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Understanding the neuroscience of narcissism
Editor’s Note: The study covered in this summary was published on ResearchSquare.com as a preprint and has not yet been peer reviewed.
Key takeaway
Why this matters
The cognitive features and phenotypic diversity of narcissism subtypes are partially unknown.
This study integrates both grandiose and vulnerable narcissism into a common framework with cognitive components connected to these traits.
Study design
This study enrolled 478 participants (397 female and 4 did not reveal their gender).
The average age of participants was 35 years (standard deviation, 14.97), with a range of 18-76 years.
A 25-item version of the Narcissistic Personality Inventory (NPI), a 40-item self-report measure of narcissism traits, was used to assess the level of authority, grandiose exhibitionism, and entitlement/exploitativeness characteristics of study participants.
The Maladaptive Covert Narcissism Scale, an expanded version of the 23-item self-report Hypersensitive Narcissism Scale, was used to assess the level of hypersensitivity, vulnerability, and entitlement of study participants.
The Rosenberg Self-Esteem Scale, a 10-item self-report scale, was used to assess the level of self-esteem of study participants.
The Young Schema Questionnaire is a 244-item measure of 19 different maladaptive schemas and was used to observe Emotional Deprivation, Vulnerability to Harm and Illness, and Entitlement schemas of study participants.
The Empathizing Quotient is a self-report measure and was used to assess the emotional intelligence of study participants.
Key results
Moderate correlation between grandiose and vulnerable narcissism and the Entitlement schema was observed.
A moderate/strong connection was observed between vulnerable narcissism and the Vulnerability to Harm and Illness schema and a moderate connection with the Emotional Deprivation schema.
No significant correlation was observed between grandiose narcissism and the Emotional Deprivation schema.
A moderate, negative correlation between vulnerable narcissism and emotional skills was observed.
A positive, weak connection between grandiose narcissism and self-esteem; and a negative, moderate connection between vulnerable narcissism and self-esteem were observed.
Gender and age were associated with empathic skills, and age was weakly/moderately connected with self-esteem and vulnerable narcissism.
Limitations
This was a cross-sectional analysis investigating a temporally specific state of personality and cognitive functioning.
The gender ratio was shifted toward women in this study.
Conclusions drawn from connections between observed components are interchangeable and cause/effect connections cannot be discerned.
Disclosures
The study was supported by the National Research, Development, and Innovation Office (Grant No. NRDI–138040) and by the Human Resource Development Operational Program – Comprehensive developments at the University of Pécs for the implementation of intelligent specialization (EFOP-3.6.1-16-2016-00004). First author Dorian Vida’s work was supported by the Collegium Talentum Programme of Hungary. None of the authors disclosed any competing interests.
This is a summary of a preprint research study, “In the mind of Narcissus: the mediating role of emotional regulation in the emergence of distorted cognitions,” written by Dorian Vida from the University of Pécs, Hungary and colleagues on ResearchSquare.com. This study has not yet been peer reviewed. The full text of the study can be found on ResearchSquare.com.
A version of this article first appeared on Medscape.com
Editor’s Note: The study covered in this summary was published on ResearchSquare.com as a preprint and has not yet been peer reviewed.
Key takeaway
Why this matters
The cognitive features and phenotypic diversity of narcissism subtypes are partially unknown.
This study integrates both grandiose and vulnerable narcissism into a common framework with cognitive components connected to these traits.
Study design
This study enrolled 478 participants (397 female and 4 did not reveal their gender).
The average age of participants was 35 years (standard deviation, 14.97), with a range of 18-76 years.
A 25-item version of the Narcissistic Personality Inventory (NPI), a 40-item self-report measure of narcissism traits, was used to assess the level of authority, grandiose exhibitionism, and entitlement/exploitativeness characteristics of study participants.
The Maladaptive Covert Narcissism Scale, an expanded version of the 23-item self-report Hypersensitive Narcissism Scale, was used to assess the level of hypersensitivity, vulnerability, and entitlement of study participants.
The Rosenberg Self-Esteem Scale, a 10-item self-report scale, was used to assess the level of self-esteem of study participants.
The Young Schema Questionnaire is a 244-item measure of 19 different maladaptive schemas and was used to observe Emotional Deprivation, Vulnerability to Harm and Illness, and Entitlement schemas of study participants.
The Empathizing Quotient is a self-report measure and was used to assess the emotional intelligence of study participants.
Key results
Moderate correlation between grandiose and vulnerable narcissism and the Entitlement schema was observed.
A moderate/strong connection was observed between vulnerable narcissism and the Vulnerability to Harm and Illness schema and a moderate connection with the Emotional Deprivation schema.
No significant correlation was observed between grandiose narcissism and the Emotional Deprivation schema.
A moderate, negative correlation between vulnerable narcissism and emotional skills was observed.
A positive, weak connection between grandiose narcissism and self-esteem; and a negative, moderate connection between vulnerable narcissism and self-esteem were observed.
Gender and age were associated with empathic skills, and age was weakly/moderately connected with self-esteem and vulnerable narcissism.
Limitations
This was a cross-sectional analysis investigating a temporally specific state of personality and cognitive functioning.
The gender ratio was shifted toward women in this study.
Conclusions drawn from connections between observed components are interchangeable and cause/effect connections cannot be discerned.
Disclosures
The study was supported by the National Research, Development, and Innovation Office (Grant No. NRDI–138040) and by the Human Resource Development Operational Program – Comprehensive developments at the University of Pécs for the implementation of intelligent specialization (EFOP-3.6.1-16-2016-00004). First author Dorian Vida’s work was supported by the Collegium Talentum Programme of Hungary. None of the authors disclosed any competing interests.
This is a summary of a preprint research study, “In the mind of Narcissus: the mediating role of emotional regulation in the emergence of distorted cognitions,” written by Dorian Vida from the University of Pécs, Hungary and colleagues on ResearchSquare.com. This study has not yet been peer reviewed. The full text of the study can be found on ResearchSquare.com.
A version of this article first appeared on Medscape.com
Editor’s Note: The study covered in this summary was published on ResearchSquare.com as a preprint and has not yet been peer reviewed.
Key takeaway
Why this matters
The cognitive features and phenotypic diversity of narcissism subtypes are partially unknown.
This study integrates both grandiose and vulnerable narcissism into a common framework with cognitive components connected to these traits.
Study design
This study enrolled 478 participants (397 female and 4 did not reveal their gender).
The average age of participants was 35 years (standard deviation, 14.97), with a range of 18-76 years.
A 25-item version of the Narcissistic Personality Inventory (NPI), a 40-item self-report measure of narcissism traits, was used to assess the level of authority, grandiose exhibitionism, and entitlement/exploitativeness characteristics of study participants.
The Maladaptive Covert Narcissism Scale, an expanded version of the 23-item self-report Hypersensitive Narcissism Scale, was used to assess the level of hypersensitivity, vulnerability, and entitlement of study participants.
The Rosenberg Self-Esteem Scale, a 10-item self-report scale, was used to assess the level of self-esteem of study participants.
The Young Schema Questionnaire is a 244-item measure of 19 different maladaptive schemas and was used to observe Emotional Deprivation, Vulnerability to Harm and Illness, and Entitlement schemas of study participants.
The Empathizing Quotient is a self-report measure and was used to assess the emotional intelligence of study participants.
Key results
Moderate correlation between grandiose and vulnerable narcissism and the Entitlement schema was observed.
A moderate/strong connection was observed between vulnerable narcissism and the Vulnerability to Harm and Illness schema and a moderate connection with the Emotional Deprivation schema.
No significant correlation was observed between grandiose narcissism and the Emotional Deprivation schema.
A moderate, negative correlation between vulnerable narcissism and emotional skills was observed.
A positive, weak connection between grandiose narcissism and self-esteem; and a negative, moderate connection between vulnerable narcissism and self-esteem were observed.
Gender and age were associated with empathic skills, and age was weakly/moderately connected with self-esteem and vulnerable narcissism.
Limitations
This was a cross-sectional analysis investigating a temporally specific state of personality and cognitive functioning.
The gender ratio was shifted toward women in this study.
Conclusions drawn from connections between observed components are interchangeable and cause/effect connections cannot be discerned.
Disclosures
The study was supported by the National Research, Development, and Innovation Office (Grant No. NRDI–138040) and by the Human Resource Development Operational Program – Comprehensive developments at the University of Pécs for the implementation of intelligent specialization (EFOP-3.6.1-16-2016-00004). First author Dorian Vida’s work was supported by the Collegium Talentum Programme of Hungary. None of the authors disclosed any competing interests.
This is a summary of a preprint research study, “In the mind of Narcissus: the mediating role of emotional regulation in the emergence of distorted cognitions,” written by Dorian Vida from the University of Pécs, Hungary and colleagues on ResearchSquare.com. This study has not yet been peer reviewed. The full text of the study can be found on ResearchSquare.com.
A version of this article first appeared on Medscape.com
Hypertension heightens risk for severe COVID-19, even in the fully vaxxed
Adults with hypertension who were vaccinated for COVID-19 with at least one booster were more than twice as likely as vaccinated and boosted individuals without hypertension to be hospitalized for severe COVID-19, according to data from more than 900 individuals.
“We were surprised to learn that many people who were hospitalized with COVID-19 had hypertension and no other risk factors,” said Susan Cheng, MD, MPH, director of the Institute for Research on Healthy Aging in the department of cardiology at the Smidt Heart Institute, Los Angeles, and a senior author of the study. “This is concerning when you consider that almost half of American adults have high blood pressure.”
COVID-19 vaccines demonstrated ability to reduce death and some of the most severe side effects from the infection in the early stages of the pandemic. Although the Omicron surge prompted recommendations for a third mRNA vaccine dose, “a proportion of individuals who received three mRNA vaccine doses still required hospitalization for COVID-19 during the Omicron surge,” and the characteristics associated with severe illness in vaccinated and boosted patients have not been explored, Joseph Ebinger, MD, of Cedars-Sinai Medical Center, Los Angeles, and colleagues wrote.
Previous research has shown an association between high blood pressure an increased risk for developing severe COVID-19 compared to several other chronic health conditions, including kidney disease, type 2 diabetes, chronic obstructive pulmonary disease, and heart failure, the researchers noted.
In a study published in Hypertension, the researchers identified 912 adults who received at least three doses of mRNA COVID-19 vaccine and were later diagnosed with COVID-19 during the surge in infections from the Omicron variant between December 2021 and April 2022.
A total of 145 of the individuals were hospitalized (16%); of these, 125 (86%) had hypertension.
Patients with hypertension were the most likely to be hospitalized, with an odds ratio of 2.9. In addition to high blood pressure, factors including older age (OR, 1.3), chronic kidney disease (OR, 2.2), prior myocardial infarction or heart failure (OR, 2.2), and longer time since the last vaccination and COVID-19 infection were associated with increased risk of hospitalization in a multivariate analysis.
However, the increased risk of severe illness and hospitalization associated with high blood pressure persisted, with an OR of 2.6, in the absence of comorbid conditions such as type 2 diabetes, kidney disease, and heart failure, the researchers emphasized.
“Although the mechanism for hypertension-associated COVID-19 risk remains unclear, prior studies have identified delayed SARS-CoV-2 viral clearance and prolonged inflammatory response among hypertensive patients, which may contribute to greater disease severity,” they wrote.
The findings were limited by several factors, including the use of data from a single center and lack of information on which Omicron variants and subvariants were behind the infections, the researchers noted.
However, the results highlight the need for more research on how to reduce the risks of severe COVID-19 in vulnerable populations, and on the mechanism for a potential connection between high blood pressure and severe COVID-19, they said.
Given the high prevalence of hypertension worldwide, increased understanding of the hypertension-specific risks and identification of individual and population-level risk reduction strategies will be important to the transition of COVID-19 from pandemic to endemic, they concluded.
Omicron changes the game
“When the pandemic initially started, many conditions were seen to increase risk for more severe COVID illness, and hypertension was one of those factors – and then things changed,” lead author Dr. Ebinger said in an interview. “First, vaccines arrived on the scene and substantially reduced risk of severe COVID for everyone who received them. Second, Omicron arrived and, while more transmissible, this variant has been less likely to cause severe COVID. On the one hand, we have vaccines and boosters that we want to think of as ‘the great equalizer’ when it comes to preexisting conditions. On the other hand, we have a dominant set of SARS-CoV-2 subvariants that seem less virulent in most people.
“Taken together, we have been hoping and even assuming that we have been doing pretty well with minimizing risks. Unfortunately, our study results indicate this is not exactly the case,” he said.
“Although vaccines and boosters appear to have equalized or minimized the risks of severe COVID for some people, this has not happened for others – even in the setting of the milder Omicron variant. Of individuals who were fully vaccinated and boosted, having hypertension increased the odds of needing to be hospitalized after getting infected with Omicron by 2.6-fold, even when accounting for or in the absence of having any major chronic disease that might otherwise predispose to more severe COVID-19 illness,” Dr. Ebinger added.
“So, while the originally seen risks of having obesity or diabetes seem to have been minimized during this current era of pandemic, the risk of having hypertension has persisted. We found this both surprising and concerning, because hypertension is very common and present in over half of people over age 50.”
Surprisingly, “we found that a fair number of people, even after being fully vaccinated plus a having gotten a booster, will not only catch Omicron but get sick enough to need hospital care,” Dr. Ebinger emphasized. “Moreover, it is not just older adults with major comorbid conditions who are vulnerable. Our data show that this can happen to an adult of any age and especially if a person has only hypertension and otherwise no major chronic disease.”
The first takeaway message for clinicians at this time is to raise awareness, Dr. Ebinger stressed in the interview. “We need to raise understanding around the fact that receiving three doses of vaccine may not prevent severe COVID-19 illness in everyone, even when the circulating viral variant is presumed to be causing only mild disease in most people. Moreover, the people who are most at risk are not whom we might think they are. They are not the sickest of the sick. They include people who might not have major conditions such as heart disease or kidney disease, but they do have hypertension.”
Second, “we need more research to understand out why there is this link between hypertension and excess risk for the more severe forms of COVID-19, despite it arising from a supposedly milder variant,” said Dr. Ebinger.
“Third, we need to determine how to reduce these risks, whether through more tailored vaccine regimens or novel therapeutics or a combination approach,” he said.
Looking ahead, “the biological mechanism underpinning the association between hypertension and severe COVID-19 remains underexplored. Future work should focus on understanding the factors linking hypertension to severe COVID-19, as this may elucidate both information on how SARS-CoV-2 effects the body and potential targets for intervention,” Dr. Ebinger added.
The study was supported in part by Cedars-Sinai Medical Center, the Erika J. Glazer Family Foundation and the National Institutes of Health. The researchers had no financial conflicts to disclose.
Adults with hypertension who were vaccinated for COVID-19 with at least one booster were more than twice as likely as vaccinated and boosted individuals without hypertension to be hospitalized for severe COVID-19, according to data from more than 900 individuals.
“We were surprised to learn that many people who were hospitalized with COVID-19 had hypertension and no other risk factors,” said Susan Cheng, MD, MPH, director of the Institute for Research on Healthy Aging in the department of cardiology at the Smidt Heart Institute, Los Angeles, and a senior author of the study. “This is concerning when you consider that almost half of American adults have high blood pressure.”
COVID-19 vaccines demonstrated ability to reduce death and some of the most severe side effects from the infection in the early stages of the pandemic. Although the Omicron surge prompted recommendations for a third mRNA vaccine dose, “a proportion of individuals who received three mRNA vaccine doses still required hospitalization for COVID-19 during the Omicron surge,” and the characteristics associated with severe illness in vaccinated and boosted patients have not been explored, Joseph Ebinger, MD, of Cedars-Sinai Medical Center, Los Angeles, and colleagues wrote.
Previous research has shown an association between high blood pressure an increased risk for developing severe COVID-19 compared to several other chronic health conditions, including kidney disease, type 2 diabetes, chronic obstructive pulmonary disease, and heart failure, the researchers noted.
In a study published in Hypertension, the researchers identified 912 adults who received at least three doses of mRNA COVID-19 vaccine and were later diagnosed with COVID-19 during the surge in infections from the Omicron variant between December 2021 and April 2022.
A total of 145 of the individuals were hospitalized (16%); of these, 125 (86%) had hypertension.
Patients with hypertension were the most likely to be hospitalized, with an odds ratio of 2.9. In addition to high blood pressure, factors including older age (OR, 1.3), chronic kidney disease (OR, 2.2), prior myocardial infarction or heart failure (OR, 2.2), and longer time since the last vaccination and COVID-19 infection were associated with increased risk of hospitalization in a multivariate analysis.
However, the increased risk of severe illness and hospitalization associated with high blood pressure persisted, with an OR of 2.6, in the absence of comorbid conditions such as type 2 diabetes, kidney disease, and heart failure, the researchers emphasized.
“Although the mechanism for hypertension-associated COVID-19 risk remains unclear, prior studies have identified delayed SARS-CoV-2 viral clearance and prolonged inflammatory response among hypertensive patients, which may contribute to greater disease severity,” they wrote.
The findings were limited by several factors, including the use of data from a single center and lack of information on which Omicron variants and subvariants were behind the infections, the researchers noted.
However, the results highlight the need for more research on how to reduce the risks of severe COVID-19 in vulnerable populations, and on the mechanism for a potential connection between high blood pressure and severe COVID-19, they said.
Given the high prevalence of hypertension worldwide, increased understanding of the hypertension-specific risks and identification of individual and population-level risk reduction strategies will be important to the transition of COVID-19 from pandemic to endemic, they concluded.
Omicron changes the game
“When the pandemic initially started, many conditions were seen to increase risk for more severe COVID illness, and hypertension was one of those factors – and then things changed,” lead author Dr. Ebinger said in an interview. “First, vaccines arrived on the scene and substantially reduced risk of severe COVID for everyone who received them. Second, Omicron arrived and, while more transmissible, this variant has been less likely to cause severe COVID. On the one hand, we have vaccines and boosters that we want to think of as ‘the great equalizer’ when it comes to preexisting conditions. On the other hand, we have a dominant set of SARS-CoV-2 subvariants that seem less virulent in most people.
“Taken together, we have been hoping and even assuming that we have been doing pretty well with minimizing risks. Unfortunately, our study results indicate this is not exactly the case,” he said.
“Although vaccines and boosters appear to have equalized or minimized the risks of severe COVID for some people, this has not happened for others – even in the setting of the milder Omicron variant. Of individuals who were fully vaccinated and boosted, having hypertension increased the odds of needing to be hospitalized after getting infected with Omicron by 2.6-fold, even when accounting for or in the absence of having any major chronic disease that might otherwise predispose to more severe COVID-19 illness,” Dr. Ebinger added.
“So, while the originally seen risks of having obesity or diabetes seem to have been minimized during this current era of pandemic, the risk of having hypertension has persisted. We found this both surprising and concerning, because hypertension is very common and present in over half of people over age 50.”
Surprisingly, “we found that a fair number of people, even after being fully vaccinated plus a having gotten a booster, will not only catch Omicron but get sick enough to need hospital care,” Dr. Ebinger emphasized. “Moreover, it is not just older adults with major comorbid conditions who are vulnerable. Our data show that this can happen to an adult of any age and especially if a person has only hypertension and otherwise no major chronic disease.”
The first takeaway message for clinicians at this time is to raise awareness, Dr. Ebinger stressed in the interview. “We need to raise understanding around the fact that receiving three doses of vaccine may not prevent severe COVID-19 illness in everyone, even when the circulating viral variant is presumed to be causing only mild disease in most people. Moreover, the people who are most at risk are not whom we might think they are. They are not the sickest of the sick. They include people who might not have major conditions such as heart disease or kidney disease, but they do have hypertension.”
Second, “we need more research to understand out why there is this link between hypertension and excess risk for the more severe forms of COVID-19, despite it arising from a supposedly milder variant,” said Dr. Ebinger.
“Third, we need to determine how to reduce these risks, whether through more tailored vaccine regimens or novel therapeutics or a combination approach,” he said.
Looking ahead, “the biological mechanism underpinning the association between hypertension and severe COVID-19 remains underexplored. Future work should focus on understanding the factors linking hypertension to severe COVID-19, as this may elucidate both information on how SARS-CoV-2 effects the body and potential targets for intervention,” Dr. Ebinger added.
The study was supported in part by Cedars-Sinai Medical Center, the Erika J. Glazer Family Foundation and the National Institutes of Health. The researchers had no financial conflicts to disclose.
Adults with hypertension who were vaccinated for COVID-19 with at least one booster were more than twice as likely as vaccinated and boosted individuals without hypertension to be hospitalized for severe COVID-19, according to data from more than 900 individuals.
“We were surprised to learn that many people who were hospitalized with COVID-19 had hypertension and no other risk factors,” said Susan Cheng, MD, MPH, director of the Institute for Research on Healthy Aging in the department of cardiology at the Smidt Heart Institute, Los Angeles, and a senior author of the study. “This is concerning when you consider that almost half of American adults have high blood pressure.”
COVID-19 vaccines demonstrated ability to reduce death and some of the most severe side effects from the infection in the early stages of the pandemic. Although the Omicron surge prompted recommendations for a third mRNA vaccine dose, “a proportion of individuals who received three mRNA vaccine doses still required hospitalization for COVID-19 during the Omicron surge,” and the characteristics associated with severe illness in vaccinated and boosted patients have not been explored, Joseph Ebinger, MD, of Cedars-Sinai Medical Center, Los Angeles, and colleagues wrote.
Previous research has shown an association between high blood pressure an increased risk for developing severe COVID-19 compared to several other chronic health conditions, including kidney disease, type 2 diabetes, chronic obstructive pulmonary disease, and heart failure, the researchers noted.
In a study published in Hypertension, the researchers identified 912 adults who received at least three doses of mRNA COVID-19 vaccine and were later diagnosed with COVID-19 during the surge in infections from the Omicron variant between December 2021 and April 2022.
A total of 145 of the individuals were hospitalized (16%); of these, 125 (86%) had hypertension.
Patients with hypertension were the most likely to be hospitalized, with an odds ratio of 2.9. In addition to high blood pressure, factors including older age (OR, 1.3), chronic kidney disease (OR, 2.2), prior myocardial infarction or heart failure (OR, 2.2), and longer time since the last vaccination and COVID-19 infection were associated with increased risk of hospitalization in a multivariate analysis.
However, the increased risk of severe illness and hospitalization associated with high blood pressure persisted, with an OR of 2.6, in the absence of comorbid conditions such as type 2 diabetes, kidney disease, and heart failure, the researchers emphasized.
“Although the mechanism for hypertension-associated COVID-19 risk remains unclear, prior studies have identified delayed SARS-CoV-2 viral clearance and prolonged inflammatory response among hypertensive patients, which may contribute to greater disease severity,” they wrote.
The findings were limited by several factors, including the use of data from a single center and lack of information on which Omicron variants and subvariants were behind the infections, the researchers noted.
However, the results highlight the need for more research on how to reduce the risks of severe COVID-19 in vulnerable populations, and on the mechanism for a potential connection between high blood pressure and severe COVID-19, they said.
Given the high prevalence of hypertension worldwide, increased understanding of the hypertension-specific risks and identification of individual and population-level risk reduction strategies will be important to the transition of COVID-19 from pandemic to endemic, they concluded.
Omicron changes the game
“When the pandemic initially started, many conditions were seen to increase risk for more severe COVID illness, and hypertension was one of those factors – and then things changed,” lead author Dr. Ebinger said in an interview. “First, vaccines arrived on the scene and substantially reduced risk of severe COVID for everyone who received them. Second, Omicron arrived and, while more transmissible, this variant has been less likely to cause severe COVID. On the one hand, we have vaccines and boosters that we want to think of as ‘the great equalizer’ when it comes to preexisting conditions. On the other hand, we have a dominant set of SARS-CoV-2 subvariants that seem less virulent in most people.
“Taken together, we have been hoping and even assuming that we have been doing pretty well with minimizing risks. Unfortunately, our study results indicate this is not exactly the case,” he said.
“Although vaccines and boosters appear to have equalized or minimized the risks of severe COVID for some people, this has not happened for others – even in the setting of the milder Omicron variant. Of individuals who were fully vaccinated and boosted, having hypertension increased the odds of needing to be hospitalized after getting infected with Omicron by 2.6-fold, even when accounting for or in the absence of having any major chronic disease that might otherwise predispose to more severe COVID-19 illness,” Dr. Ebinger added.
“So, while the originally seen risks of having obesity or diabetes seem to have been minimized during this current era of pandemic, the risk of having hypertension has persisted. We found this both surprising and concerning, because hypertension is very common and present in over half of people over age 50.”
Surprisingly, “we found that a fair number of people, even after being fully vaccinated plus a having gotten a booster, will not only catch Omicron but get sick enough to need hospital care,” Dr. Ebinger emphasized. “Moreover, it is not just older adults with major comorbid conditions who are vulnerable. Our data show that this can happen to an adult of any age and especially if a person has only hypertension and otherwise no major chronic disease.”
The first takeaway message for clinicians at this time is to raise awareness, Dr. Ebinger stressed in the interview. “We need to raise understanding around the fact that receiving three doses of vaccine may not prevent severe COVID-19 illness in everyone, even when the circulating viral variant is presumed to be causing only mild disease in most people. Moreover, the people who are most at risk are not whom we might think they are. They are not the sickest of the sick. They include people who might not have major conditions such as heart disease or kidney disease, but they do have hypertension.”
Second, “we need more research to understand out why there is this link between hypertension and excess risk for the more severe forms of COVID-19, despite it arising from a supposedly milder variant,” said Dr. Ebinger.
“Third, we need to determine how to reduce these risks, whether through more tailored vaccine regimens or novel therapeutics or a combination approach,” he said.
Looking ahead, “the biological mechanism underpinning the association between hypertension and severe COVID-19 remains underexplored. Future work should focus on understanding the factors linking hypertension to severe COVID-19, as this may elucidate both information on how SARS-CoV-2 effects the body and potential targets for intervention,” Dr. Ebinger added.
The study was supported in part by Cedars-Sinai Medical Center, the Erika J. Glazer Family Foundation and the National Institutes of Health. The researchers had no financial conflicts to disclose.
FROM HYPERTENSION
A Special Supplement on Hot Topics in Primary Care 2022
Hot Topics in Primary Care 2022 is a resource that explores the newest developments in primary care topics that impact your daily clinical practice.
Click on the link below to access the entire supplement. You can also click on the video panes below to view brief summaries of individual chapters. Titles above the video panes link directly to each article.
- A Paradigm Shift for Asthma Care
- Common Questions on Continuous Glucose Monitoring in Primary Care
- Detecting and Managing ASCVD in Women: A Focus on Statins
- Improving Detection and Management of Anemia in CKD
- OTC Analgesics vs Opioids for Pain Management
- Practical Considerations for Use of Insulin/Glucagon-Like Peptide 1 Receptor Agonist Combinations in Older Adults With Type 2 Diabetes
- Practical Screening for Islet Autoantibodies: The Time Has Come
- Reducing Thrombotic Risk From Polyvascular Disease in Primary Care
- Strategies to Improve Outcomes in COPD
- The Evolving Landscape of ASCVD Risk Among Patients With HIV
- The New Face of Preadolescent and Adolescent Acne: Beyond the Guidelines
- The Role of Eggs in Healthy Diets
- Update on the Gut Microbiome for the Primary Care Clinician
- Updates in the Management of Mild Cognitive Impairment and Alzheimer Disease
- Use of SGLT-2 Inhibitors for Chronic Kidney Disease in Primary Care
This supplement offers the opportunity to earn a total of 4 continuing medical education (CME) credits. Credit is awarded for successful completion of the evaluation after reading the article. The links can be found within the supplement on the first page of each article where CME credits are offered.
Click here to read Hot Topics in Primary Care 2022
This supplement to The Journal of Family Practice was sponsored by the Primary Care Education Consortium and Primary Care Metabolic Group.
Check out these short video segments, which were prepared by the supplement authors and summarize the individual articles.
The title above each video links to the related article.
A Paradigm Shift for Asthma Care, Njira Lugogo, MD; Neil Skolnik, MD; Yihui Jiang, DO
Common Questions on Continuous Glucose Monitoring in Primary Care, Eden M. Miller, DO
Detecting and Managing ASCVD in Women: A Focus on Statins, Pam Kushner, MD
Improving Detection and Management of Anemia in CKD, Steven Fishbane, MD; Stephen Brunton, MD, FAAFP
OTC Analgesics vs Opioids for Pain Management, Gary M. Ruoff, MD
Practical Screening for Islet Autoantibodies: The Time Has Come, Timothy Reid, MD
Reducing Thrombotic Risk From Polyvascular Disease in Primary Care, Stephen Brunton, MD, FAAFP
Strategies to Improve Outcomes in COPD, Barbara Yawn, MD, MSc, FAAFP
The Evolving Landscape of ASCVD Risk Among Patients With HIV, Carlos Malvestutto, MD, MPH
The Role of Eggs in Healthy Diets, Maria Luz Fernandez, PhD
Update on the Gut Microbiome for the Primary Care Clinician, Eden M. Miller, DO
Updates in the Management of Mild Cognitive Impairment and Alzheimer Disease, Gary Small, MD
Use of SGLT-2 Inhibitors for Chronic Kidney Disease in Primary Care, George Bakris, MD
Hot Topics in Primary Care 2022 is a resource that explores the newest developments in primary care topics that impact your daily clinical practice.
Click on the link below to access the entire supplement. You can also click on the video panes below to view brief summaries of individual chapters. Titles above the video panes link directly to each article.
- A Paradigm Shift for Asthma Care
- Common Questions on Continuous Glucose Monitoring in Primary Care
- Detecting and Managing ASCVD in Women: A Focus on Statins
- Improving Detection and Management of Anemia in CKD
- OTC Analgesics vs Opioids for Pain Management
- Practical Considerations for Use of Insulin/Glucagon-Like Peptide 1 Receptor Agonist Combinations in Older Adults With Type 2 Diabetes
- Practical Screening for Islet Autoantibodies: The Time Has Come
- Reducing Thrombotic Risk From Polyvascular Disease in Primary Care
- Strategies to Improve Outcomes in COPD
- The Evolving Landscape of ASCVD Risk Among Patients With HIV
- The New Face of Preadolescent and Adolescent Acne: Beyond the Guidelines
- The Role of Eggs in Healthy Diets
- Update on the Gut Microbiome for the Primary Care Clinician
- Updates in the Management of Mild Cognitive Impairment and Alzheimer Disease
- Use of SGLT-2 Inhibitors for Chronic Kidney Disease in Primary Care
This supplement offers the opportunity to earn a total of 4 continuing medical education (CME) credits. Credit is awarded for successful completion of the evaluation after reading the article. The links can be found within the supplement on the first page of each article where CME credits are offered.
Click here to read Hot Topics in Primary Care 2022
This supplement to The Journal of Family Practice was sponsored by the Primary Care Education Consortium and Primary Care Metabolic Group.
Check out these short video segments, which were prepared by the supplement authors and summarize the individual articles.
The title above each video links to the related article.
A Paradigm Shift for Asthma Care, Njira Lugogo, MD; Neil Skolnik, MD; Yihui Jiang, DO
Common Questions on Continuous Glucose Monitoring in Primary Care, Eden M. Miller, DO
Detecting and Managing ASCVD in Women: A Focus on Statins, Pam Kushner, MD
Improving Detection and Management of Anemia in CKD, Steven Fishbane, MD; Stephen Brunton, MD, FAAFP
OTC Analgesics vs Opioids for Pain Management, Gary M. Ruoff, MD
Practical Screening for Islet Autoantibodies: The Time Has Come, Timothy Reid, MD
Reducing Thrombotic Risk From Polyvascular Disease in Primary Care, Stephen Brunton, MD, FAAFP
Strategies to Improve Outcomes in COPD, Barbara Yawn, MD, MSc, FAAFP
The Evolving Landscape of ASCVD Risk Among Patients With HIV, Carlos Malvestutto, MD, MPH
The Role of Eggs in Healthy Diets, Maria Luz Fernandez, PhD
Update on the Gut Microbiome for the Primary Care Clinician, Eden M. Miller, DO
Updates in the Management of Mild Cognitive Impairment and Alzheimer Disease, Gary Small, MD
Use of SGLT-2 Inhibitors for Chronic Kidney Disease in Primary Care, George Bakris, MD
Hot Topics in Primary Care 2022 is a resource that explores the newest developments in primary care topics that impact your daily clinical practice.
Click on the link below to access the entire supplement. You can also click on the video panes below to view brief summaries of individual chapters. Titles above the video panes link directly to each article.
- A Paradigm Shift for Asthma Care
- Common Questions on Continuous Glucose Monitoring in Primary Care
- Detecting and Managing ASCVD in Women: A Focus on Statins
- Improving Detection and Management of Anemia in CKD
- OTC Analgesics vs Opioids for Pain Management
- Practical Considerations for Use of Insulin/Glucagon-Like Peptide 1 Receptor Agonist Combinations in Older Adults With Type 2 Diabetes
- Practical Screening for Islet Autoantibodies: The Time Has Come
- Reducing Thrombotic Risk From Polyvascular Disease in Primary Care
- Strategies to Improve Outcomes in COPD
- The Evolving Landscape of ASCVD Risk Among Patients With HIV
- The New Face of Preadolescent and Adolescent Acne: Beyond the Guidelines
- The Role of Eggs in Healthy Diets
- Update on the Gut Microbiome for the Primary Care Clinician
- Updates in the Management of Mild Cognitive Impairment and Alzheimer Disease
- Use of SGLT-2 Inhibitors for Chronic Kidney Disease in Primary Care
This supplement offers the opportunity to earn a total of 4 continuing medical education (CME) credits. Credit is awarded for successful completion of the evaluation after reading the article. The links can be found within the supplement on the first page of each article where CME credits are offered.
Click here to read Hot Topics in Primary Care 2022
This supplement to The Journal of Family Practice was sponsored by the Primary Care Education Consortium and Primary Care Metabolic Group.
Check out these short video segments, which were prepared by the supplement authors and summarize the individual articles.
The title above each video links to the related article.
A Paradigm Shift for Asthma Care, Njira Lugogo, MD; Neil Skolnik, MD; Yihui Jiang, DO
Common Questions on Continuous Glucose Monitoring in Primary Care, Eden M. Miller, DO
Detecting and Managing ASCVD in Women: A Focus on Statins, Pam Kushner, MD
Improving Detection and Management of Anemia in CKD, Steven Fishbane, MD; Stephen Brunton, MD, FAAFP
OTC Analgesics vs Opioids for Pain Management, Gary M. Ruoff, MD
Practical Screening for Islet Autoantibodies: The Time Has Come, Timothy Reid, MD
Reducing Thrombotic Risk From Polyvascular Disease in Primary Care, Stephen Brunton, MD, FAAFP
Strategies to Improve Outcomes in COPD, Barbara Yawn, MD, MSc, FAAFP
The Evolving Landscape of ASCVD Risk Among Patients With HIV, Carlos Malvestutto, MD, MPH
The Role of Eggs in Healthy Diets, Maria Luz Fernandez, PhD
Update on the Gut Microbiome for the Primary Care Clinician, Eden M. Miller, DO
Updates in the Management of Mild Cognitive Impairment and Alzheimer Disease, Gary Small, MD
Use of SGLT-2 Inhibitors for Chronic Kidney Disease in Primary Care, George Bakris, MD
‘Case closed’: Bridging thrombolysis remains ‘gold standard’ in stroke thrombectomy
Two new noninferiority trials address the controversial question of whether thrombolytic therapy can be omitted for acute ischemic stroke in patients undergoing endovascular thrombectomy for large-vessel occlusion.
Both trials show better outcomes when standard bridging thrombolytic therapy is used before thrombectomy, with comparable safety.
The results of SWIFT-DIRECT and DIRECT-SAFE were published online June 22 in The Lancet.
“The case appears closed. Bypass intravenous thrombolysis is highly unlikely to be noninferior to standard care by a clinically acceptable margin for most patients,” writes Pooja Khatri, MD, MSc, department of neurology, University of Cincinnati, in a linked comment.
SWIFT-DIRECT
SWIFT-DIRECT enrolled 408 patients (median age 72; 51% women) with acute stroke due to large vessel occlusion admitted to stroke centers in Europe and Canada. Half were randomly allocated to thrombectomy alone and half to intravenous alteplase and thrombectomy.
Successful reperfusion was less common in patients who had thrombectomy alone (91% vs. 96%; risk difference −5.1%; 95% confidence interval, −10.2 to 0.0, P = .047).
With combination therapy, more patients achieved functional independence with a modified Rankin scale score of 0-2 at 90 days (65% vs. 57%; adjusted risk difference −7.3%; 95% CI, −16·6 to 2·1, lower limit of one-sided 95% CI, −15·1%, crossing the noninferiority margin of −12%).
“Despite a very liberal noninferiority margin and strict inclusion and exclusion criteria aimed at studying a population most likely to benefit from thrombectomy alone, point estimates directionally favored intravenous thrombolysis plus thrombectomy,” Urs Fischer, MD, cochair of the Stroke Center, University Hospital Basel, Switzerland, told this news organization.
“Furthermore, we could demonstrate that overall reperfusion rates were extremely high and yet significantly better in patients receiving intravenous thrombolysis plus thrombectomy than in patients treated with thrombectomy alone, a finding which has not been shown before,” Dr. Fischer said.
There was no significant difference in the risk of symptomatic intracranial bleeding (3% with combination therapy and 2% with thrombectomy alone).
Based on the results, in patients suitable for thrombolysis, skipping it before thrombectomy “is not justified,” the study team concludes.
DIRECT-SAFE
DIRECT-SAFE enrolled 295 patients (median age 69; 43% women) with stroke and large vessel occlusion from Australia, New Zealand, China, and Vietnam, with half undergoing direct thrombectomy and half bridging therapy first.
Functional independence (modified Rankin Scale 0-2 or return to baseline at 90 days) was more common in the bridging group (61% vs. 55%).
Safety outcomes were similar between groups. Symptomatic intracerebral hemorrhage occurred in 2 (1%) patients in the direct group and 1 (1%) patient in the bridging group. There were 22 (15%) deaths in the direct group and 24 in the bridging group.
“There has been concern across the world regarding cost of treatment, together with fears of increasing bleeding risk or clot migration with intravenous thrombolytic,” lead investigator Peter Mitchell, MBBS, director, NeuroIntervention Service, The Royal Melbourne Hospital, Parkville, Victoria, Australia, told this news organization.
“We showed that patients in the bridging treatment arm had better outcomes across the entire study, especially in Asian region patients” and therefore remains “the gold standard,” Dr. Mitchell said.
To date, six published trials have addressed this question of endovascular therapy alone or with thrombolysis – SKIP, DIRECT-MT, MR CLEAN NO IV, SWIFT-DIRECT, and DIRECT-SAFE.
Dr. Fischer said the SWIFT-DIRECT study group plans to perform an individual participant data meta-analysis known as Improving Reperfusion Strategies in Ischemic Stroke (IRIS) of all six trials to see whether there are subgroups of patients in whom thrombectomy alone is as effective as thrombolysis plus thrombectomy.
Subgroups of interest, he said, include patients with early ischemic signs on imaging, those at increased risk for hemorrhagic complications, and patients with a high clot burden.
SWIFT-DIRECT was funding by Medtronic and University Hospital Bern. DIRECT-SAFE was funded by Australian National Health and Medical Research Council and Stryker USA. A complete list of author disclosures is available with the original articles.
A version of this article first appeared on Medscape.com.
Two new noninferiority trials address the controversial question of whether thrombolytic therapy can be omitted for acute ischemic stroke in patients undergoing endovascular thrombectomy for large-vessel occlusion.
Both trials show better outcomes when standard bridging thrombolytic therapy is used before thrombectomy, with comparable safety.
The results of SWIFT-DIRECT and DIRECT-SAFE were published online June 22 in The Lancet.
“The case appears closed. Bypass intravenous thrombolysis is highly unlikely to be noninferior to standard care by a clinically acceptable margin for most patients,” writes Pooja Khatri, MD, MSc, department of neurology, University of Cincinnati, in a linked comment.
SWIFT-DIRECT
SWIFT-DIRECT enrolled 408 patients (median age 72; 51% women) with acute stroke due to large vessel occlusion admitted to stroke centers in Europe and Canada. Half were randomly allocated to thrombectomy alone and half to intravenous alteplase and thrombectomy.
Successful reperfusion was less common in patients who had thrombectomy alone (91% vs. 96%; risk difference −5.1%; 95% confidence interval, −10.2 to 0.0, P = .047).
With combination therapy, more patients achieved functional independence with a modified Rankin scale score of 0-2 at 90 days (65% vs. 57%; adjusted risk difference −7.3%; 95% CI, −16·6 to 2·1, lower limit of one-sided 95% CI, −15·1%, crossing the noninferiority margin of −12%).
“Despite a very liberal noninferiority margin and strict inclusion and exclusion criteria aimed at studying a population most likely to benefit from thrombectomy alone, point estimates directionally favored intravenous thrombolysis plus thrombectomy,” Urs Fischer, MD, cochair of the Stroke Center, University Hospital Basel, Switzerland, told this news organization.
“Furthermore, we could demonstrate that overall reperfusion rates were extremely high and yet significantly better in patients receiving intravenous thrombolysis plus thrombectomy than in patients treated with thrombectomy alone, a finding which has not been shown before,” Dr. Fischer said.
There was no significant difference in the risk of symptomatic intracranial bleeding (3% with combination therapy and 2% with thrombectomy alone).
Based on the results, in patients suitable for thrombolysis, skipping it before thrombectomy “is not justified,” the study team concludes.
DIRECT-SAFE
DIRECT-SAFE enrolled 295 patients (median age 69; 43% women) with stroke and large vessel occlusion from Australia, New Zealand, China, and Vietnam, with half undergoing direct thrombectomy and half bridging therapy first.
Functional independence (modified Rankin Scale 0-2 or return to baseline at 90 days) was more common in the bridging group (61% vs. 55%).
Safety outcomes were similar between groups. Symptomatic intracerebral hemorrhage occurred in 2 (1%) patients in the direct group and 1 (1%) patient in the bridging group. There were 22 (15%) deaths in the direct group and 24 in the bridging group.
“There has been concern across the world regarding cost of treatment, together with fears of increasing bleeding risk or clot migration with intravenous thrombolytic,” lead investigator Peter Mitchell, MBBS, director, NeuroIntervention Service, The Royal Melbourne Hospital, Parkville, Victoria, Australia, told this news organization.
“We showed that patients in the bridging treatment arm had better outcomes across the entire study, especially in Asian region patients” and therefore remains “the gold standard,” Dr. Mitchell said.
To date, six published trials have addressed this question of endovascular therapy alone or with thrombolysis – SKIP, DIRECT-MT, MR CLEAN NO IV, SWIFT-DIRECT, and DIRECT-SAFE.
Dr. Fischer said the SWIFT-DIRECT study group plans to perform an individual participant data meta-analysis known as Improving Reperfusion Strategies in Ischemic Stroke (IRIS) of all six trials to see whether there are subgroups of patients in whom thrombectomy alone is as effective as thrombolysis plus thrombectomy.
Subgroups of interest, he said, include patients with early ischemic signs on imaging, those at increased risk for hemorrhagic complications, and patients with a high clot burden.
SWIFT-DIRECT was funding by Medtronic and University Hospital Bern. DIRECT-SAFE was funded by Australian National Health and Medical Research Council and Stryker USA. A complete list of author disclosures is available with the original articles.
A version of this article first appeared on Medscape.com.
Two new noninferiority trials address the controversial question of whether thrombolytic therapy can be omitted for acute ischemic stroke in patients undergoing endovascular thrombectomy for large-vessel occlusion.
Both trials show better outcomes when standard bridging thrombolytic therapy is used before thrombectomy, with comparable safety.
The results of SWIFT-DIRECT and DIRECT-SAFE were published online June 22 in The Lancet.
“The case appears closed. Bypass intravenous thrombolysis is highly unlikely to be noninferior to standard care by a clinically acceptable margin for most patients,” writes Pooja Khatri, MD, MSc, department of neurology, University of Cincinnati, in a linked comment.
SWIFT-DIRECT
SWIFT-DIRECT enrolled 408 patients (median age 72; 51% women) with acute stroke due to large vessel occlusion admitted to stroke centers in Europe and Canada. Half were randomly allocated to thrombectomy alone and half to intravenous alteplase and thrombectomy.
Successful reperfusion was less common in patients who had thrombectomy alone (91% vs. 96%; risk difference −5.1%; 95% confidence interval, −10.2 to 0.0, P = .047).
With combination therapy, more patients achieved functional independence with a modified Rankin scale score of 0-2 at 90 days (65% vs. 57%; adjusted risk difference −7.3%; 95% CI, −16·6 to 2·1, lower limit of one-sided 95% CI, −15·1%, crossing the noninferiority margin of −12%).
“Despite a very liberal noninferiority margin and strict inclusion and exclusion criteria aimed at studying a population most likely to benefit from thrombectomy alone, point estimates directionally favored intravenous thrombolysis plus thrombectomy,” Urs Fischer, MD, cochair of the Stroke Center, University Hospital Basel, Switzerland, told this news organization.
“Furthermore, we could demonstrate that overall reperfusion rates were extremely high and yet significantly better in patients receiving intravenous thrombolysis plus thrombectomy than in patients treated with thrombectomy alone, a finding which has not been shown before,” Dr. Fischer said.
There was no significant difference in the risk of symptomatic intracranial bleeding (3% with combination therapy and 2% with thrombectomy alone).
Based on the results, in patients suitable for thrombolysis, skipping it before thrombectomy “is not justified,” the study team concludes.
DIRECT-SAFE
DIRECT-SAFE enrolled 295 patients (median age 69; 43% women) with stroke and large vessel occlusion from Australia, New Zealand, China, and Vietnam, with half undergoing direct thrombectomy and half bridging therapy first.
Functional independence (modified Rankin Scale 0-2 or return to baseline at 90 days) was more common in the bridging group (61% vs. 55%).
Safety outcomes were similar between groups. Symptomatic intracerebral hemorrhage occurred in 2 (1%) patients in the direct group and 1 (1%) patient in the bridging group. There were 22 (15%) deaths in the direct group and 24 in the bridging group.
“There has been concern across the world regarding cost of treatment, together with fears of increasing bleeding risk or clot migration with intravenous thrombolytic,” lead investigator Peter Mitchell, MBBS, director, NeuroIntervention Service, The Royal Melbourne Hospital, Parkville, Victoria, Australia, told this news organization.
“We showed that patients in the bridging treatment arm had better outcomes across the entire study, especially in Asian region patients” and therefore remains “the gold standard,” Dr. Mitchell said.
To date, six published trials have addressed this question of endovascular therapy alone or with thrombolysis – SKIP, DIRECT-MT, MR CLEAN NO IV, SWIFT-DIRECT, and DIRECT-SAFE.
Dr. Fischer said the SWIFT-DIRECT study group plans to perform an individual participant data meta-analysis known as Improving Reperfusion Strategies in Ischemic Stroke (IRIS) of all six trials to see whether there are subgroups of patients in whom thrombectomy alone is as effective as thrombolysis plus thrombectomy.
Subgroups of interest, he said, include patients with early ischemic signs on imaging, those at increased risk for hemorrhagic complications, and patients with a high clot burden.
SWIFT-DIRECT was funding by Medtronic and University Hospital Bern. DIRECT-SAFE was funded by Australian National Health and Medical Research Council and Stryker USA. A complete list of author disclosures is available with the original articles.
A version of this article first appeared on Medscape.com.
FROM THE LANCET
Science lags behind for kids with long COVID
Emma Sherman, a 13-year-old girl in Ascot, England, woke up to a dizzying aura of blind spots and flashing lights in her field of vision. It was May 2020, and she also had crippling nausea and headaches. By August, her dizziness was so overwhelming, she couldn’t hold her head up, lying in her mother’s lap for hours, too fatigued to attend school.
The former competitive gymnast, who had hoped to try out for the cheerleading squad, now used a wheelchair and was a shadow of her former self. She had been diagnosed with COVID-induced postural orthostatic tachycardia syndrome, a condition often caused by an infection that results in a higher heart rate, extreme nausea, dizziness, and fatigue.
“I was so into sports before I got long COVID, and afterwards I could barely walk,” Emma said.
Even minor movements sent her heart rate sky-high. Her long chestnut hair turned gray and fell out in clumps. In the hospital, she was pricked and prodded, her blood tested for numerous conditions.
“They ran every scan known to man and took an MRI of her brain,” said Emma’s mother, Marie Sherman. “All was clear.”
Emma’s pediatrician determined that the teen had long COVID after having had a mild case of the virus in March, about 2 months before her puzzling symptoms began. But beyond a positive antibody test, doctors have found little evidence of what was causing Emma’s symptoms.
For Emma and others with long COVID, there are no medications shown to directly target the condition. Instead, caregivers target their symptoms, which include nausea, dizziness, fatigue, headaches, and a racing heart, said Laura Malone, MD, codirector of the Johns Hopkins Kennedy Krieger Pediatric Post–COVID-19 Rehabilitation Clinic in Baltimore.
“Right now, it’s a rehabilitation-based approach focused on improving symptoms and functioning so that kids can go back to their usual activities as much as possible,” she says.
Depression and anxiety are common, although doctors are struggling to figure out whether COVID is changing the brain or whether mental health symptoms result from all the life disruptions. There’s little research to show how may kids have depression because of long COVID. Dr. Malone said about half of her patients at the Kennedy Krieger Institute›s long COVID clinic are also dealing with mental health issues.
Patients with headaches, dizziness, and nausea are given pain and nausea medications and recommendations for a healthy diet with added fruits and vegetables, monounsaturated fats, lower sodium, unprocessed foods, and whole grains. Kids with irregular or racing heart rates are referred to cardiologists and potentially prescribed beta-blockers to treat their heart arrhythmias, while children with breathing problems may be referred to pulmonologists and those with depression to a psychiatrist.
Still, many patients like Emma go to their doctors with phantom symptoms that don’t show up on scans or blood tests.
“We’re not seeing any evidence of structural damage to the brain, for example,” said Dr. Malone. “When we do MRIs, they often come out normal.”
It’s possible that the virus lingers in some patients, said Rajeev Fernando, MD, an infectious disease specialist and a fellow at Harvard Medical School, Boston. Kids’ strong immune systems often fend off problems that can be noticed. But on the inside, dead fragments of the virus persist, floating in hidden parts of the body and activating the immune system long after the threat has passed.
The virus can be in the gut and in the brain, which may help explain why symptoms like brain fog and nausea can linger in children.
“The immune system doesn’t recognize whether fragments of the virus are dead or alive. It continues to think it’s fighting active COVID,” said Dr. Fernando.
There is little data on how long symptoms last, Dr. Fernando said, as well as how many kids get them and why some are more vulnerable than others. Some research has found that about 5%-15% of children with COVID may get long COVID, but the statistics vary globally.
“Children with long COVID have largely been ignored. And while we’re talking about it now, we’ve got some work to do,” said Dr. Fernando.
As for Emma, she recovered in January of 2021, heading back to school and her friends, although her cardiologist advised her to skip gym classes.
“For the first time in months, I was feeling like myself again,” she said.
But the coronavirus found its way to Emma again. Although she was fully vaccinated in the fall of 2021, when the Omicron variant swept the world late that year, she was infected again.
“When the wave of Omicron descended, Emma was like a sitting duck,” her mother said.
She was bedridden with a high fever and cough. The cold-like symptoms eventually went away, but the issues in her gut stuck around. Since then, Emma has had extreme nausea, losing most of the weight she had gained back.
For her part, Ms. Sherman has found solace in a group called Long COVID Kids, a nonprofit in Europe and the United States. The group is raising awareness about the condition in kids to increase funding, boost understanding, and improve treatment and outcomes.
“There’s nothing worse than watching your child suffer and not being able to do anything about it,” she said. “I tell Emma all the time: If I could just crawl in your body and take it, I would do it in a second.”
Emma is hoping for a fresh start with her family’s move in the coming weeks to Sotogrande in southern Spain.
“I miss the simplest things like going for a run, going to the fair with my friends, and just feeling well,” she said. “I have a long list of things I’ll do once this is all done.”
A version of this article first appeared on WebMD.com.
Emma Sherman, a 13-year-old girl in Ascot, England, woke up to a dizzying aura of blind spots and flashing lights in her field of vision. It was May 2020, and she also had crippling nausea and headaches. By August, her dizziness was so overwhelming, she couldn’t hold her head up, lying in her mother’s lap for hours, too fatigued to attend school.
The former competitive gymnast, who had hoped to try out for the cheerleading squad, now used a wheelchair and was a shadow of her former self. She had been diagnosed with COVID-induced postural orthostatic tachycardia syndrome, a condition often caused by an infection that results in a higher heart rate, extreme nausea, dizziness, and fatigue.
“I was so into sports before I got long COVID, and afterwards I could barely walk,” Emma said.
Even minor movements sent her heart rate sky-high. Her long chestnut hair turned gray and fell out in clumps. In the hospital, she was pricked and prodded, her blood tested for numerous conditions.
“They ran every scan known to man and took an MRI of her brain,” said Emma’s mother, Marie Sherman. “All was clear.”
Emma’s pediatrician determined that the teen had long COVID after having had a mild case of the virus in March, about 2 months before her puzzling symptoms began. But beyond a positive antibody test, doctors have found little evidence of what was causing Emma’s symptoms.
For Emma and others with long COVID, there are no medications shown to directly target the condition. Instead, caregivers target their symptoms, which include nausea, dizziness, fatigue, headaches, and a racing heart, said Laura Malone, MD, codirector of the Johns Hopkins Kennedy Krieger Pediatric Post–COVID-19 Rehabilitation Clinic in Baltimore.
“Right now, it’s a rehabilitation-based approach focused on improving symptoms and functioning so that kids can go back to their usual activities as much as possible,” she says.
Depression and anxiety are common, although doctors are struggling to figure out whether COVID is changing the brain or whether mental health symptoms result from all the life disruptions. There’s little research to show how may kids have depression because of long COVID. Dr. Malone said about half of her patients at the Kennedy Krieger Institute›s long COVID clinic are also dealing with mental health issues.
Patients with headaches, dizziness, and nausea are given pain and nausea medications and recommendations for a healthy diet with added fruits and vegetables, monounsaturated fats, lower sodium, unprocessed foods, and whole grains. Kids with irregular or racing heart rates are referred to cardiologists and potentially prescribed beta-blockers to treat their heart arrhythmias, while children with breathing problems may be referred to pulmonologists and those with depression to a psychiatrist.
Still, many patients like Emma go to their doctors with phantom symptoms that don’t show up on scans or blood tests.
“We’re not seeing any evidence of structural damage to the brain, for example,” said Dr. Malone. “When we do MRIs, they often come out normal.”
It’s possible that the virus lingers in some patients, said Rajeev Fernando, MD, an infectious disease specialist and a fellow at Harvard Medical School, Boston. Kids’ strong immune systems often fend off problems that can be noticed. But on the inside, dead fragments of the virus persist, floating in hidden parts of the body and activating the immune system long after the threat has passed.
The virus can be in the gut and in the brain, which may help explain why symptoms like brain fog and nausea can linger in children.
“The immune system doesn’t recognize whether fragments of the virus are dead or alive. It continues to think it’s fighting active COVID,” said Dr. Fernando.
There is little data on how long symptoms last, Dr. Fernando said, as well as how many kids get them and why some are more vulnerable than others. Some research has found that about 5%-15% of children with COVID may get long COVID, but the statistics vary globally.
“Children with long COVID have largely been ignored. And while we’re talking about it now, we’ve got some work to do,” said Dr. Fernando.
As for Emma, she recovered in January of 2021, heading back to school and her friends, although her cardiologist advised her to skip gym classes.
“For the first time in months, I was feeling like myself again,” she said.
But the coronavirus found its way to Emma again. Although she was fully vaccinated in the fall of 2021, when the Omicron variant swept the world late that year, she was infected again.
“When the wave of Omicron descended, Emma was like a sitting duck,” her mother said.
She was bedridden with a high fever and cough. The cold-like symptoms eventually went away, but the issues in her gut stuck around. Since then, Emma has had extreme nausea, losing most of the weight she had gained back.
For her part, Ms. Sherman has found solace in a group called Long COVID Kids, a nonprofit in Europe and the United States. The group is raising awareness about the condition in kids to increase funding, boost understanding, and improve treatment and outcomes.
“There’s nothing worse than watching your child suffer and not being able to do anything about it,” she said. “I tell Emma all the time: If I could just crawl in your body and take it, I would do it in a second.”
Emma is hoping for a fresh start with her family’s move in the coming weeks to Sotogrande in southern Spain.
“I miss the simplest things like going for a run, going to the fair with my friends, and just feeling well,” she said. “I have a long list of things I’ll do once this is all done.”
A version of this article first appeared on WebMD.com.
Emma Sherman, a 13-year-old girl in Ascot, England, woke up to a dizzying aura of blind spots and flashing lights in her field of vision. It was May 2020, and she also had crippling nausea and headaches. By August, her dizziness was so overwhelming, she couldn’t hold her head up, lying in her mother’s lap for hours, too fatigued to attend school.
The former competitive gymnast, who had hoped to try out for the cheerleading squad, now used a wheelchair and was a shadow of her former self. She had been diagnosed with COVID-induced postural orthostatic tachycardia syndrome, a condition often caused by an infection that results in a higher heart rate, extreme nausea, dizziness, and fatigue.
“I was so into sports before I got long COVID, and afterwards I could barely walk,” Emma said.
Even minor movements sent her heart rate sky-high. Her long chestnut hair turned gray and fell out in clumps. In the hospital, she was pricked and prodded, her blood tested for numerous conditions.
“They ran every scan known to man and took an MRI of her brain,” said Emma’s mother, Marie Sherman. “All was clear.”
Emma’s pediatrician determined that the teen had long COVID after having had a mild case of the virus in March, about 2 months before her puzzling symptoms began. But beyond a positive antibody test, doctors have found little evidence of what was causing Emma’s symptoms.
For Emma and others with long COVID, there are no medications shown to directly target the condition. Instead, caregivers target their symptoms, which include nausea, dizziness, fatigue, headaches, and a racing heart, said Laura Malone, MD, codirector of the Johns Hopkins Kennedy Krieger Pediatric Post–COVID-19 Rehabilitation Clinic in Baltimore.
“Right now, it’s a rehabilitation-based approach focused on improving symptoms and functioning so that kids can go back to their usual activities as much as possible,” she says.
Depression and anxiety are common, although doctors are struggling to figure out whether COVID is changing the brain or whether mental health symptoms result from all the life disruptions. There’s little research to show how may kids have depression because of long COVID. Dr. Malone said about half of her patients at the Kennedy Krieger Institute›s long COVID clinic are also dealing with mental health issues.
Patients with headaches, dizziness, and nausea are given pain and nausea medications and recommendations for a healthy diet with added fruits and vegetables, monounsaturated fats, lower sodium, unprocessed foods, and whole grains. Kids with irregular or racing heart rates are referred to cardiologists and potentially prescribed beta-blockers to treat their heart arrhythmias, while children with breathing problems may be referred to pulmonologists and those with depression to a psychiatrist.
Still, many patients like Emma go to their doctors with phantom symptoms that don’t show up on scans or blood tests.
“We’re not seeing any evidence of structural damage to the brain, for example,” said Dr. Malone. “When we do MRIs, they often come out normal.”
It’s possible that the virus lingers in some patients, said Rajeev Fernando, MD, an infectious disease specialist and a fellow at Harvard Medical School, Boston. Kids’ strong immune systems often fend off problems that can be noticed. But on the inside, dead fragments of the virus persist, floating in hidden parts of the body and activating the immune system long after the threat has passed.
The virus can be in the gut and in the brain, which may help explain why symptoms like brain fog and nausea can linger in children.
“The immune system doesn’t recognize whether fragments of the virus are dead or alive. It continues to think it’s fighting active COVID,” said Dr. Fernando.
There is little data on how long symptoms last, Dr. Fernando said, as well as how many kids get them and why some are more vulnerable than others. Some research has found that about 5%-15% of children with COVID may get long COVID, but the statistics vary globally.
“Children with long COVID have largely been ignored. And while we’re talking about it now, we’ve got some work to do,” said Dr. Fernando.
As for Emma, she recovered in January of 2021, heading back to school and her friends, although her cardiologist advised her to skip gym classes.
“For the first time in months, I was feeling like myself again,” she said.
But the coronavirus found its way to Emma again. Although she was fully vaccinated in the fall of 2021, when the Omicron variant swept the world late that year, she was infected again.
“When the wave of Omicron descended, Emma was like a sitting duck,” her mother said.
She was bedridden with a high fever and cough. The cold-like symptoms eventually went away, but the issues in her gut stuck around. Since then, Emma has had extreme nausea, losing most of the weight she had gained back.
For her part, Ms. Sherman has found solace in a group called Long COVID Kids, a nonprofit in Europe and the United States. The group is raising awareness about the condition in kids to increase funding, boost understanding, and improve treatment and outcomes.
“There’s nothing worse than watching your child suffer and not being able to do anything about it,” she said. “I tell Emma all the time: If I could just crawl in your body and take it, I would do it in a second.”
Emma is hoping for a fresh start with her family’s move in the coming weeks to Sotogrande in southern Spain.
“I miss the simplest things like going for a run, going to the fair with my friends, and just feeling well,” she said. “I have a long list of things I’ll do once this is all done.”
A version of this article first appeared on WebMD.com.
Body-brain neuroinflammation loop may cause chronic ME/CFS, long COVID symptoms
ME/CFS has been established as resulting from infections, environmental exposures, stressors, and surgery. Similarities have been drawn during the COVID-19 pandemic between ME/CFS and a large subgroup of patients with post-acute sequelae of SARS-CoV-2 infection – also known as post-COVID conditions, or long COVID – who continue to have viral fatigue and other lingering symptoms after their infection resolves.
What has been less clearly understood, the researchers said, is the reason behind why ME/CFS and other postviral fatigue tends to be chronic and can sometime develop into a lifelong condition.
“These diseases are very closely related, and it is clear the biological basis of long COVID is unequivocally connected to the original COVID infection – so there should no longer be any debate and doubt about the fact that postviral fatigue syndromes like ME/CFS are biologically based and involve much disturbed physiology,” Warren Tate, MSc, PhD, emeritus professor in the department of biochemistry at the University of Otago in Dunedin, New Zealand, stated in a press release.
Their hypothesis, set forth in a study published in Frontiers of Neurology, proposes that the systemic immune/inflammatory response that occurs after an infection or stressful event does not revolve, which results in a “fluctuating chronic neuroinflammation that sustains and controls the complex neurological symptoms of ME/CFS and long COVID and facilitates frequent more serious relapses in response to life stress, as evidenced from a comprehensive disruption to the cellular molecular biology and body’s physiological pathways.”
Dr. Tate and colleagues said that it is still unclear how the neuroinflammation occurs, why it’s persistent in ME/CFS, and how it causes symptoms associated with ME/CFS. In their hypothesis, “abnormal signaling or transport of molecules/cells occurs through one or both of neurovascular pathways and/or a dysfunctional blood brain barrier,” they said, noting “the normally separate and contained brain/CNS compartment in the healthy person becomes more porous.” The neurological symptoms associated with ME/CFS occur due to strong signals sent because of persistent “inflammatory signals or immune cells/molecules migrating into the brain,” they explained.
This results in a continuous loop where the central nervous system sends signals back to the body through the hypothalamus/paraventricular nucleus and the brain stem. “The resulting symptoms and the neurologically driven ‘sickness response’ for the ME/CFS patient would persist, preventing healing and a return to the preinfectious/stress-related state,” Dr. Tate and colleagues said.
Lingering inflammation may be the culprit
Commenting on the study, Achillefs Ntranos, MD, a board-certified neurologist in private practice in Scarsdale, N.Y., who was not involved with the research, said previous studies have shown that long COVID is linked to chronic activation of microglia in the brain, which has also been seen to activate in patients with ME/CFS.
“The hypothesis that lingering inflammation in the brain is the culprit behind the neurological symptoms of long COVID and ME/CFS is valid,” he said. “If these cells remain activated in the brain, they can cause a state of increased and lingering inflammation, which can interfere with the function of neurons, thus producing neurological symptoms. Since the neurological symptoms are similar between these entities, the mechanisms that produce them might also be similar.”
While the exact cause of ME/CFS is still unclear, it is often tied to the aftereffects of a flu-like illness, Dr. Ntranos said. “This has led researchers to propose that it arises after a viral infection, with many different types of viruses being associated with it. Other ways researchers think ME/CFS is being brought on after a viral illness is via changes in the immune system, such as chronic production of cytokines, neuroinflammation, and disruption of the hypothalamic-pituitary-adrenal axis, which regulates the body’s response to stress,” he explained.
While a newer condition, long COVID is not all that different from ME/CFS, Dr. Ntranos noted, sharing the catalyst of a viral infection and core neurological symptoms such as fatigue, postexertional malaise, a “brain fog” that makes thinking or concentrating difficult, sleep problems, and lightheadedness, but there are differences that set it apart from ME/CFS.
“Long COVID is unique in having additional symptoms that are specific to the SARS-CoV-2 virus, such as respiratory and cardiovascular symptoms and loss of smell and taste. However most central nervous system effects are the same between these two entities,” he said.
Dr. Ntranos said long COVID’s neurological symptoms are similar to that of multiple sclerosis (MS), such as “brain fog” and postexertional malaise. “Since MS only affects the brain and spinal cord, there are no symptoms from other organ systems, such as the lungs, heart, or digestive system, contrary to long COVID. Furthermore, MS rarely affects smell and taste, making these symptoms unique to COVID,” he said.
However, he pointed out that brain fog and fatigue symptoms on their own can be nonspecific and attributed to many different conditions, such as obstructive sleep apnea, migraines, depression, anxiety, thyroid problems, vitamin deficiencies, dehydration, sleep disorders, and side effects of medications.
“More research needs to be done to understand how these cells are being activated, how they interfere with neuronal function, and why they remain in that state in some people, who then go on to develop fatigue and brain fog,” he said.
This study was funded by the Healthcare Otago Charitable Trust, the Associated New Zealand Myalgic Encephalomyelitis Society, and donations from families of patients with ME/CFS. The authors and Dr. Ntranos report no relevant financial disclosures.
ME/CFS has been established as resulting from infections, environmental exposures, stressors, and surgery. Similarities have been drawn during the COVID-19 pandemic between ME/CFS and a large subgroup of patients with post-acute sequelae of SARS-CoV-2 infection – also known as post-COVID conditions, or long COVID – who continue to have viral fatigue and other lingering symptoms after their infection resolves.
What has been less clearly understood, the researchers said, is the reason behind why ME/CFS and other postviral fatigue tends to be chronic and can sometime develop into a lifelong condition.
“These diseases are very closely related, and it is clear the biological basis of long COVID is unequivocally connected to the original COVID infection – so there should no longer be any debate and doubt about the fact that postviral fatigue syndromes like ME/CFS are biologically based and involve much disturbed physiology,” Warren Tate, MSc, PhD, emeritus professor in the department of biochemistry at the University of Otago in Dunedin, New Zealand, stated in a press release.
Their hypothesis, set forth in a study published in Frontiers of Neurology, proposes that the systemic immune/inflammatory response that occurs after an infection or stressful event does not revolve, which results in a “fluctuating chronic neuroinflammation that sustains and controls the complex neurological symptoms of ME/CFS and long COVID and facilitates frequent more serious relapses in response to life stress, as evidenced from a comprehensive disruption to the cellular molecular biology and body’s physiological pathways.”
Dr. Tate and colleagues said that it is still unclear how the neuroinflammation occurs, why it’s persistent in ME/CFS, and how it causes symptoms associated with ME/CFS. In their hypothesis, “abnormal signaling or transport of molecules/cells occurs through one or both of neurovascular pathways and/or a dysfunctional blood brain barrier,” they said, noting “the normally separate and contained brain/CNS compartment in the healthy person becomes more porous.” The neurological symptoms associated with ME/CFS occur due to strong signals sent because of persistent “inflammatory signals or immune cells/molecules migrating into the brain,” they explained.
This results in a continuous loop where the central nervous system sends signals back to the body through the hypothalamus/paraventricular nucleus and the brain stem. “The resulting symptoms and the neurologically driven ‘sickness response’ for the ME/CFS patient would persist, preventing healing and a return to the preinfectious/stress-related state,” Dr. Tate and colleagues said.
Lingering inflammation may be the culprit
Commenting on the study, Achillefs Ntranos, MD, a board-certified neurologist in private practice in Scarsdale, N.Y., who was not involved with the research, said previous studies have shown that long COVID is linked to chronic activation of microglia in the brain, which has also been seen to activate in patients with ME/CFS.
“The hypothesis that lingering inflammation in the brain is the culprit behind the neurological symptoms of long COVID and ME/CFS is valid,” he said. “If these cells remain activated in the brain, they can cause a state of increased and lingering inflammation, which can interfere with the function of neurons, thus producing neurological symptoms. Since the neurological symptoms are similar between these entities, the mechanisms that produce them might also be similar.”
While the exact cause of ME/CFS is still unclear, it is often tied to the aftereffects of a flu-like illness, Dr. Ntranos said. “This has led researchers to propose that it arises after a viral infection, with many different types of viruses being associated with it. Other ways researchers think ME/CFS is being brought on after a viral illness is via changes in the immune system, such as chronic production of cytokines, neuroinflammation, and disruption of the hypothalamic-pituitary-adrenal axis, which regulates the body’s response to stress,” he explained.
While a newer condition, long COVID is not all that different from ME/CFS, Dr. Ntranos noted, sharing the catalyst of a viral infection and core neurological symptoms such as fatigue, postexertional malaise, a “brain fog” that makes thinking or concentrating difficult, sleep problems, and lightheadedness, but there are differences that set it apart from ME/CFS.
“Long COVID is unique in having additional symptoms that are specific to the SARS-CoV-2 virus, such as respiratory and cardiovascular symptoms and loss of smell and taste. However most central nervous system effects are the same between these two entities,” he said.
Dr. Ntranos said long COVID’s neurological symptoms are similar to that of multiple sclerosis (MS), such as “brain fog” and postexertional malaise. “Since MS only affects the brain and spinal cord, there are no symptoms from other organ systems, such as the lungs, heart, or digestive system, contrary to long COVID. Furthermore, MS rarely affects smell and taste, making these symptoms unique to COVID,” he said.
However, he pointed out that brain fog and fatigue symptoms on their own can be nonspecific and attributed to many different conditions, such as obstructive sleep apnea, migraines, depression, anxiety, thyroid problems, vitamin deficiencies, dehydration, sleep disorders, and side effects of medications.
“More research needs to be done to understand how these cells are being activated, how they interfere with neuronal function, and why they remain in that state in some people, who then go on to develop fatigue and brain fog,” he said.
This study was funded by the Healthcare Otago Charitable Trust, the Associated New Zealand Myalgic Encephalomyelitis Society, and donations from families of patients with ME/CFS. The authors and Dr. Ntranos report no relevant financial disclosures.
ME/CFS has been established as resulting from infections, environmental exposures, stressors, and surgery. Similarities have been drawn during the COVID-19 pandemic between ME/CFS and a large subgroup of patients with post-acute sequelae of SARS-CoV-2 infection – also known as post-COVID conditions, or long COVID – who continue to have viral fatigue and other lingering symptoms after their infection resolves.
What has been less clearly understood, the researchers said, is the reason behind why ME/CFS and other postviral fatigue tends to be chronic and can sometime develop into a lifelong condition.
“These diseases are very closely related, and it is clear the biological basis of long COVID is unequivocally connected to the original COVID infection – so there should no longer be any debate and doubt about the fact that postviral fatigue syndromes like ME/CFS are biologically based and involve much disturbed physiology,” Warren Tate, MSc, PhD, emeritus professor in the department of biochemistry at the University of Otago in Dunedin, New Zealand, stated in a press release.
Their hypothesis, set forth in a study published in Frontiers of Neurology, proposes that the systemic immune/inflammatory response that occurs after an infection or stressful event does not revolve, which results in a “fluctuating chronic neuroinflammation that sustains and controls the complex neurological symptoms of ME/CFS and long COVID and facilitates frequent more serious relapses in response to life stress, as evidenced from a comprehensive disruption to the cellular molecular biology and body’s physiological pathways.”
Dr. Tate and colleagues said that it is still unclear how the neuroinflammation occurs, why it’s persistent in ME/CFS, and how it causes symptoms associated with ME/CFS. In their hypothesis, “abnormal signaling or transport of molecules/cells occurs through one or both of neurovascular pathways and/or a dysfunctional blood brain barrier,” they said, noting “the normally separate and contained brain/CNS compartment in the healthy person becomes more porous.” The neurological symptoms associated with ME/CFS occur due to strong signals sent because of persistent “inflammatory signals or immune cells/molecules migrating into the brain,” they explained.
This results in a continuous loop where the central nervous system sends signals back to the body through the hypothalamus/paraventricular nucleus and the brain stem. “The resulting symptoms and the neurologically driven ‘sickness response’ for the ME/CFS patient would persist, preventing healing and a return to the preinfectious/stress-related state,” Dr. Tate and colleagues said.
Lingering inflammation may be the culprit
Commenting on the study, Achillefs Ntranos, MD, a board-certified neurologist in private practice in Scarsdale, N.Y., who was not involved with the research, said previous studies have shown that long COVID is linked to chronic activation of microglia in the brain, which has also been seen to activate in patients with ME/CFS.
“The hypothesis that lingering inflammation in the brain is the culprit behind the neurological symptoms of long COVID and ME/CFS is valid,” he said. “If these cells remain activated in the brain, they can cause a state of increased and lingering inflammation, which can interfere with the function of neurons, thus producing neurological symptoms. Since the neurological symptoms are similar between these entities, the mechanisms that produce them might also be similar.”
While the exact cause of ME/CFS is still unclear, it is often tied to the aftereffects of a flu-like illness, Dr. Ntranos said. “This has led researchers to propose that it arises after a viral infection, with many different types of viruses being associated with it. Other ways researchers think ME/CFS is being brought on after a viral illness is via changes in the immune system, such as chronic production of cytokines, neuroinflammation, and disruption of the hypothalamic-pituitary-adrenal axis, which regulates the body’s response to stress,” he explained.
While a newer condition, long COVID is not all that different from ME/CFS, Dr. Ntranos noted, sharing the catalyst of a viral infection and core neurological symptoms such as fatigue, postexertional malaise, a “brain fog” that makes thinking or concentrating difficult, sleep problems, and lightheadedness, but there are differences that set it apart from ME/CFS.
“Long COVID is unique in having additional symptoms that are specific to the SARS-CoV-2 virus, such as respiratory and cardiovascular symptoms and loss of smell and taste. However most central nervous system effects are the same between these two entities,” he said.
Dr. Ntranos said long COVID’s neurological symptoms are similar to that of multiple sclerosis (MS), such as “brain fog” and postexertional malaise. “Since MS only affects the brain and spinal cord, there are no symptoms from other organ systems, such as the lungs, heart, or digestive system, contrary to long COVID. Furthermore, MS rarely affects smell and taste, making these symptoms unique to COVID,” he said.
However, he pointed out that brain fog and fatigue symptoms on their own can be nonspecific and attributed to many different conditions, such as obstructive sleep apnea, migraines, depression, anxiety, thyroid problems, vitamin deficiencies, dehydration, sleep disorders, and side effects of medications.
“More research needs to be done to understand how these cells are being activated, how they interfere with neuronal function, and why they remain in that state in some people, who then go on to develop fatigue and brain fog,” he said.
This study was funded by the Healthcare Otago Charitable Trust, the Associated New Zealand Myalgic Encephalomyelitis Society, and donations from families of patients with ME/CFS. The authors and Dr. Ntranos report no relevant financial disclosures.
FROM FRONTIERS IN NEUROLOGY
Cross-training across the map
There was a recent post on Sermo about medical office staff cross-training. It talked about the importance of the scheduler being able to cover for the medical assistant (to an extent), a billing person being able to room patients, and so on.
Here, in my little three-person office, the only thing my staff can’t do is see patients.
Actually, more than 2 years out since the pandemic changed everyone’s lives, we’ve settled into a very different cross-training routine. I’m the only one at my office. My medical assistant works from home, far north of me, and so does my scheduler, who is across town.
So, at the office, I handle it all. I check people in, copy insurance cards, collect copays, see patients, and make follow-ups.
At this time, I’ve not only gotten used to it, but really don’t mind it.
We don’t worry about freeway traffic. My staff starts at the exact time each day, and so I don’t worry about one of them being an hour late, trapped behind a rush-hour pile-up on the 101. Staying at home with a sick kid isn’t an issue either, anymore. If my secretary has to make her young daughter lunch, or run her over to a birthday party, I don’t even notice it. If there are any problems, she knows how to reach me. Same with my medical assistant.
Nobody worries about what to throw together for dinner if they get home late.
It saves money on rent, and money and time on transportation.
Gas prices, at least for driving to and from work for them, don’t have to be factored into the wage equations. I’d guess it’s about 1,000 gallons of gas a year saved. On a national scale that’s nothing, but to my staff right now that’s $3,000-$4,000 more in their pockets at the end of the year. Not to mention it’s two more cars off the road.
Granted, this doesn’t change what I’m doing. Seeing patients in person is a key part of being a doctor. Some things can be handled equally well over the phone or Zoom, but many can’t. It’s what I signed up for, and I really don’t mind it. Seeing patients is still what I enjoy.
My staff is a lot happier with this arrangement, and I don’t mind it either. I always, by nature, kept a reasonably paced schedule. Trying to shoehorn patients in has never been my way, so I have time to run a credit card or scan insurance information.
When one of my staff goes out of town, the other covers her calls and relays messages to me. Yes, it’s extra work, but no more so than if they were here in person. Probably less.
I’m sure many physicians wouldn’t agree with my office model, but it suits me fine. Cross-training and all.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
There was a recent post on Sermo about medical office staff cross-training. It talked about the importance of the scheduler being able to cover for the medical assistant (to an extent), a billing person being able to room patients, and so on.
Here, in my little three-person office, the only thing my staff can’t do is see patients.
Actually, more than 2 years out since the pandemic changed everyone’s lives, we’ve settled into a very different cross-training routine. I’m the only one at my office. My medical assistant works from home, far north of me, and so does my scheduler, who is across town.
So, at the office, I handle it all. I check people in, copy insurance cards, collect copays, see patients, and make follow-ups.
At this time, I’ve not only gotten used to it, but really don’t mind it.
We don’t worry about freeway traffic. My staff starts at the exact time each day, and so I don’t worry about one of them being an hour late, trapped behind a rush-hour pile-up on the 101. Staying at home with a sick kid isn’t an issue either, anymore. If my secretary has to make her young daughter lunch, or run her over to a birthday party, I don’t even notice it. If there are any problems, she knows how to reach me. Same with my medical assistant.
Nobody worries about what to throw together for dinner if they get home late.
It saves money on rent, and money and time on transportation.
Gas prices, at least for driving to and from work for them, don’t have to be factored into the wage equations. I’d guess it’s about 1,000 gallons of gas a year saved. On a national scale that’s nothing, but to my staff right now that’s $3,000-$4,000 more in their pockets at the end of the year. Not to mention it’s two more cars off the road.
Granted, this doesn’t change what I’m doing. Seeing patients in person is a key part of being a doctor. Some things can be handled equally well over the phone or Zoom, but many can’t. It’s what I signed up for, and I really don’t mind it. Seeing patients is still what I enjoy.
My staff is a lot happier with this arrangement, and I don’t mind it either. I always, by nature, kept a reasonably paced schedule. Trying to shoehorn patients in has never been my way, so I have time to run a credit card or scan insurance information.
When one of my staff goes out of town, the other covers her calls and relays messages to me. Yes, it’s extra work, but no more so than if they were here in person. Probably less.
I’m sure many physicians wouldn’t agree with my office model, but it suits me fine. Cross-training and all.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
There was a recent post on Sermo about medical office staff cross-training. It talked about the importance of the scheduler being able to cover for the medical assistant (to an extent), a billing person being able to room patients, and so on.
Here, in my little three-person office, the only thing my staff can’t do is see patients.
Actually, more than 2 years out since the pandemic changed everyone’s lives, we’ve settled into a very different cross-training routine. I’m the only one at my office. My medical assistant works from home, far north of me, and so does my scheduler, who is across town.
So, at the office, I handle it all. I check people in, copy insurance cards, collect copays, see patients, and make follow-ups.
At this time, I’ve not only gotten used to it, but really don’t mind it.
We don’t worry about freeway traffic. My staff starts at the exact time each day, and so I don’t worry about one of them being an hour late, trapped behind a rush-hour pile-up on the 101. Staying at home with a sick kid isn’t an issue either, anymore. If my secretary has to make her young daughter lunch, or run her over to a birthday party, I don’t even notice it. If there are any problems, she knows how to reach me. Same with my medical assistant.
Nobody worries about what to throw together for dinner if they get home late.
It saves money on rent, and money and time on transportation.
Gas prices, at least for driving to and from work for them, don’t have to be factored into the wage equations. I’d guess it’s about 1,000 gallons of gas a year saved. On a national scale that’s nothing, but to my staff right now that’s $3,000-$4,000 more in their pockets at the end of the year. Not to mention it’s two more cars off the road.
Granted, this doesn’t change what I’m doing. Seeing patients in person is a key part of being a doctor. Some things can be handled equally well over the phone or Zoom, but many can’t. It’s what I signed up for, and I really don’t mind it. Seeing patients is still what I enjoy.
My staff is a lot happier with this arrangement, and I don’t mind it either. I always, by nature, kept a reasonably paced schedule. Trying to shoehorn patients in has never been my way, so I have time to run a credit card or scan insurance information.
When one of my staff goes out of town, the other covers her calls and relays messages to me. Yes, it’s extra work, but no more so than if they were here in person. Probably less.
I’m sure many physicians wouldn’t agree with my office model, but it suits me fine. Cross-training and all.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
Topical gene therapy for dystrophic epidermolysis bullosa shows promise
INDIANAPOLIS – An investigational compared with placebo, according to results from a small phase 3 study.
DEB is a serious, ultra-rare genetic blistering disease caused by mutations in the COL7A1 gene, encoding for type VII collagen and leading to skin fragility and wounds. No approved therapies are currently available. In the study, treatment was generally well tolerated.
“B-VEC is the first treatment that has not only been shown to be effective, but the first to directly target the defect through topical application,” the study’s principal investigator, Shireen V. Guide, MD, said in an interview during a poster session at the annual meeting of the Society for Pediatric Dermatology. “It delivers type VII collagen gene therapy to these patients, which allows healing in areas that they may have had open since birth. It’s been life-changing for them.”
B-VEC is a herpes simplex virus (HSV-1)-based topical, redosable gene therapy being developed by Krystal Biotech that is designed to restore functional COL7 protein by delivering the COL7A1 gene. For the phase 3, multicenter, double-blind, placebo-controlled study known GEM-3, Dr. Guide, who practices dermatology in Rancho Santa Margarita, Calif., and her colleagues, including Peter Marinkovich, MD, from Stanford (Calif.) University, and Mercedes Gonzalez, MD, from the University of Miami, enrolled 31 patients aged 6 months and older with genetically confirmed DEB. Each patient had one wound treated randomized 1:1 to treatment with B-VEC once a week or placebo for 6 months. The mean age of the 31 study participants was 17 years, 65% were male, 65% were White, and 19% were Asian.
The primary endpoint was complete wound healing (defined as 100% wound closure from exact wound area at baseline, specified as skin re-epithelialization without drainage) at 6 months. Additional endpoints included complete wound healing at 3 months and change in pain associated with wound dressing changes.
At 3 months, 70% of wounds treated with B-VEC met the endpoint of complete wound healing, compared with 20% of wounds treated with placebo (P < .005). At 6 months, 67% of wounds treated with B-VEC met the endpoint of complete wound healing compared with 22% of those treated with placebo (P < .005).
Of the total wounds that closed at 3 months, 67% of wounds treated with B-VEC were also closed at 6 months, compared with 33% of those treated with placebo (P = .02). In other findings, a trend toward decreased pain was observed in wounds treated with B-VEC vs. those treated with placebo.
B-VEC was well tolerated with no treatment-related serious adverse events or discontinuations. Three patients experienced a total of five serious adverse events during the study: anemia (two events), and cellulitis, diarrhea, and positive blood culture (one event each). None were considered related to the study drug.
Dr. Guide, who is on staff at Children’s Health of Orange County, Orange, Calif., characterized B-VEC as “very novel because it’s very practical.”
To date, all treatments for DEB “have been extremely labor intensive, including skin grafting and hospitalizations. It’s a topical application that can be done in the office and potentially applied at home in the future. It’s also durable. Not only are the [treated] areas closing, but they are staying closed.”
Kalyani S. Marathe, MD, MPH, director of the dermatology division at Cincinnati Children’s Hospital, who was asked to comment on the study, said that topical application of B-VEC “allows the side effect profile to be very favorable. The results are remarkable in the amount of wound healing and reduction in pain.”
The tolerability of this medication “is crucial,” she added. “EB patients have a lot of pain from their wounds and so any treatment needs to be as painless as possible for it to be usable. I’m very excited about the next phase of studies for this medication and hopeful that it heralds new treatments for our EB patients.”
In June 2022, the manufacturer announced that it had submitted a biologics license application to the Food and Drug Administration for approval of B-VEC for the treatment of DEB, and that it anticipates submitting an application for marketing authorization with the European Medical Agency (EMA) in the second half of 2022.
Dr. Guide disclosed that she has served as an investigator for Krystal Biotech, Innovaderm Research, Arcutis, Premier Research, Paidion, and Castle Biosciences. Dr. Marathe disclosed that she has served as an adviser for Verrica, and that Cincinnati Children’s Hospital is a site for the next phase studies for B-VEC.
*This story was updated on July 25.
INDIANAPOLIS – An investigational compared with placebo, according to results from a small phase 3 study.
DEB is a serious, ultra-rare genetic blistering disease caused by mutations in the COL7A1 gene, encoding for type VII collagen and leading to skin fragility and wounds. No approved therapies are currently available. In the study, treatment was generally well tolerated.
“B-VEC is the first treatment that has not only been shown to be effective, but the first to directly target the defect through topical application,” the study’s principal investigator, Shireen V. Guide, MD, said in an interview during a poster session at the annual meeting of the Society for Pediatric Dermatology. “It delivers type VII collagen gene therapy to these patients, which allows healing in areas that they may have had open since birth. It’s been life-changing for them.”
B-VEC is a herpes simplex virus (HSV-1)-based topical, redosable gene therapy being developed by Krystal Biotech that is designed to restore functional COL7 protein by delivering the COL7A1 gene. For the phase 3, multicenter, double-blind, placebo-controlled study known GEM-3, Dr. Guide, who practices dermatology in Rancho Santa Margarita, Calif., and her colleagues, including Peter Marinkovich, MD, from Stanford (Calif.) University, and Mercedes Gonzalez, MD, from the University of Miami, enrolled 31 patients aged 6 months and older with genetically confirmed DEB. Each patient had one wound treated randomized 1:1 to treatment with B-VEC once a week or placebo for 6 months. The mean age of the 31 study participants was 17 years, 65% were male, 65% were White, and 19% were Asian.
The primary endpoint was complete wound healing (defined as 100% wound closure from exact wound area at baseline, specified as skin re-epithelialization without drainage) at 6 months. Additional endpoints included complete wound healing at 3 months and change in pain associated with wound dressing changes.
At 3 months, 70% of wounds treated with B-VEC met the endpoint of complete wound healing, compared with 20% of wounds treated with placebo (P < .005). At 6 months, 67% of wounds treated with B-VEC met the endpoint of complete wound healing compared with 22% of those treated with placebo (P < .005).
Of the total wounds that closed at 3 months, 67% of wounds treated with B-VEC were also closed at 6 months, compared with 33% of those treated with placebo (P = .02). In other findings, a trend toward decreased pain was observed in wounds treated with B-VEC vs. those treated with placebo.
B-VEC was well tolerated with no treatment-related serious adverse events or discontinuations. Three patients experienced a total of five serious adverse events during the study: anemia (two events), and cellulitis, diarrhea, and positive blood culture (one event each). None were considered related to the study drug.
Dr. Guide, who is on staff at Children’s Health of Orange County, Orange, Calif., characterized B-VEC as “very novel because it’s very practical.”
To date, all treatments for DEB “have been extremely labor intensive, including skin grafting and hospitalizations. It’s a topical application that can be done in the office and potentially applied at home in the future. It’s also durable. Not only are the [treated] areas closing, but they are staying closed.”
Kalyani S. Marathe, MD, MPH, director of the dermatology division at Cincinnati Children’s Hospital, who was asked to comment on the study, said that topical application of B-VEC “allows the side effect profile to be very favorable. The results are remarkable in the amount of wound healing and reduction in pain.”
The tolerability of this medication “is crucial,” she added. “EB patients have a lot of pain from their wounds and so any treatment needs to be as painless as possible for it to be usable. I’m very excited about the next phase of studies for this medication and hopeful that it heralds new treatments for our EB patients.”
In June 2022, the manufacturer announced that it had submitted a biologics license application to the Food and Drug Administration for approval of B-VEC for the treatment of DEB, and that it anticipates submitting an application for marketing authorization with the European Medical Agency (EMA) in the second half of 2022.
Dr. Guide disclosed that she has served as an investigator for Krystal Biotech, Innovaderm Research, Arcutis, Premier Research, Paidion, and Castle Biosciences. Dr. Marathe disclosed that she has served as an adviser for Verrica, and that Cincinnati Children’s Hospital is a site for the next phase studies for B-VEC.
*This story was updated on July 25.
INDIANAPOLIS – An investigational compared with placebo, according to results from a small phase 3 study.
DEB is a serious, ultra-rare genetic blistering disease caused by mutations in the COL7A1 gene, encoding for type VII collagen and leading to skin fragility and wounds. No approved therapies are currently available. In the study, treatment was generally well tolerated.
“B-VEC is the first treatment that has not only been shown to be effective, but the first to directly target the defect through topical application,” the study’s principal investigator, Shireen V. Guide, MD, said in an interview during a poster session at the annual meeting of the Society for Pediatric Dermatology. “It delivers type VII collagen gene therapy to these patients, which allows healing in areas that they may have had open since birth. It’s been life-changing for them.”
B-VEC is a herpes simplex virus (HSV-1)-based topical, redosable gene therapy being developed by Krystal Biotech that is designed to restore functional COL7 protein by delivering the COL7A1 gene. For the phase 3, multicenter, double-blind, placebo-controlled study known GEM-3, Dr. Guide, who practices dermatology in Rancho Santa Margarita, Calif., and her colleagues, including Peter Marinkovich, MD, from Stanford (Calif.) University, and Mercedes Gonzalez, MD, from the University of Miami, enrolled 31 patients aged 6 months and older with genetically confirmed DEB. Each patient had one wound treated randomized 1:1 to treatment with B-VEC once a week or placebo for 6 months. The mean age of the 31 study participants was 17 years, 65% were male, 65% were White, and 19% were Asian.
The primary endpoint was complete wound healing (defined as 100% wound closure from exact wound area at baseline, specified as skin re-epithelialization without drainage) at 6 months. Additional endpoints included complete wound healing at 3 months and change in pain associated with wound dressing changes.
At 3 months, 70% of wounds treated with B-VEC met the endpoint of complete wound healing, compared with 20% of wounds treated with placebo (P < .005). At 6 months, 67% of wounds treated with B-VEC met the endpoint of complete wound healing compared with 22% of those treated with placebo (P < .005).
Of the total wounds that closed at 3 months, 67% of wounds treated with B-VEC were also closed at 6 months, compared with 33% of those treated with placebo (P = .02). In other findings, a trend toward decreased pain was observed in wounds treated with B-VEC vs. those treated with placebo.
B-VEC was well tolerated with no treatment-related serious adverse events or discontinuations. Three patients experienced a total of five serious adverse events during the study: anemia (two events), and cellulitis, diarrhea, and positive blood culture (one event each). None were considered related to the study drug.
Dr. Guide, who is on staff at Children’s Health of Orange County, Orange, Calif., characterized B-VEC as “very novel because it’s very practical.”
To date, all treatments for DEB “have been extremely labor intensive, including skin grafting and hospitalizations. It’s a topical application that can be done in the office and potentially applied at home in the future. It’s also durable. Not only are the [treated] areas closing, but they are staying closed.”
Kalyani S. Marathe, MD, MPH, director of the dermatology division at Cincinnati Children’s Hospital, who was asked to comment on the study, said that topical application of B-VEC “allows the side effect profile to be very favorable. The results are remarkable in the amount of wound healing and reduction in pain.”
The tolerability of this medication “is crucial,” she added. “EB patients have a lot of pain from their wounds and so any treatment needs to be as painless as possible for it to be usable. I’m very excited about the next phase of studies for this medication and hopeful that it heralds new treatments for our EB patients.”
In June 2022, the manufacturer announced that it had submitted a biologics license application to the Food and Drug Administration for approval of B-VEC for the treatment of DEB, and that it anticipates submitting an application for marketing authorization with the European Medical Agency (EMA) in the second half of 2022.
Dr. Guide disclosed that she has served as an investigator for Krystal Biotech, Innovaderm Research, Arcutis, Premier Research, Paidion, and Castle Biosciences. Dr. Marathe disclosed that she has served as an adviser for Verrica, and that Cincinnati Children’s Hospital is a site for the next phase studies for B-VEC.
*This story was updated on July 25.
AT SPD 2022
‘Stunning variation’ in CV test, procedure costs revealed at top U.S. hospitals
Wide variation in the cost of common cardiovascular (CV) tests and procedures, from stress tests to coronary interventions, was revealed in a cross-sectional analysis based on publicly available data from 20 top-ranked hospitals in the United States.
The analysis also suggested a low level of compliance with the 2021 Hospital Price Transparency Final Rule among the 20 centers.
“The variation we found in payer-negotiated prices for identical cardiovascular tests and procedures was stunning,” Rishi K. Wadhera, MD, MPP, MPhil, Beth Israel Deaconess Medical Center, Boston, told this news organization.
“For example, there was a 10-fold difference in the median price of an echocardiogram, and these differences were even larger for common procedures” such as percutaneous coronary intervention (PCI) and pacemaker implantation, he said. “It’s hard to argue that this variation reflects quality of care, given that we looked at a top group of highly ranked hospitals.”
“Even more striking was how the price of a cardiovascular test within the very same hospital could differ across commercial insurance companies,” he said. “For example, the price of a stress test varied 5-fold in one hospital, and in another hospital, more than 4-fold for a coronary angiogram.”
Dr. Wadhera is senior author on the study published online as a research letter in JAMA Internal Medicine, with lead author Andrew S. Oseran, MD, MBA, also from Beth Israel Deaconess Medical Center.
Difficulties with data, interpretation
The researchers looked at payer and self-pay cash prices for noninvasive and invasive CV tests and procedures at the U.S. News & World Report 2021 top 20–ranked U.S. hospitals, based in part on Current Procedural Terminology codes.
Price differences among the hospitals were derived from median negotiated prices for each test and procedure at the centers across all payers. The interquartile ratio (IQR) of prices for each test or procedure across payers was used to evaluate within-hospital price variation.
“Only 80% of the hospitals reported prices for some cardiovascular tests and procedures,” Dr. Wadhera said. “For the most part, even among the hospitals that did report this information, it was extremely challenging to navigate and interpret the data provided.”
Further, the team found that only 7 of the 20 hospitals reported prices for all CV tests and procedures. Centers that did not post prices for some tests or procedures are named in the report’s Figure 1 and Figure 2.
The number of insurance plans listed for each test or procedure ranged from 1 to 432 in the analysis. Median prices ranged from $204 to $2,588 for an echocardiogram, $463 to $3,230 for a stress test, $2,821 to $9,382 for right heart catheterization, $2,868 to $9,203 for a coronary angiogram, $657 to $25,521 for a PCI, and $506 to $20,002 for pacemaker implantation, the report states.
A similar pattern was seen for self-pay cash prices.
Within-hospital variation also ranged broadly. For example, the widest IQR ranges were $3,143-$12,926 for a right heart catheterization, $4,011-$14,486 for a coronary angiogram, $11,325-$23,392 for a PCI, and $8,474-$22,694 for pacemaker implantation.
The report cites a number of limitations to the analysis, among those, the need to rely on the hospitals themselves for data quality and accuracy.
‘More needed besides transparency’
“As a means to better understand health care costs, many opined that full price transparency would leverage market dynamics and result in lower costs,” observed Clyde W. Yancy, MD, MSc, professor of medicine and chief of cardiology at Northwestern Medicine, Chicago. The findings “by an expert group of outcomes scientists make clear that more is needed besides price transparency to lower cost,” he said in an interview.
That said, he added, “there are sufficient variations and allowances made for data collection that it is preferable to hold the current findings circumspect at best. Importantly, the voice of the hospitals does not appear.”
Although “price variation among the top 20 hospitals is substantial,” he observed, “without a better assessment of root cause, actual charge capture, prevailing market dynamics – especially nursing and ancillary staff costs – and the general influence of inflation, it is too difficult to emerge with a precise interpretation.”
Across the 20 hospitals, “there are likely to be 20 different business models,” he added, with negotiated prices reflecting “at least regional, if not institutional, variations.”
“These are complex issues. The several-fold price differences in standard procedures are a concern and an area worth further study with the intention of lowering health care costs,” Dr. Yancy said. “But clearly our next efforts should not address lowering prices per se but understanding how prices are set [and] the connection with reimbursement and actual payments.”
Dr. Wadhera discloses receiving personal fees from Abbott and CVS Health unrelated to the current study; disclosures for the other authors are in the report. Dr. Yancy is deputy editor of JAMA Cardiology.
A version of this article first appeared on Medscape.com.
Wide variation in the cost of common cardiovascular (CV) tests and procedures, from stress tests to coronary interventions, was revealed in a cross-sectional analysis based on publicly available data from 20 top-ranked hospitals in the United States.
The analysis also suggested a low level of compliance with the 2021 Hospital Price Transparency Final Rule among the 20 centers.
“The variation we found in payer-negotiated prices for identical cardiovascular tests and procedures was stunning,” Rishi K. Wadhera, MD, MPP, MPhil, Beth Israel Deaconess Medical Center, Boston, told this news organization.
“For example, there was a 10-fold difference in the median price of an echocardiogram, and these differences were even larger for common procedures” such as percutaneous coronary intervention (PCI) and pacemaker implantation, he said. “It’s hard to argue that this variation reflects quality of care, given that we looked at a top group of highly ranked hospitals.”
“Even more striking was how the price of a cardiovascular test within the very same hospital could differ across commercial insurance companies,” he said. “For example, the price of a stress test varied 5-fold in one hospital, and in another hospital, more than 4-fold for a coronary angiogram.”
Dr. Wadhera is senior author on the study published online as a research letter in JAMA Internal Medicine, with lead author Andrew S. Oseran, MD, MBA, also from Beth Israel Deaconess Medical Center.
Difficulties with data, interpretation
The researchers looked at payer and self-pay cash prices for noninvasive and invasive CV tests and procedures at the U.S. News & World Report 2021 top 20–ranked U.S. hospitals, based in part on Current Procedural Terminology codes.
Price differences among the hospitals were derived from median negotiated prices for each test and procedure at the centers across all payers. The interquartile ratio (IQR) of prices for each test or procedure across payers was used to evaluate within-hospital price variation.
“Only 80% of the hospitals reported prices for some cardiovascular tests and procedures,” Dr. Wadhera said. “For the most part, even among the hospitals that did report this information, it was extremely challenging to navigate and interpret the data provided.”
Further, the team found that only 7 of the 20 hospitals reported prices for all CV tests and procedures. Centers that did not post prices for some tests or procedures are named in the report’s Figure 1 and Figure 2.
The number of insurance plans listed for each test or procedure ranged from 1 to 432 in the analysis. Median prices ranged from $204 to $2,588 for an echocardiogram, $463 to $3,230 for a stress test, $2,821 to $9,382 for right heart catheterization, $2,868 to $9,203 for a coronary angiogram, $657 to $25,521 for a PCI, and $506 to $20,002 for pacemaker implantation, the report states.
A similar pattern was seen for self-pay cash prices.
Within-hospital variation also ranged broadly. For example, the widest IQR ranges were $3,143-$12,926 for a right heart catheterization, $4,011-$14,486 for a coronary angiogram, $11,325-$23,392 for a PCI, and $8,474-$22,694 for pacemaker implantation.
The report cites a number of limitations to the analysis, among those, the need to rely on the hospitals themselves for data quality and accuracy.
‘More needed besides transparency’
“As a means to better understand health care costs, many opined that full price transparency would leverage market dynamics and result in lower costs,” observed Clyde W. Yancy, MD, MSc, professor of medicine and chief of cardiology at Northwestern Medicine, Chicago. The findings “by an expert group of outcomes scientists make clear that more is needed besides price transparency to lower cost,” he said in an interview.
That said, he added, “there are sufficient variations and allowances made for data collection that it is preferable to hold the current findings circumspect at best. Importantly, the voice of the hospitals does not appear.”
Although “price variation among the top 20 hospitals is substantial,” he observed, “without a better assessment of root cause, actual charge capture, prevailing market dynamics – especially nursing and ancillary staff costs – and the general influence of inflation, it is too difficult to emerge with a precise interpretation.”
Across the 20 hospitals, “there are likely to be 20 different business models,” he added, with negotiated prices reflecting “at least regional, if not institutional, variations.”
“These are complex issues. The several-fold price differences in standard procedures are a concern and an area worth further study with the intention of lowering health care costs,” Dr. Yancy said. “But clearly our next efforts should not address lowering prices per se but understanding how prices are set [and] the connection with reimbursement and actual payments.”
Dr. Wadhera discloses receiving personal fees from Abbott and CVS Health unrelated to the current study; disclosures for the other authors are in the report. Dr. Yancy is deputy editor of JAMA Cardiology.
A version of this article first appeared on Medscape.com.
Wide variation in the cost of common cardiovascular (CV) tests and procedures, from stress tests to coronary interventions, was revealed in a cross-sectional analysis based on publicly available data from 20 top-ranked hospitals in the United States.
The analysis also suggested a low level of compliance with the 2021 Hospital Price Transparency Final Rule among the 20 centers.
“The variation we found in payer-negotiated prices for identical cardiovascular tests and procedures was stunning,” Rishi K. Wadhera, MD, MPP, MPhil, Beth Israel Deaconess Medical Center, Boston, told this news organization.
“For example, there was a 10-fold difference in the median price of an echocardiogram, and these differences were even larger for common procedures” such as percutaneous coronary intervention (PCI) and pacemaker implantation, he said. “It’s hard to argue that this variation reflects quality of care, given that we looked at a top group of highly ranked hospitals.”
“Even more striking was how the price of a cardiovascular test within the very same hospital could differ across commercial insurance companies,” he said. “For example, the price of a stress test varied 5-fold in one hospital, and in another hospital, more than 4-fold for a coronary angiogram.”
Dr. Wadhera is senior author on the study published online as a research letter in JAMA Internal Medicine, with lead author Andrew S. Oseran, MD, MBA, also from Beth Israel Deaconess Medical Center.
Difficulties with data, interpretation
The researchers looked at payer and self-pay cash prices for noninvasive and invasive CV tests and procedures at the U.S. News & World Report 2021 top 20–ranked U.S. hospitals, based in part on Current Procedural Terminology codes.
Price differences among the hospitals were derived from median negotiated prices for each test and procedure at the centers across all payers. The interquartile ratio (IQR) of prices for each test or procedure across payers was used to evaluate within-hospital price variation.
“Only 80% of the hospitals reported prices for some cardiovascular tests and procedures,” Dr. Wadhera said. “For the most part, even among the hospitals that did report this information, it was extremely challenging to navigate and interpret the data provided.”
Further, the team found that only 7 of the 20 hospitals reported prices for all CV tests and procedures. Centers that did not post prices for some tests or procedures are named in the report’s Figure 1 and Figure 2.
The number of insurance plans listed for each test or procedure ranged from 1 to 432 in the analysis. Median prices ranged from $204 to $2,588 for an echocardiogram, $463 to $3,230 for a stress test, $2,821 to $9,382 for right heart catheterization, $2,868 to $9,203 for a coronary angiogram, $657 to $25,521 for a PCI, and $506 to $20,002 for pacemaker implantation, the report states.
A similar pattern was seen for self-pay cash prices.
Within-hospital variation also ranged broadly. For example, the widest IQR ranges were $3,143-$12,926 for a right heart catheterization, $4,011-$14,486 for a coronary angiogram, $11,325-$23,392 for a PCI, and $8,474-$22,694 for pacemaker implantation.
The report cites a number of limitations to the analysis, among those, the need to rely on the hospitals themselves for data quality and accuracy.
‘More needed besides transparency’
“As a means to better understand health care costs, many opined that full price transparency would leverage market dynamics and result in lower costs,” observed Clyde W. Yancy, MD, MSc, professor of medicine and chief of cardiology at Northwestern Medicine, Chicago. The findings “by an expert group of outcomes scientists make clear that more is needed besides price transparency to lower cost,” he said in an interview.
That said, he added, “there are sufficient variations and allowances made for data collection that it is preferable to hold the current findings circumspect at best. Importantly, the voice of the hospitals does not appear.”
Although “price variation among the top 20 hospitals is substantial,” he observed, “without a better assessment of root cause, actual charge capture, prevailing market dynamics – especially nursing and ancillary staff costs – and the general influence of inflation, it is too difficult to emerge with a precise interpretation.”
Across the 20 hospitals, “there are likely to be 20 different business models,” he added, with negotiated prices reflecting “at least regional, if not institutional, variations.”
“These are complex issues. The several-fold price differences in standard procedures are a concern and an area worth further study with the intention of lowering health care costs,” Dr. Yancy said. “But clearly our next efforts should not address lowering prices per se but understanding how prices are set [and] the connection with reimbursement and actual payments.”
Dr. Wadhera discloses receiving personal fees from Abbott and CVS Health unrelated to the current study; disclosures for the other authors are in the report. Dr. Yancy is deputy editor of JAMA Cardiology.
A version of this article first appeared on Medscape.com.
Neuroscientist alleges irregularities in Alzheimer’s research
A U.S. neuroscientist claims that some of the studies of the experimental agent, simufilam (Cassava Sciences), a drug that targets amyloid beta (Abeta) in Alzheimer’s disease (AD), are flawed, and, as a result, has taken his concerns to the National Institutes of Health.
Matthew Schrag, MD, PhD, department of neurology, Vanderbilt University Medical Center, Nashville, Tenn., uncovered what he calls inconsistencies in major studies examining the drug.
to support the hypothesis that buildup of amyloid in the brain causes AD. The NIH has funded research into Abeta as a potential cause of AD to the tune of millions of dollars for years.
“This hypothesis has been the central dominant thinking of the field,” Dr. Schrag told this news organization. “A lot of the therapies that have been developed and tested clinically over the last decade focused on the amyloid hypothesis in one formulation or another. So, it’s an important component of the way we think about Alzheimer’s disease,” he added.
In an in-depth article published in Science and written by investigative reporter Charles Piller, Dr. Schrag said he became involved after a colleague suggested he work with an attorney investigating simufilam. The lawyer paid Dr. Schrag $18,000 to investigate the research behind the agent. Cassava Sciences denies any misconduct, according to the article.
Dr. Schrag ran many AD studies through sophisticated imaging software. The effort revealed multiple Western blot images – which scientists use to detect the presence and amount of proteins in a sample – that appeared to be altered.
High stakes
Dr. Schrag found “apparently altered or duplicated images in dozens of journal articles,” the Science article states.
“A lot is at stake in terms of getting this right and it’s also important to acknowledge the limitations of what we can do. We were working with what’s published, what’s publicly available, and I think that it raises quite a lot of red flags, but we’ve also not reviewed the original material because it’s simply not available to us,” Dr. Schrag said in an interview.
However, he added that despite these limitations he believes “there’s enough here that it’s important for regulatory bodies to take a closer look at it to make sure that the data is right.”
Science reports that it launched its own independent review, asking several neuroscience experts to also review the research. They agreed with Dr. Schrag’s overall conclusions that something was amiss.
Many of the studies questioned in the whistleblower report involve Sylvain Lesné, PhD, who runs The Lesné Laboratory at the University of Minnesota, Minneapolis, and is an associate professor of neuroscience. His colleague Karen Ashe, MD, PhD, a professor of neurology at the same institution, was also mentioned in the whistleblower report. She was coauthor of a 2006 report in Nature that identified an Abeta subtype as a potential culprit behind AD.
This news organization reached out to Dr. Lesné and Dr. Ashe for comment, but has not received a response.
However, an email from a University of Minnesota spokesperson said the institution is “aware that questions have arisen regarding certain images used in peer-reviewed research publications authored by University faculty Dr. Ashe and Dr. Lesné. The University will follow its processes to review the questions any claims have raised. At this time, we have no further information to provide.”
A matter of trust
Dr. Schrag noted the “important trust relationship between patients, physicians and scientists. When we’re exploring diseases that we don’t have good treatments for.” He added that when patients agree to participate in trials and accept the associated risks, “we owe them a very high degree of integrity regarding the foundational data.”
Dr. Schrag also pointed out that there are limited resources to study these diseases. “There is some potential for that to be misdirected. It’s important for us to pay attention to data integrity issues, to make sure that we’re investing in the right places.”
The term “fraud” does not appear in Dr. Schrag’s whistleblower report, nor does he claim misconduct in the report. However, his work has spurred some independent, ongoing investigation into the claims by several journals that published the works in question, including Nature and Science Signaling.
Dr. Schrag said that if his findings are validated through an investigation he would like to see the scientific record corrected.
“Ultimately, I’d like to see a new set of hypotheses given a chance to look at this disease from a new perspective,” he added.
Dr. Schrag noted that the work described in the Science article was performed outside of his employment with Vanderbilt University Medical Center and that his opinions do not necessarily represent the views of Vanderbilt University or Vanderbilt University Medical Center.
A version of this article first appeared on Medscape.com.
A U.S. neuroscientist claims that some of the studies of the experimental agent, simufilam (Cassava Sciences), a drug that targets amyloid beta (Abeta) in Alzheimer’s disease (AD), are flawed, and, as a result, has taken his concerns to the National Institutes of Health.
Matthew Schrag, MD, PhD, department of neurology, Vanderbilt University Medical Center, Nashville, Tenn., uncovered what he calls inconsistencies in major studies examining the drug.
to support the hypothesis that buildup of amyloid in the brain causes AD. The NIH has funded research into Abeta as a potential cause of AD to the tune of millions of dollars for years.
“This hypothesis has been the central dominant thinking of the field,” Dr. Schrag told this news organization. “A lot of the therapies that have been developed and tested clinically over the last decade focused on the amyloid hypothesis in one formulation or another. So, it’s an important component of the way we think about Alzheimer’s disease,” he added.
In an in-depth article published in Science and written by investigative reporter Charles Piller, Dr. Schrag said he became involved after a colleague suggested he work with an attorney investigating simufilam. The lawyer paid Dr. Schrag $18,000 to investigate the research behind the agent. Cassava Sciences denies any misconduct, according to the article.
Dr. Schrag ran many AD studies through sophisticated imaging software. The effort revealed multiple Western blot images – which scientists use to detect the presence and amount of proteins in a sample – that appeared to be altered.
High stakes
Dr. Schrag found “apparently altered or duplicated images in dozens of journal articles,” the Science article states.
“A lot is at stake in terms of getting this right and it’s also important to acknowledge the limitations of what we can do. We were working with what’s published, what’s publicly available, and I think that it raises quite a lot of red flags, but we’ve also not reviewed the original material because it’s simply not available to us,” Dr. Schrag said in an interview.
However, he added that despite these limitations he believes “there’s enough here that it’s important for regulatory bodies to take a closer look at it to make sure that the data is right.”
Science reports that it launched its own independent review, asking several neuroscience experts to also review the research. They agreed with Dr. Schrag’s overall conclusions that something was amiss.
Many of the studies questioned in the whistleblower report involve Sylvain Lesné, PhD, who runs The Lesné Laboratory at the University of Minnesota, Minneapolis, and is an associate professor of neuroscience. His colleague Karen Ashe, MD, PhD, a professor of neurology at the same institution, was also mentioned in the whistleblower report. She was coauthor of a 2006 report in Nature that identified an Abeta subtype as a potential culprit behind AD.
This news organization reached out to Dr. Lesné and Dr. Ashe for comment, but has not received a response.
However, an email from a University of Minnesota spokesperson said the institution is “aware that questions have arisen regarding certain images used in peer-reviewed research publications authored by University faculty Dr. Ashe and Dr. Lesné. The University will follow its processes to review the questions any claims have raised. At this time, we have no further information to provide.”
A matter of trust
Dr. Schrag noted the “important trust relationship between patients, physicians and scientists. When we’re exploring diseases that we don’t have good treatments for.” He added that when patients agree to participate in trials and accept the associated risks, “we owe them a very high degree of integrity regarding the foundational data.”
Dr. Schrag also pointed out that there are limited resources to study these diseases. “There is some potential for that to be misdirected. It’s important for us to pay attention to data integrity issues, to make sure that we’re investing in the right places.”
The term “fraud” does not appear in Dr. Schrag’s whistleblower report, nor does he claim misconduct in the report. However, his work has spurred some independent, ongoing investigation into the claims by several journals that published the works in question, including Nature and Science Signaling.
Dr. Schrag said that if his findings are validated through an investigation he would like to see the scientific record corrected.
“Ultimately, I’d like to see a new set of hypotheses given a chance to look at this disease from a new perspective,” he added.
Dr. Schrag noted that the work described in the Science article was performed outside of his employment with Vanderbilt University Medical Center and that his opinions do not necessarily represent the views of Vanderbilt University or Vanderbilt University Medical Center.
A version of this article first appeared on Medscape.com.
A U.S. neuroscientist claims that some of the studies of the experimental agent, simufilam (Cassava Sciences), a drug that targets amyloid beta (Abeta) in Alzheimer’s disease (AD), are flawed, and, as a result, has taken his concerns to the National Institutes of Health.
Matthew Schrag, MD, PhD, department of neurology, Vanderbilt University Medical Center, Nashville, Tenn., uncovered what he calls inconsistencies in major studies examining the drug.
to support the hypothesis that buildup of amyloid in the brain causes AD. The NIH has funded research into Abeta as a potential cause of AD to the tune of millions of dollars for years.
“This hypothesis has been the central dominant thinking of the field,” Dr. Schrag told this news organization. “A lot of the therapies that have been developed and tested clinically over the last decade focused on the amyloid hypothesis in one formulation or another. So, it’s an important component of the way we think about Alzheimer’s disease,” he added.
In an in-depth article published in Science and written by investigative reporter Charles Piller, Dr. Schrag said he became involved after a colleague suggested he work with an attorney investigating simufilam. The lawyer paid Dr. Schrag $18,000 to investigate the research behind the agent. Cassava Sciences denies any misconduct, according to the article.
Dr. Schrag ran many AD studies through sophisticated imaging software. The effort revealed multiple Western blot images – which scientists use to detect the presence and amount of proteins in a sample – that appeared to be altered.
High stakes
Dr. Schrag found “apparently altered or duplicated images in dozens of journal articles,” the Science article states.
“A lot is at stake in terms of getting this right and it’s also important to acknowledge the limitations of what we can do. We were working with what’s published, what’s publicly available, and I think that it raises quite a lot of red flags, but we’ve also not reviewed the original material because it’s simply not available to us,” Dr. Schrag said in an interview.
However, he added that despite these limitations he believes “there’s enough here that it’s important for regulatory bodies to take a closer look at it to make sure that the data is right.”
Science reports that it launched its own independent review, asking several neuroscience experts to also review the research. They agreed with Dr. Schrag’s overall conclusions that something was amiss.
Many of the studies questioned in the whistleblower report involve Sylvain Lesné, PhD, who runs The Lesné Laboratory at the University of Minnesota, Minneapolis, and is an associate professor of neuroscience. His colleague Karen Ashe, MD, PhD, a professor of neurology at the same institution, was also mentioned in the whistleblower report. She was coauthor of a 2006 report in Nature that identified an Abeta subtype as a potential culprit behind AD.
This news organization reached out to Dr. Lesné and Dr. Ashe for comment, but has not received a response.
However, an email from a University of Minnesota spokesperson said the institution is “aware that questions have arisen regarding certain images used in peer-reviewed research publications authored by University faculty Dr. Ashe and Dr. Lesné. The University will follow its processes to review the questions any claims have raised. At this time, we have no further information to provide.”
A matter of trust
Dr. Schrag noted the “important trust relationship between patients, physicians and scientists. When we’re exploring diseases that we don’t have good treatments for.” He added that when patients agree to participate in trials and accept the associated risks, “we owe them a very high degree of integrity regarding the foundational data.”
Dr. Schrag also pointed out that there are limited resources to study these diseases. “There is some potential for that to be misdirected. It’s important for us to pay attention to data integrity issues, to make sure that we’re investing in the right places.”
The term “fraud” does not appear in Dr. Schrag’s whistleblower report, nor does he claim misconduct in the report. However, his work has spurred some independent, ongoing investigation into the claims by several journals that published the works in question, including Nature and Science Signaling.
Dr. Schrag said that if his findings are validated through an investigation he would like to see the scientific record corrected.
“Ultimately, I’d like to see a new set of hypotheses given a chance to look at this disease from a new perspective,” he added.
Dr. Schrag noted that the work described in the Science article was performed outside of his employment with Vanderbilt University Medical Center and that his opinions do not necessarily represent the views of Vanderbilt University or Vanderbilt University Medical Center.
A version of this article first appeared on Medscape.com.