. Harmon said. “The AMA has acknowledged that it is a public health threat. We have acknowledged that it is ... a political description versus a biologic construct. So, I would anticipate that you’ll find changes.”

The AMA began developing its strategic plan to advance equity several years ago, Dr. Harmon noted. “I think we are very well poised to move forward and attack this enemy of health disparity.”
 

AAFP president supporting Dr. Harmon’s inauguration

Among those congratulating Dr. Harmon on his inauguration was Ada Stewart, MD, a fellow family physician and South Carolina resident who is the president of the American Academy of Family Physicians.

“We are very excited that family physician Dr. Gerald Harmon will serve as president of the AMA this coming year,” Dr. Stewart said. “Family medicine encompasses the very essence of medicine – treating the whole person, in the context of family, community, and each individual’s unique circumstances. As a family physician, Dr. Harmon brings important perspectives from the front lines of primary care. His commitment to health equity and evidence-based care, as well as his concern for practice sustainability and physician well-being, will serve him well as he leads the house of medicine into the future.”

Dr. Harmon has practiced as a family medicine specialist in Georgetown, S.C., for more than 30 years. He is a member of the clinical faculty for the Tidelands Health Medical University of South Carolina family medicine residency program, advises a community health system, and is vice president of a multispecialty physician practice. In addition, Dr. Harmon is the medical director of a nonprofit hospice and volunteers as medical supervisor for his local school district.

Dr. Harmon received his undergraduate degree in physics and mathematics from the University of South Carolina, Columbia, and received his medical degree from the Medical University of South Carolina, Charleston. He completed a residency training program in family medicine with the U.S. Air Force at Eglin (Fla.) AFB, Florida.

During a 35-year military career, Dr. Harmon served as chief surgeon for the National Guard Bureau and assistant surgeon general for the U.S. Air Force. He retired from the military as a major general.

Dr. Harmon and his wife, Linda, have three married children and eight grandchildren.

Every now and then, a bucket of tomatoes or even a half bushel of corn shows up in the back of Dr. Harmon’s pickup truck, with a note on the window thanking him. “That really touches you deeply,” Dr. Harmon said. “I practice that type of medicine and I’m honored to be able to do that every day.”

jremaly@mdedge.com

Gerald E. Harmon, MD, a family physician in South Carolina whose patients sometimes leave produce in the back of his pickup truck, has practiced medicine during military deployments and during 15-hour shifts in the COVID-19 pandemic.

He has encountered “all manner of unexpected situations” and feels “more than prepared” to serve as president of the American Medical Association, he said.

At the same time, “I still find myself a little nervous about it,” Dr. Harmon said in an interview the day after he was sworn in as president. “I would be less than candid if I didn’t tell you that. I don’t mean intimidated. ... It’s almost like before an athletic event.”

Dr. Harmon was sworn in June 15 as the 176th president of the AMA during the virtual Special Meeting of the AMA House of Delegates. He follows Susan R. Bailey, MD, an allergist from Fort Worth, Tex., in leading the organization, which has more than 270,000 members.
 

Advancing health equity

During his inaugural address, Dr. Harmon discussed the pandemic and the AMA’s plan to advance health equity.

COVID-19 “has revealed enormous gaps in how we care for people and communities in America, demonstrated in the disproportionate impact of this pandemic on communities of color and in the weaknesses of our underfunded and underresourced public health infrastructure,” Dr. Harmon said.

He described medical professionals as being “at war against seemingly formidable adversaries,” including the pandemic, the effects of prolonged isolation on emotional and behavioral health, and political and racial tension. There is an “immense battle to rid our health system – and society – of health disparities and racism,” he said. “As we face these battles, we must remember that our actions as physicians and as leaders will have far-reaching consequences.”

Other challenges before the AMA include vaccinating patients, recovering from the ongoing pandemic, removing unnecessary obstacles to care, ending an epidemic of drug overdoses, improving outcomes for patients with chronic disease, incorporating technology in ways that benefit doctors and patients, and preparing future physicians, Dr. Harmon noted.

“We are going to embed the principles of equity and racial justice within the AMA and throughout our health system,” added Dr. Harmon, who has been an AMA board member since 2013 and served as board chair from 2017 to 2018. He highlighted the AMA’s strategic plan, released in May 2021, to advance health equity and justice and improve the quality of care for people who have been marginalized.

“Meaningful progress won’t happen until we, as doctors, recognize how profoundly systemic racism influences the health of our patients, and until we commit to taking action within our own spheres of influence,” Dr. Harmon said. “As a family doctor in a very diverse state, I have treated people from all backgrounds, and have seen inequities up close, inequities that understandably lead to distrust.”

Commenting in an interview on JAMA’s controversial tweet and podcast related to structural racism from earlier this year that have been deleted and removed from JAMA’s website, Dr. Harmon said, JAMA maintains editorial independence from the AMA, but that direction from a journal oversight committee could lead to changes at the journal that could help prevent similar incidents.

“We’ll support whatever the journal oversight committee suggests,” Dr. Harmon said.

“We had public statements about [the podcast]. I do think that we’ll be able to move very quickly in a stronger direction to address the issue of systemic racism,” Dr. Harmon said. “The AMA has acknowledged that it is a public health threat. We have acknowledged that it is ... a political description versus a biologic construct. So, I would anticipate that you’ll find changes.”

The AMA began developing its strategic plan to advance equity several years ago, Dr. Harmon noted. “I think we are very well poised to move forward and attack this enemy of health disparity.”
 

AAFP president supporting Dr. Harmon’s inauguration

Among those congratulating Dr. Harmon on his inauguration was Ada Stewart, MD, a fellow family physician and South Carolina resident who is the president of the American Academy of Family Physicians.

“We are very excited that family physician Dr. Gerald Harmon will serve as president of the AMA this coming year,” Dr. Stewart said. “Family medicine encompasses the very essence of medicine – treating the whole person, in the context of family, community, and each individual’s unique circumstances. As a family physician, Dr. Harmon brings important perspectives from the front lines of primary care. His commitment to health equity and evidence-based care, as well as his concern for practice sustainability and physician well-being, will serve him well as he leads the house of medicine into the future.”

Dr. Harmon has practiced as a family medicine specialist in Georgetown, S.C., for more than 30 years. He is a member of the clinical faculty for the Tidelands Health Medical University of South Carolina family medicine residency program, advises a community health system, and is vice president of a multispecialty physician practice. In addition, Dr. Harmon is the medical director of a nonprofit hospice and volunteers as medical supervisor for his local school district.

Dr. Harmon received his undergraduate degree in physics and mathematics from the University of South Carolina, Columbia, and received his medical degree from the Medical University of South Carolina, Charleston. He completed a residency training program in family medicine with the U.S. Air Force at Eglin (Fla.) AFB, Florida.

During a 35-year military career, Dr. Harmon served as chief surgeon for the National Guard Bureau and assistant surgeon general for the U.S. Air Force. He retired from the military as a major general.

Dr. Harmon and his wife, Linda, have three married children and eight grandchildren.

Every now and then, a bucket of tomatoes or even a half bushel of corn shows up in the back of Dr. Harmon’s pickup truck, with a note on the window thanking him. “That really touches you deeply,” Dr. Harmon said. “I practice that type of medicine and I’m honored to be able to do that every day.”

jremaly@mdedge.com

Gerald E. Harmon, MD, a family physician in South Carolina whose patients sometimes leave produce in the back of his pickup truck, has practiced medicine during military deployments and during 15-hour shifts in the COVID-19 pandemic.

He has encountered “all manner of unexpected situations” and feels “more than prepared” to serve as president of the American Medical Association, he said.

At the same time, “I still find myself a little nervous about it,” Dr. Harmon said in an interview the day after he was sworn in as president. “I would be less than candid if I didn’t tell you that. I don’t mean intimidated. ... It’s almost like before an athletic event.”

Dr. Harmon was sworn in June 15 as the 176th president of the AMA during the virtual Special Meeting of the AMA House of Delegates. He follows Susan R. Bailey, MD, an allergist from Fort Worth, Tex., in leading the organization, which has more than 270,000 members.
 

Advancing health equity

During his inaugural address, Dr. Harmon discussed the pandemic and the AMA’s plan to advance health equity.

COVID-19 “has revealed enormous gaps in how we care for people and communities in America, demonstrated in the disproportionate impact of this pandemic on communities of color and in the weaknesses of our underfunded and underresourced public health infrastructure,” Dr. Harmon said.

He described medical professionals as being “at war against seemingly formidable adversaries,” including the pandemic, the effects of prolonged isolation on emotional and behavioral health, and political and racial tension. There is an “immense battle to rid our health system – and society – of health disparities and racism,” he said. “As we face these battles, we must remember that our actions as physicians and as leaders will have far-reaching consequences.”

Other challenges before the AMA include vaccinating patients, recovering from the ongoing pandemic, removing unnecessary obstacles to care, ending an epidemic of drug overdoses, improving outcomes for patients with chronic disease, incorporating technology in ways that benefit doctors and patients, and preparing future physicians, Dr. Harmon noted.

“We are going to embed the principles of equity and racial justice within the AMA and throughout our health system,” added Dr. Harmon, who has been an AMA board member since 2013 and served as board chair from 2017 to 2018. He highlighted the AMA’s strategic plan, released in May 2021, to advance health equity and justice and improve the quality of care for people who have been marginalized.

“Meaningful progress won’t happen until we, as doctors, recognize how profoundly systemic racism influences the health of our patients, and until we commit to taking action within our own spheres of influence,” Dr. Harmon said. “As a family doctor in a very diverse state, I have treated people from all backgrounds, and have seen inequities up close, inequities that understandably lead to distrust.”

Commenting in an interview on JAMA’s controversial tweet and podcast related to structural racism from earlier this year that have been deleted and removed from JAMA’s website, Dr. Harmon said, JAMA maintains editorial independence from the AMA, but that direction from a journal oversight committee could lead to changes at the journal that could help prevent similar incidents.

“We’ll support whatever the journal oversight committee suggests,” Dr. Harmon said.

“We had public statements about [the podcast]. I do think that we’ll be able to move very quickly in a stronger direction to address the issue of systemic racism,” Dr. Harmon said. “The AMA has acknowledged that it is a public health threat. We have acknowledged that it is ... a political description versus a biologic construct. So, I would anticipate that you’ll find changes.”

The AMA began developing its strategic plan to advance equity several years ago, Dr. Harmon noted. “I think we are very well poised to move forward and attack this enemy of health disparity.”
 

AAFP president supporting Dr. Harmon’s inauguration

Among those congratulating Dr. Harmon on his inauguration was Ada Stewart, MD, a fellow family physician and South Carolina resident who is the president of the American Academy of Family Physicians.

“We are very excited that family physician Dr. Gerald Harmon will serve as president of the AMA this coming year,” Dr. Stewart said. “Family medicine encompasses the very essence of medicine – treating the whole person, in the context of family, community, and each individual’s unique circumstances. As a family physician, Dr. Harmon brings important perspectives from the front lines of primary care. His commitment to health equity and evidence-based care, as well as his concern for practice sustainability and physician well-being, will serve him well as he leads the house of medicine into the future.”

Dr. Harmon has practiced as a family medicine specialist in Georgetown, S.C., for more than 30 years. He is a member of the clinical faculty for the Tidelands Health Medical University of South Carolina family medicine residency program, advises a community health system, and is vice president of a multispecialty physician practice. In addition, Dr. Harmon is the medical director of a nonprofit hospice and volunteers as medical supervisor for his local school district.

Dr. Harmon received his undergraduate degree in physics and mathematics from the University of South Carolina, Columbia, and received his medical degree from the Medical University of South Carolina, Charleston. He completed a residency training program in family medicine with the U.S. Air Force at Eglin (Fla.) AFB, Florida.

During a 35-year military career, Dr. Harmon served as chief surgeon for the National Guard Bureau and assistant surgeon general for the U.S. Air Force. He retired from the military as a major general.

Dr. Harmon and his wife, Linda, have three married children and eight grandchildren.

Every now and then, a bucket of tomatoes or even a half bushel of corn shows up in the back of Dr. Harmon’s pickup truck, with a note on the window thanking him. “That really touches you deeply,” Dr. Harmon said. “I practice that type of medicine and I’m honored to be able to do that every day.”

jremaly@mdedge.com

A high-profile, Washington-based consumer advocacy group is calling for the removal of the U.S. Food and Drug Administration’s acting commissioner and two other top officials, saying that the agency’s approval of the Alzheimer’s drug aducanumab (Aduhelm, Biogen) was “reckless.”

In a letter to the U.S. Department of Health and Human Services Secretary Xavier Becerra, Michael A. Carome, MD, director of Public Citizen’s Health Research Group, said: “The FDA’s decision to approve aducanumab for anyone with Alzheimer’s disease, regardless of severity, showed a stunning disregard for science, eviscerated the agency’s standards for approving new drugs, and ranks as one of the most irresponsible and egregious decisions in the history of the agency.”

Public Citizen urged Mr. Becerra to seek the resignations or the removal of the three FDA officials it said were most responsible for the approval – Acting FDA Commissioner Janet Woodcock, MD; Center for Drug Evaluation and Research (CDER) Director Patrizia Cavazzoni, MD; and CDER’s Office of Neuroscience Director Billy Dunn, MD.

“This decision is a disastrous blow to the agency’s credibility, public health, and the financial sustainability of the Medicare program,” writes Dr. Carome, noting that Biogen said it would charge $56,000 annually for the infusion.

Aaron Kesselheim, MD, one of three FDA Peripheral and Central Nervous System Drugs advisory committee members who resigned in the wake of the approval, agreed with Public Citizen that the agency’s credibility is suffering.

“The aducanumab decision is the worst example yet of the FDA’s movement away from its high standards,” Dr. Kesselheim, a professor of medicine at Harvard Medical School, Boston, and Harvard colleague Jerry Avorn, MD, wrote in the New York Times on June 15.

“As physicians, we know well that Alzheimer’s disease is a terrible condition,” they wrote. However, they added, “approving a drug that has such poor evidence that it works and causes such worrisome side effects is not the solution.”

In his resignation letter, Dr. Kesselheim said he had also been dismayed by the agency’s 2016 approval of eteplirsen (Exondys 51, Sarepta Therapeutics) for Duchenne muscular dystrophy. In both the eteplirsen and aducanumab approvals, the agency went against its advisers’ recommendations, Dr. Kesselheim said.
 

Advocates who backed approval decry cost

Aducanumab had a rocky road to approval but had unwavering backing from the Alzheimer’s Association and at least one other organization, UsAgainstAlzheimer’s.

The Alzheimer’s Association was particularly outspoken in its support and, in March, was accused of potential conflict of interest by Public Citizen and several neurologists because the association accepted at least $1.4 million from Biogen and its partner Eisai since fiscal year 2018.

The association applauded the FDA approval but, a few days later, expressed outrage over the $56,000-a-year price tag.

“This price is simply unacceptable,” the Alzheimer’s Association said in the statement. “For many, this price will pose an insurmountable barrier to access, it complicates and jeopardizes sustainable access to this treatment, and may further deepen issues of health equity,” the association said, adding, “We call on Biogen to change this price.”

UsAgainstAlzheimer’s also expressed concerns about access, even before it knew aducanumab’s price.  

“Shockingly, Medicare does not reimburse patients for the expensive PET scans important to determine whether someone is appropriate for this drug,” noted George Vradenburg, chairman and cofounder of the group, in a June 7 statement. “We intend to work with Biogen and Medicare to make access to this drug affordable for every American who needs it,” Mr. Vradenburg said.

Dr. Carome said the advocates’ complaints were hard to fathom.

“This should not have come as a surprise to anyone,” Dr. Carome said, adding that “it’s essentially the ballpark figure the company threw out weeks ago.”

“Fifty-six-thousand-dollars is particularly egregiously overpriced for a drug that doesn’t work,” Dr. Carome said. “If the [Alzheimer’s Association] truly finds this objectionable, hopefully they’ll stop accepting money from Biogen and its partner Eisai,” he added.

“The Alzheimer’s Association is recognizing that the genie is out of the bottle and that they are going to have trouble reining in the inevitable run-away costs,” said Mike Greicius, MD, MPH, associate professor of neurology at Stanford University’s Wu Tsai Neurosciences Institute, Stanford, California.

“In addition to the eye-popping annual cost that Biogen has invented, I hope the Alzheimer’s Association is also concerned about the dangerously loose and broad FDA labeling which does not require screening for amyloid-positivity and does not restrict use to the milder forms of disease studied in the Phase 3 trials,” Dr. Greicius said.

Another advocacy group, Patients For Affordable Drugs, commended the Alzheimer’s Association. Its statement “was nothing short of courageous, especially in light of the Alzheimer’s Association’s reliance on funding from drug corporations, including Biogen,” said David Mitchell, a cancer patient and founder of Patients For Affordable Drugs, in a statement.

Mr. Mitchell said his members “stand with the Alzheimer’s Association in its denunciation of the price set by Biogen” and called for a new law that would allow Medicare to negotiate drug prices.

A version of this article first appeared on Medscape.com.

A high-profile, Washington-based consumer advocacy group is calling for the removal of the U.S. Food and Drug Administration’s acting commissioner and two other top officials, saying that the agency’s approval of the Alzheimer’s drug aducanumab (Aduhelm, Biogen) was “reckless.”

In a letter to the U.S. Department of Health and Human Services Secretary Xavier Becerra, Michael A. Carome, MD, director of Public Citizen’s Health Research Group, said: “The FDA’s decision to approve aducanumab for anyone with Alzheimer’s disease, regardless of severity, showed a stunning disregard for science, eviscerated the agency’s standards for approving new drugs, and ranks as one of the most irresponsible and egregious decisions in the history of the agency.”

Public Citizen urged Mr. Becerra to seek the resignations or the removal of the three FDA officials it said were most responsible for the approval – Acting FDA Commissioner Janet Woodcock, MD; Center for Drug Evaluation and Research (CDER) Director Patrizia Cavazzoni, MD; and CDER’s Office of Neuroscience Director Billy Dunn, MD.

“This decision is a disastrous blow to the agency’s credibility, public health, and the financial sustainability of the Medicare program,” writes Dr. Carome, noting that Biogen said it would charge $56,000 annually for the infusion.

Aaron Kesselheim, MD, one of three FDA Peripheral and Central Nervous System Drugs advisory committee members who resigned in the wake of the approval, agreed with Public Citizen that the agency’s credibility is suffering.

“The aducanumab decision is the worst example yet of the FDA’s movement away from its high standards,” Dr. Kesselheim, a professor of medicine at Harvard Medical School, Boston, and Harvard colleague Jerry Avorn, MD, wrote in the New York Times on June 15.

“As physicians, we know well that Alzheimer’s disease is a terrible condition,” they wrote. However, they added, “approving a drug that has such poor evidence that it works and causes such worrisome side effects is not the solution.”

In his resignation letter, Dr. Kesselheim said he had also been dismayed by the agency’s 2016 approval of eteplirsen (Exondys 51, Sarepta Therapeutics) for Duchenne muscular dystrophy. In both the eteplirsen and aducanumab approvals, the agency went against its advisers’ recommendations, Dr. Kesselheim said.
 

Advocates who backed approval decry cost

Aducanumab had a rocky road to approval but had unwavering backing from the Alzheimer’s Association and at least one other organization, UsAgainstAlzheimer’s.

The Alzheimer’s Association was particularly outspoken in its support and, in March, was accused of potential conflict of interest by Public Citizen and several neurologists because the association accepted at least $1.4 million from Biogen and its partner Eisai since fiscal year 2018.

The association applauded the FDA approval but, a few days later, expressed outrage over the $56,000-a-year price tag.

“This price is simply unacceptable,” the Alzheimer’s Association said in the statement. “For many, this price will pose an insurmountable barrier to access, it complicates and jeopardizes sustainable access to this treatment, and may further deepen issues of health equity,” the association said, adding, “We call on Biogen to change this price.”

UsAgainstAlzheimer’s also expressed concerns about access, even before it knew aducanumab’s price.  

“Shockingly, Medicare does not reimburse patients for the expensive PET scans important to determine whether someone is appropriate for this drug,” noted George Vradenburg, chairman and cofounder of the group, in a June 7 statement. “We intend to work with Biogen and Medicare to make access to this drug affordable for every American who needs it,” Mr. Vradenburg said.

Dr. Carome said the advocates’ complaints were hard to fathom.

“This should not have come as a surprise to anyone,” Dr. Carome said, adding that “it’s essentially the ballpark figure the company threw out weeks ago.”

“Fifty-six-thousand-dollars is particularly egregiously overpriced for a drug that doesn’t work,” Dr. Carome said. “If the [Alzheimer’s Association] truly finds this objectionable, hopefully they’ll stop accepting money from Biogen and its partner Eisai,” he added.

“The Alzheimer’s Association is recognizing that the genie is out of the bottle and that they are going to have trouble reining in the inevitable run-away costs,” said Mike Greicius, MD, MPH, associate professor of neurology at Stanford University’s Wu Tsai Neurosciences Institute, Stanford, California.

“In addition to the eye-popping annual cost that Biogen has invented, I hope the Alzheimer’s Association is also concerned about the dangerously loose and broad FDA labeling which does not require screening for amyloid-positivity and does not restrict use to the milder forms of disease studied in the Phase 3 trials,” Dr. Greicius said.

Another advocacy group, Patients For Affordable Drugs, commended the Alzheimer’s Association. Its statement “was nothing short of courageous, especially in light of the Alzheimer’s Association’s reliance on funding from drug corporations, including Biogen,” said David Mitchell, a cancer patient and founder of Patients For Affordable Drugs, in a statement.

Mr. Mitchell said his members “stand with the Alzheimer’s Association in its denunciation of the price set by Biogen” and called for a new law that would allow Medicare to negotiate drug prices.

A version of this article first appeared on Medscape.com.

A high-profile, Washington-based consumer advocacy group is calling for the removal of the U.S. Food and Drug Administration’s acting commissioner and two other top officials, saying that the agency’s approval of the Alzheimer’s drug aducanumab (Aduhelm, Biogen) was “reckless.”

In a letter to the U.S. Department of Health and Human Services Secretary Xavier Becerra, Michael A. Carome, MD, director of Public Citizen’s Health Research Group, said: “The FDA’s decision to approve aducanumab for anyone with Alzheimer’s disease, regardless of severity, showed a stunning disregard for science, eviscerated the agency’s standards for approving new drugs, and ranks as one of the most irresponsible and egregious decisions in the history of the agency.”

Public Citizen urged Mr. Becerra to seek the resignations or the removal of the three FDA officials it said were most responsible for the approval – Acting FDA Commissioner Janet Woodcock, MD; Center for Drug Evaluation and Research (CDER) Director Patrizia Cavazzoni, MD; and CDER’s Office of Neuroscience Director Billy Dunn, MD.

“This decision is a disastrous blow to the agency’s credibility, public health, and the financial sustainability of the Medicare program,” writes Dr. Carome, noting that Biogen said it would charge $56,000 annually for the infusion.

Aaron Kesselheim, MD, one of three FDA Peripheral and Central Nervous System Drugs advisory committee members who resigned in the wake of the approval, agreed with Public Citizen that the agency’s credibility is suffering.

“The aducanumab decision is the worst example yet of the FDA’s movement away from its high standards,” Dr. Kesselheim, a professor of medicine at Harvard Medical School, Boston, and Harvard colleague Jerry Avorn, MD, wrote in the New York Times on June 15.

“As physicians, we know well that Alzheimer’s disease is a terrible condition,” they wrote. However, they added, “approving a drug that has such poor evidence that it works and causes such worrisome side effects is not the solution.”

In his resignation letter, Dr. Kesselheim said he had also been dismayed by the agency’s 2016 approval of eteplirsen (Exondys 51, Sarepta Therapeutics) for Duchenne muscular dystrophy. In both the eteplirsen and aducanumab approvals, the agency went against its advisers’ recommendations, Dr. Kesselheim said.
 

Advocates who backed approval decry cost

Aducanumab had a rocky road to approval but had unwavering backing from the Alzheimer’s Association and at least one other organization, UsAgainstAlzheimer’s.

The Alzheimer’s Association was particularly outspoken in its support and, in March, was accused of potential conflict of interest by Public Citizen and several neurologists because the association accepted at least $1.4 million from Biogen and its partner Eisai since fiscal year 2018.

The association applauded the FDA approval but, a few days later, expressed outrage over the $56,000-a-year price tag.

“This price is simply unacceptable,” the Alzheimer’s Association said in the statement. “For many, this price will pose an insurmountable barrier to access, it complicates and jeopardizes sustainable access to this treatment, and may further deepen issues of health equity,” the association said, adding, “We call on Biogen to change this price.”

UsAgainstAlzheimer’s also expressed concerns about access, even before it knew aducanumab’s price.  

“Shockingly, Medicare does not reimburse patients for the expensive PET scans important to determine whether someone is appropriate for this drug,” noted George Vradenburg, chairman and cofounder of the group, in a June 7 statement. “We intend to work with Biogen and Medicare to make access to this drug affordable for every American who needs it,” Mr. Vradenburg said.

Dr. Carome said the advocates’ complaints were hard to fathom.

“This should not have come as a surprise to anyone,” Dr. Carome said, adding that “it’s essentially the ballpark figure the company threw out weeks ago.”

“Fifty-six-thousand-dollars is particularly egregiously overpriced for a drug that doesn’t work,” Dr. Carome said. “If the [Alzheimer’s Association] truly finds this objectionable, hopefully they’ll stop accepting money from Biogen and its partner Eisai,” he added.

“The Alzheimer’s Association is recognizing that the genie is out of the bottle and that they are going to have trouble reining in the inevitable run-away costs,” said Mike Greicius, MD, MPH, associate professor of neurology at Stanford University’s Wu Tsai Neurosciences Institute, Stanford, California.

“In addition to the eye-popping annual cost that Biogen has invented, I hope the Alzheimer’s Association is also concerned about the dangerously loose and broad FDA labeling which does not require screening for amyloid-positivity and does not restrict use to the milder forms of disease studied in the Phase 3 trials,” Dr. Greicius said.

Another advocacy group, Patients For Affordable Drugs, commended the Alzheimer’s Association. Its statement “was nothing short of courageous, especially in light of the Alzheimer’s Association’s reliance on funding from drug corporations, including Biogen,” said David Mitchell, a cancer patient and founder of Patients For Affordable Drugs, in a statement.

Mr. Mitchell said his members “stand with the Alzheimer’s Association in its denunciation of the price set by Biogen” and called for a new law that would allow Medicare to negotiate drug prices.

A version of this article first appeared on Medscape.com.

Gradually, we are emerging from the chaos, isolation, and anxiety of COVID-19. As the Centers for Disease Control and Prevention adjusts its recommendations and vaccinations become more widely available, our communities are beginning to return to normalcy. We are encouraged to put aside our masks if vaccinated and rejoin society, to venture out with less hesitancy and anxiety. As family and friends reunite, memories of confusion, frustration, and fear are beginning to fade to black. Despite the prevailing belief that we should move on, look forward, and remember the past to safeguard our future, remnants of the pandemic remain.

shironosov/Getty Images

Unvaccinated individuals, notably children under the age of 12, are quite significant in number. The use of telehealth is now standard practice.

For several years, we were warned about the looming “mental health crisis.” The past year has demonstrated that a crisis no longer looms – it has arrived. Our patients can reveal the vulnerability COVID-19 has wrought – from the devastation of lives lost, supply shortages, loss of employment and financial stability – to a lack of access to computers and thereby, the risk of educational decline. Those factors, coupled with isolation and uncertainty about the future, have led to an influx of individuals with anxiety, depression, and other mood disorders seeking mental health treatment.
 

Doctors, others suffering

As result of a medical culture guided by the sacred oath to which care, compassion, and dedication held as true in ancient Greece as it does today, the focus centers on those around us – while signs of our own weariness are waved away as “a bad day.” Even though several support groups are readily available to offer a listening ear and mental health physicians who focus on the treatment of health care professionals are becoming more ubiquitous, the vestiges of past doctrine remain.

In this modern age of medical training, there is often as much sacrifice as there is attainment of knowledge. This philosophy is so ingrained that throughout training and practice one may come across colleagues experiencing an abundance of guilt when leave is needed for personal reasons. We are quick to recommend such steps for our patients, family, and friends, but hesitant to consider such for ourselves. Yet, of all the lessons this past year has wrought, the importance of mental health and self-care cannot be overstated. This raises the question: How do we incorporate wellness into our routines while navigating the complexity of medicine?

It is vital to accept our humanity as something not to repair, treat, or overcome but to understand. There is strength and power in vulnerability. If we do not perceive and validate this process within ourselves, how can we do so for others? In other words, the oxygen mask must be placed on us first before we can place it on anyone else – patients or otherwise.

Chiefly and above all else, the importance of identifying individual signs of stress is essential. Where do you hold tension? Are you prone to GI distress or headaches when taxed? Do you tend toward irritability, apathy, or exhaustion?

Once this is determined, it is important to assess your stress on a numerical scale, such as those used for pain. Are you a 5 or an 8? Finally, are there identifiable triggers or reliable alleviators? Is there a time of day or day of the week that is most difficult to manage? Can you anticipate potential stressors? Understanding your triggers, listening to your body, and practicing the language of self is the first step toward wellness.

Following introspection and observation, the next step is inventory. Take stock of your reserves. What replenishes? What depletes? What brings joy? What brings dread? Are there certain activities that mitigate stress? If so, how much time do they entail? Identify your number on a scale and associate that number with specific strategies or techniques. Remember that decompression for a 6 might be excessive for a 4. Furthermore, what is the duration of these feelings? Chronic stressors may incur gradual change verses sudden impact if acute. Through identifying personal signs, devising and using a scale, as well as escalating or de-escalating factors, individuals become more in tune with their bodies and therefore, more likely to intervene before burnout takes hold.

With this process well integrated, one can now consider stylized approaches for stress management. For example, those inclined toward mindfulness practices may find yoga, meditation, and relaxation exercises beneficial. Others may thrive on positive affirmations, gratitude, and thankfulness. While some might find relief in physical activity, be it strenuous or casual, the creative arts might appeal to those who find joy in painting, writing, or doing crafts. In addition, baking, reading, dancing, and/or listening to music might help lift stress.

Along with those discoveries, or in some cases, rediscoveries, basic needs such as dietary habits and nutrition, hydration, and sleep are vital toward emotional regulation, physiological homeostasis, and stress modulation. Remember HALT: Hungry, Angry, Lonely, Tired, Too hot, Too cold, Sad or Stressed. Those strategies are meant to guide self-care and highlight the importance of allowing time for self-awareness. Imagine yourself as if you are meeting a new patient. Establish rapport, identify symptoms, and explore options for treatment. When we give time to ourselves, we can give time more freely to others. With this in mind, try following the 5-minute wellness check that I formulated:

1. How am I feeling? What am I feeling?

2. Assess HALTS.

3. Identify the number on your scale.

4. Methods of quick de-escalation:

• Designate and schedule personal time.
• Write down daily goals.
• Repeat positive affirmations or write down words of gratitude.
• Use deep breathing exercises.
• Stretch or take a brief walk.
• Engage in mindfulness practices, such as meditation.

Once we develop a habit of monitoring, assessing, and practicing self-care, the process becomes more efficient and effective. Think of the way a seasoned attending can manage workflow with ease, compared with an intern. Recognizing signs and using these strategies routinely can become a quick daily measure of well-being.
 

Dr. Thomas is a board-certified adult psychiatrist with interests in chronic illness, women’s behavioral health, and minority mental health. She currently practices in North Kingstown and East Providence, R.I. Dr. Thomas has no conflicts of interest.

Gradually, we are emerging from the chaos, isolation, and anxiety of COVID-19. As the Centers for Disease Control and Prevention adjusts its recommendations and vaccinations become more widely available, our communities are beginning to return to normalcy. We are encouraged to put aside our masks if vaccinated and rejoin society, to venture out with less hesitancy and anxiety. As family and friends reunite, memories of confusion, frustration, and fear are beginning to fade to black. Despite the prevailing belief that we should move on, look forward, and remember the past to safeguard our future, remnants of the pandemic remain.

shironosov/Getty Images

Unvaccinated individuals, notably children under the age of 12, are quite significant in number. The use of telehealth is now standard practice.

For several years, we were warned about the looming “mental health crisis.” The past year has demonstrated that a crisis no longer looms – it has arrived. Our patients can reveal the vulnerability COVID-19 has wrought – from the devastation of lives lost, supply shortages, loss of employment and financial stability – to a lack of access to computers and thereby, the risk of educational decline. Those factors, coupled with isolation and uncertainty about the future, have led to an influx of individuals with anxiety, depression, and other mood disorders seeking mental health treatment.
 

Doctors, others suffering

As result of a medical culture guided by the sacred oath to which care, compassion, and dedication held as true in ancient Greece as it does today, the focus centers on those around us – while signs of our own weariness are waved away as “a bad day.” Even though several support groups are readily available to offer a listening ear and mental health physicians who focus on the treatment of health care professionals are becoming more ubiquitous, the vestiges of past doctrine remain.

In this modern age of medical training, there is often as much sacrifice as there is attainment of knowledge. This philosophy is so ingrained that throughout training and practice one may come across colleagues experiencing an abundance of guilt when leave is needed for personal reasons. We are quick to recommend such steps for our patients, family, and friends, but hesitant to consider such for ourselves. Yet, of all the lessons this past year has wrought, the importance of mental health and self-care cannot be overstated. This raises the question: How do we incorporate wellness into our routines while navigating the complexity of medicine?

It is vital to accept our humanity as something not to repair, treat, or overcome but to understand. There is strength and power in vulnerability. If we do not perceive and validate this process within ourselves, how can we do so for others? In other words, the oxygen mask must be placed on us first before we can place it on anyone else – patients or otherwise.

Chiefly and above all else, the importance of identifying individual signs of stress is essential. Where do you hold tension? Are you prone to GI distress or headaches when taxed? Do you tend toward irritability, apathy, or exhaustion?

Once this is determined, it is important to assess your stress on a numerical scale, such as those used for pain. Are you a 5 or an 8? Finally, are there identifiable triggers or reliable alleviators? Is there a time of day or day of the week that is most difficult to manage? Can you anticipate potential stressors? Understanding your triggers, listening to your body, and practicing the language of self is the first step toward wellness.

Following introspection and observation, the next step is inventory. Take stock of your reserves. What replenishes? What depletes? What brings joy? What brings dread? Are there certain activities that mitigate stress? If so, how much time do they entail? Identify your number on a scale and associate that number with specific strategies or techniques. Remember that decompression for a 6 might be excessive for a 4. Furthermore, what is the duration of these feelings? Chronic stressors may incur gradual change verses sudden impact if acute. Through identifying personal signs, devising and using a scale, as well as escalating or de-escalating factors, individuals become more in tune with their bodies and therefore, more likely to intervene before burnout takes hold.

With this process well integrated, one can now consider stylized approaches for stress management. For example, those inclined toward mindfulness practices may find yoga, meditation, and relaxation exercises beneficial. Others may thrive on positive affirmations, gratitude, and thankfulness. While some might find relief in physical activity, be it strenuous or casual, the creative arts might appeal to those who find joy in painting, writing, or doing crafts. In addition, baking, reading, dancing, and/or listening to music might help lift stress.

Along with those discoveries, or in some cases, rediscoveries, basic needs such as dietary habits and nutrition, hydration, and sleep are vital toward emotional regulation, physiological homeostasis, and stress modulation. Remember HALT: Hungry, Angry, Lonely, Tired, Too hot, Too cold, Sad or Stressed. Those strategies are meant to guide self-care and highlight the importance of allowing time for self-awareness. Imagine yourself as if you are meeting a new patient. Establish rapport, identify symptoms, and explore options for treatment. When we give time to ourselves, we can give time more freely to others. With this in mind, try following the 5-minute wellness check that I formulated:

1. How am I feeling? What am I feeling?

2. Assess HALTS.

3. Identify the number on your scale.

4. Methods of quick de-escalation:

• Designate and schedule personal time.
• Write down daily goals.
• Repeat positive affirmations or write down words of gratitude.
• Use deep breathing exercises.
• Stretch or take a brief walk.
• Engage in mindfulness practices, such as meditation.

Once we develop a habit of monitoring, assessing, and practicing self-care, the process becomes more efficient and effective. Think of the way a seasoned attending can manage workflow with ease, compared with an intern. Recognizing signs and using these strategies routinely can become a quick daily measure of well-being.
 

Dr. Thomas is a board-certified adult psychiatrist with interests in chronic illness, women’s behavioral health, and minority mental health. She currently practices in North Kingstown and East Providence, R.I. Dr. Thomas has no conflicts of interest.

Gradually, we are emerging from the chaos, isolation, and anxiety of COVID-19. As the Centers for Disease Control and Prevention adjusts its recommendations and vaccinations become more widely available, our communities are beginning to return to normalcy. We are encouraged to put aside our masks if vaccinated and rejoin society, to venture out with less hesitancy and anxiety. As family and friends reunite, memories of confusion, frustration, and fear are beginning to fade to black. Despite the prevailing belief that we should move on, look forward, and remember the past to safeguard our future, remnants of the pandemic remain.

shironosov/Getty Images

Unvaccinated individuals, notably children under the age of 12, are quite significant in number. The use of telehealth is now standard practice.

For several years, we were warned about the looming “mental health crisis.” The past year has demonstrated that a crisis no longer looms – it has arrived. Our patients can reveal the vulnerability COVID-19 has wrought – from the devastation of lives lost, supply shortages, loss of employment and financial stability – to a lack of access to computers and thereby, the risk of educational decline. Those factors, coupled with isolation and uncertainty about the future, have led to an influx of individuals with anxiety, depression, and other mood disorders seeking mental health treatment.
 

Doctors, others suffering

As result of a medical culture guided by the sacred oath to which care, compassion, and dedication held as true in ancient Greece as it does today, the focus centers on those around us – while signs of our own weariness are waved away as “a bad day.” Even though several support groups are readily available to offer a listening ear and mental health physicians who focus on the treatment of health care professionals are becoming more ubiquitous, the vestiges of past doctrine remain.

In this modern age of medical training, there is often as much sacrifice as there is attainment of knowledge. This philosophy is so ingrained that throughout training and practice one may come across colleagues experiencing an abundance of guilt when leave is needed for personal reasons. We are quick to recommend such steps for our patients, family, and friends, but hesitant to consider such for ourselves. Yet, of all the lessons this past year has wrought, the importance of mental health and self-care cannot be overstated. This raises the question: How do we incorporate wellness into our routines while navigating the complexity of medicine?

It is vital to accept our humanity as something not to repair, treat, or overcome but to understand. There is strength and power in vulnerability. If we do not perceive and validate this process within ourselves, how can we do so for others? In other words, the oxygen mask must be placed on us first before we can place it on anyone else – patients or otherwise.

Chiefly and above all else, the importance of identifying individual signs of stress is essential. Where do you hold tension? Are you prone to GI distress or headaches when taxed? Do you tend toward irritability, apathy, or exhaustion?

Once this is determined, it is important to assess your stress on a numerical scale, such as those used for pain. Are you a 5 or an 8? Finally, are there identifiable triggers or reliable alleviators? Is there a time of day or day of the week that is most difficult to manage? Can you anticipate potential stressors? Understanding your triggers, listening to your body, and practicing the language of self is the first step toward wellness.

Following introspection and observation, the next step is inventory. Take stock of your reserves. What replenishes? What depletes? What brings joy? What brings dread? Are there certain activities that mitigate stress? If so, how much time do they entail? Identify your number on a scale and associate that number with specific strategies or techniques. Remember that decompression for a 6 might be excessive for a 4. Furthermore, what is the duration of these feelings? Chronic stressors may incur gradual change verses sudden impact if acute. Through identifying personal signs, devising and using a scale, as well as escalating or de-escalating factors, individuals become more in tune with their bodies and therefore, more likely to intervene before burnout takes hold.

With this process well integrated, one can now consider stylized approaches for stress management. For example, those inclined toward mindfulness practices may find yoga, meditation, and relaxation exercises beneficial. Others may thrive on positive affirmations, gratitude, and thankfulness. While some might find relief in physical activity, be it strenuous or casual, the creative arts might appeal to those who find joy in painting, writing, or doing crafts. In addition, baking, reading, dancing, and/or listening to music might help lift stress.

Along with those discoveries, or in some cases, rediscoveries, basic needs such as dietary habits and nutrition, hydration, and sleep are vital toward emotional regulation, physiological homeostasis, and stress modulation. Remember HALT: Hungry, Angry, Lonely, Tired, Too hot, Too cold, Sad or Stressed. Those strategies are meant to guide self-care and highlight the importance of allowing time for self-awareness. Imagine yourself as if you are meeting a new patient. Establish rapport, identify symptoms, and explore options for treatment. When we give time to ourselves, we can give time more freely to others. With this in mind, try following the 5-minute wellness check that I formulated:

1. How am I feeling? What am I feeling?

2. Assess HALTS.

3. Identify the number on your scale.

4. Methods of quick de-escalation:

• Designate and schedule personal time.
• Write down daily goals.
• Repeat positive affirmations or write down words of gratitude.
• Use deep breathing exercises.
• Stretch or take a brief walk.
• Engage in mindfulness practices, such as meditation.

Once we develop a habit of monitoring, assessing, and practicing self-care, the process becomes more efficient and effective. Think of the way a seasoned attending can manage workflow with ease, compared with an intern. Recognizing signs and using these strategies routinely can become a quick daily measure of well-being.
 

Dr. Thomas is a board-certified adult psychiatrist with interests in chronic illness, women’s behavioral health, and minority mental health. She currently practices in North Kingstown and East Providence, R.I. Dr. Thomas has no conflicts of interest.