MDedge Neurology

Pursuing fellowship training is often financially costly in terms of lifetime earnings, compared with starting a career as a general pediatrician immediately after residency, a report suggests.

Researchers found that most pediatric subspecialists – including those practicing neurology, pulmonology, and adolescent medicine – do not see a financial return from additional training because of the delays in receiving increased compensation and the repayment of educational debt.

“Most pediatric subspecialists don’t experience a relative increase in compensation after training compared to a general pediatrician, so there isn’t a financial benefit to additional training,” lead author Eva Catenaccio, MD, from the division of pediatric neurology, department of neurology, Johns Hopkins University, Baltimore, told this news organization.

The findings, published online March 8 in Pediatrics, contribute to the ongoing debate about the length of pediatric fellowship training programs. The data also provide evidence for the potential effect of a pediatric subspecialty loan repayment program.
 

Pediatric subspecialty training rarely pays off

However, not all practitioners in pediatric subspecialties would find themselves in the red relative to their generalist peers. Three subspecialties had a positive financial return: cardiology, critical care, and neonatology. Dr. Catenaccio explained that this may be because these subspecialties tend to be “inpatient procedure oriented, which are often more [lucrative] than outpatient cognitive–oriented subspecialties, such as pediatric infectious diseases, endocrinology, or adolescent medicine.”

Enrolling in a pediatric fellowship program resulted in lifetime financial returns that ranged from an increase of $852,129 for cardiology, relative to general pediatrics, to a loss of $1,594,366 for adolescent medicine, researchers found.

For the study, researchers calculated the financial returns of 15 pediatric subspecialties – emergency medicine, neurology, cardiology, critical care, neonatology, hematology and oncology, pulmonology, hospitalist medicine, allergy and immunology, gastroenterology, rheumatology, nephrology, adolescent medicine, infectious diseases, and endocrinology – in comparison with returns of private practice general pediatrics on the basis of 2018-2019 data on fellowship stipends, compensation, and educational debt.

They obtained most of the data from the Association of American Medical Colleges Survey of Resident/Fellow Stipends and Benefits, AAMC’s annual Medical School Faculty Salary Report, and the AAMC Medical School Graduation Questionnaire.

Richard Mink, MD, department of pediatrics, Harbor-UCLA Medical Center, Torrance, Calif., noted that it would have been helpful to have also compared the lifetime earnings of practitioners in pediatric subspecialties to academic general pediatricians and not just those in private practice.
 

The financial gap has worsened

To better understand which aspects of fellowship training have the greatest effect on lifetime compensation, Dr. Catenaccio and colleagues evaluated the potential effects of shortening fellowship length, eliminating school debt, and implementing a federal loan repayment plan. These changes enhanced the returns of cardiology, critical care, and neonatology – subspecialties that had already seen financial returns before these changes – and resulted in a positive financial return for emergency medicine.

The changes also narrowed the financial gap between subspecialties and general pediatrics. However, the remaining subspecialties still earned less than private practice pediatrics.

The new study is an update to a 2011 report, which reflected 2007-2008 data for 11 subspecialties. This time around, the researchers included the subspecialty of hospitalist medicine, which was approved as a board-certified subspecialty by the American Board of Pediatrics in 2014, as well as neurology, allergy and immunology, and adolescent medicine.

“I was most surprised that the additional pediatric subspecialties we included since the 2011 report followed the same general trend, with pediatric subspecialty training having a lower lifetime earning potential than general pediatrics,” Dr. Catenaccio said.

Comparing results from the two study periods showed that the financial gap between general pediatrics and subspecialty pediatrics worsened over time. For example, the financial return for pediatric endocrinology decreased an additional $500,000 between 2007 and 2018.

The researchers believe a combination of increased educational debt burden, slow growth in compensation, and changing interest rates over time have caused the financial differences between general pediatrics and subspecialty pediatrics to become more pronounced.
 

‘Pediatric subspecialty training is worth it!’

Despite the financial gaps, Dr. Catenaccio and colleagues say pediatric subspecialty training is still worthwhile but that policymakers should address these financial differences to help guide workforce distribution in a way that meets the needs of patients.

“I think pediatric subspecialty training is worth it,” said Dr. Catenaccio, who’s pursuing pediatric subspecialty training. “There are so many factors that go into choosing a specialty or subspecialty in medicine, including the desire to care for a particular patient population, interest in certain diseases or organ systems, lifestyle considerations, and research opportunities.”

But it’s also important for trainees to be aware of economic considerations in their decision-making.

Dr. Mink, who wrote an accompanying commentary, agrees that young clinicians should not make career decisions on the basis of metrics such as lifetime earning measures.

“I think people who go into pediatrics have decided that money is not the driving force,” said Dr. Mink. He noted that pediatricians are usually not paid well, compared with other specialists. “To me the important thing is you have to like what you’re doing.”

A 2020 study found that trainees who chose a career in pediatric pulmonology, a subspecialty, said that financial considerations were not the driving factor in their decision-making. Nevertheless, Dr. Mink also believes young clinicians should take into account their educational debt.

The further widening of the financial gap between general pediatrics and pediatric subspecialties could lead to shortages in the pediatric subspecialty workforce.

The authors and Dr. Mink have disclosed no relevant financial relationships.

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

Pursuing fellowship training is often financially costly in terms of lifetime earnings, compared with starting a career as a general pediatrician immediately after residency, a report suggests.

Researchers found that most pediatric subspecialists – including those practicing neurology, pulmonology, and adolescent medicine – do not see a financial return from additional training because of the delays in receiving increased compensation and the repayment of educational debt.

“Most pediatric subspecialists don’t experience a relative increase in compensation after training compared to a general pediatrician, so there isn’t a financial benefit to additional training,” lead author Eva Catenaccio, MD, from the division of pediatric neurology, department of neurology, Johns Hopkins University, Baltimore, told this news organization.

The findings, published online March 8 in Pediatrics, contribute to the ongoing debate about the length of pediatric fellowship training programs. The data also provide evidence for the potential effect of a pediatric subspecialty loan repayment program.
 

Pediatric subspecialty training rarely pays off

However, not all practitioners in pediatric subspecialties would find themselves in the red relative to their generalist peers. Three subspecialties had a positive financial return: cardiology, critical care, and neonatology. Dr. Catenaccio explained that this may be because these subspecialties tend to be “inpatient procedure oriented, which are often more [lucrative] than outpatient cognitive–oriented subspecialties, such as pediatric infectious diseases, endocrinology, or adolescent medicine.”

Enrolling in a pediatric fellowship program resulted in lifetime financial returns that ranged from an increase of $852,129 for cardiology, relative to general pediatrics, to a loss of $1,594,366 for adolescent medicine, researchers found.

For the study, researchers calculated the financial returns of 15 pediatric subspecialties – emergency medicine, neurology, cardiology, critical care, neonatology, hematology and oncology, pulmonology, hospitalist medicine, allergy and immunology, gastroenterology, rheumatology, nephrology, adolescent medicine, infectious diseases, and endocrinology – in comparison with returns of private practice general pediatrics on the basis of 2018-2019 data on fellowship stipends, compensation, and educational debt.

They obtained most of the data from the Association of American Medical Colleges Survey of Resident/Fellow Stipends and Benefits, AAMC’s annual Medical School Faculty Salary Report, and the AAMC Medical School Graduation Questionnaire.

Richard Mink, MD, department of pediatrics, Harbor-UCLA Medical Center, Torrance, Calif., noted that it would have been helpful to have also compared the lifetime earnings of practitioners in pediatric subspecialties to academic general pediatricians and not just those in private practice.
 

The financial gap has worsened

To better understand which aspects of fellowship training have the greatest effect on lifetime compensation, Dr. Catenaccio and colleagues evaluated the potential effects of shortening fellowship length, eliminating school debt, and implementing a federal loan repayment plan. These changes enhanced the returns of cardiology, critical care, and neonatology – subspecialties that had already seen financial returns before these changes – and resulted in a positive financial return for emergency medicine.

The changes also narrowed the financial gap between subspecialties and general pediatrics. However, the remaining subspecialties still earned less than private practice pediatrics.

The new study is an update to a 2011 report, which reflected 2007-2008 data for 11 subspecialties. This time around, the researchers included the subspecialty of hospitalist medicine, which was approved as a board-certified subspecialty by the American Board of Pediatrics in 2014, as well as neurology, allergy and immunology, and adolescent medicine.

“I was most surprised that the additional pediatric subspecialties we included since the 2011 report followed the same general trend, with pediatric subspecialty training having a lower lifetime earning potential than general pediatrics,” Dr. Catenaccio said.

Comparing results from the two study periods showed that the financial gap between general pediatrics and subspecialty pediatrics worsened over time. For example, the financial return for pediatric endocrinology decreased an additional $500,000 between 2007 and 2018.

The researchers believe a combination of increased educational debt burden, slow growth in compensation, and changing interest rates over time have caused the financial differences between general pediatrics and subspecialty pediatrics to become more pronounced.
 

‘Pediatric subspecialty training is worth it!’

Despite the financial gaps, Dr. Catenaccio and colleagues say pediatric subspecialty training is still worthwhile but that policymakers should address these financial differences to help guide workforce distribution in a way that meets the needs of patients.

“I think pediatric subspecialty training is worth it,” said Dr. Catenaccio, who’s pursuing pediatric subspecialty training. “There are so many factors that go into choosing a specialty or subspecialty in medicine, including the desire to care for a particular patient population, interest in certain diseases or organ systems, lifestyle considerations, and research opportunities.”

But it’s also important for trainees to be aware of economic considerations in their decision-making.

Dr. Mink, who wrote an accompanying commentary, agrees that young clinicians should not make career decisions on the basis of metrics such as lifetime earning measures.

“I think people who go into pediatrics have decided that money is not the driving force,” said Dr. Mink. He noted that pediatricians are usually not paid well, compared with other specialists. “To me the important thing is you have to like what you’re doing.”

A 2020 study found that trainees who chose a career in pediatric pulmonology, a subspecialty, said that financial considerations were not the driving factor in their decision-making. Nevertheless, Dr. Mink also believes young clinicians should take into account their educational debt.

The further widening of the financial gap between general pediatrics and pediatric subspecialties could lead to shortages in the pediatric subspecialty workforce.

The authors and Dr. Mink have disclosed no relevant financial relationships.

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

Pursuing fellowship training is often financially costly in terms of lifetime earnings, compared with starting a career as a general pediatrician immediately after residency, a report suggests.

Researchers found that most pediatric subspecialists – including those practicing neurology, pulmonology, and adolescent medicine – do not see a financial return from additional training because of the delays in receiving increased compensation and the repayment of educational debt.

“Most pediatric subspecialists don’t experience a relative increase in compensation after training compared to a general pediatrician, so there isn’t a financial benefit to additional training,” lead author Eva Catenaccio, MD, from the division of pediatric neurology, department of neurology, Johns Hopkins University, Baltimore, told this news organization.

The findings, published online March 8 in Pediatrics, contribute to the ongoing debate about the length of pediatric fellowship training programs. The data also provide evidence for the potential effect of a pediatric subspecialty loan repayment program.
 

Pediatric subspecialty training rarely pays off

However, not all practitioners in pediatric subspecialties would find themselves in the red relative to their generalist peers. Three subspecialties had a positive financial return: cardiology, critical care, and neonatology. Dr. Catenaccio explained that this may be because these subspecialties tend to be “inpatient procedure oriented, which are often more [lucrative] than outpatient cognitive–oriented subspecialties, such as pediatric infectious diseases, endocrinology, or adolescent medicine.”

Enrolling in a pediatric fellowship program resulted in lifetime financial returns that ranged from an increase of $852,129 for cardiology, relative to general pediatrics, to a loss of $1,594,366 for adolescent medicine, researchers found.

For the study, researchers calculated the financial returns of 15 pediatric subspecialties – emergency medicine, neurology, cardiology, critical care, neonatology, hematology and oncology, pulmonology, hospitalist medicine, allergy and immunology, gastroenterology, rheumatology, nephrology, adolescent medicine, infectious diseases, and endocrinology – in comparison with returns of private practice general pediatrics on the basis of 2018-2019 data on fellowship stipends, compensation, and educational debt.

They obtained most of the data from the Association of American Medical Colleges Survey of Resident/Fellow Stipends and Benefits, AAMC’s annual Medical School Faculty Salary Report, and the AAMC Medical School Graduation Questionnaire.

Richard Mink, MD, department of pediatrics, Harbor-UCLA Medical Center, Torrance, Calif., noted that it would have been helpful to have also compared the lifetime earnings of practitioners in pediatric subspecialties to academic general pediatricians and not just those in private practice.
 

The financial gap has worsened

To better understand which aspects of fellowship training have the greatest effect on lifetime compensation, Dr. Catenaccio and colleagues evaluated the potential effects of shortening fellowship length, eliminating school debt, and implementing a federal loan repayment plan. These changes enhanced the returns of cardiology, critical care, and neonatology – subspecialties that had already seen financial returns before these changes – and resulted in a positive financial return for emergency medicine.

The changes also narrowed the financial gap between subspecialties and general pediatrics. However, the remaining subspecialties still earned less than private practice pediatrics.

The new study is an update to a 2011 report, which reflected 2007-2008 data for 11 subspecialties. This time around, the researchers included the subspecialty of hospitalist medicine, which was approved as a board-certified subspecialty by the American Board of Pediatrics in 2014, as well as neurology, allergy and immunology, and adolescent medicine.

“I was most surprised that the additional pediatric subspecialties we included since the 2011 report followed the same general trend, with pediatric subspecialty training having a lower lifetime earning potential than general pediatrics,” Dr. Catenaccio said.

Comparing results from the two study periods showed that the financial gap between general pediatrics and subspecialty pediatrics worsened over time. For example, the financial return for pediatric endocrinology decreased an additional $500,000 between 2007 and 2018.

The researchers believe a combination of increased educational debt burden, slow growth in compensation, and changing interest rates over time have caused the financial differences between general pediatrics and subspecialty pediatrics to become more pronounced.
 

‘Pediatric subspecialty training is worth it!’

Despite the financial gaps, Dr. Catenaccio and colleagues say pediatric subspecialty training is still worthwhile but that policymakers should address these financial differences to help guide workforce distribution in a way that meets the needs of patients.

“I think pediatric subspecialty training is worth it,” said Dr. Catenaccio, who’s pursuing pediatric subspecialty training. “There are so many factors that go into choosing a specialty or subspecialty in medicine, including the desire to care for a particular patient population, interest in certain diseases or organ systems, lifestyle considerations, and research opportunities.”

But it’s also important for trainees to be aware of economic considerations in their decision-making.

Dr. Mink, who wrote an accompanying commentary, agrees that young clinicians should not make career decisions on the basis of metrics such as lifetime earning measures.

“I think people who go into pediatrics have decided that money is not the driving force,” said Dr. Mink. He noted that pediatricians are usually not paid well, compared with other specialists. “To me the important thing is you have to like what you’re doing.”

A 2020 study found that trainees who chose a career in pediatric pulmonology, a subspecialty, said that financial considerations were not the driving factor in their decision-making. Nevertheless, Dr. Mink also believes young clinicians should take into account their educational debt.

The further widening of the financial gap between general pediatrics and pediatric subspecialties could lead to shortages in the pediatric subspecialty workforce.

The authors and Dr. Mink have disclosed no relevant financial relationships.

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

Children who have higher levels of sun exposure appear to have a substantially lower risk of developing pediatric multiple sclerosis (MS) than children who are less exposed to the sun, research shows. The use of sunscreen does not appear to affect the risk.

“This is the first study, as far as we are aware, to investigate the effect of sun exposure in pediatric MS,” first author Prince Sebastian, of the ANU Medical School, Australian National University, Canberra, said during a presentation at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

“In order to reduce the incidence of MS, parents should be encouraged to allow their children to spend at least 30 minutes outdoors in the sun every day, while using adequate sun protection,” Mr. Sebastian said.

“This is especially important for children with a family history of MS,” he said. As the findings show, “you can use adequate sun protection and still get the benefit of sun exposure in terms of MS risk reduction.”

Low sun exposure, exposure to ultraviolet light, and vitamin D have been well established as modifiable risk factors for MS in adults. However, research is lacking on the effect of these factors upon patients younger than 18 years who have pediatric MS, a less common form of the disease. Pediatric MS constitutes about 5% of all MS cases.

To investigate the issue, Mr. Sebastian and colleagues evaluated data on 332 patients with pediatric MS who were between the ages of 4 and 22 years. The patients were enrolled at 16 MS centers around the United States. They were compared by sex and age with 534 control persons aged 3-22 years who did not have MS.

For the patients with MS, the median disease duration was 7.3 months, and 63% were female. The median age of the patients was 15.9 years.

Compared with those who did not have MS, patients with MS were significantly less likely to have been exposed to cigarette smoke (17.8% vs. 14.2%). They were significantly more likely to be overweight (23.8% vs. 14.2%), and the median anti-VCA level was higher (3.7 vs. 2.2).

Those who were exposed to the sun during the most recent summer for a duration of 30 minutes to 1 hour daily, as determined on the basis of self-report or parent report, had a 2.6-fold reduced risk of having MS, compared with those who spent less than 30 minutes outdoors daily (odds ratio, 0.39; P < .05), after adjusting for age, sex, birth season, the child’s skin color, the mother’s education, smoke exposure, being overweight, and Epstein-Barr virus infection.

Sun exposure for 1-2 hours daily was associated with a 7.4-fold reduced risk for MS, compared with exposure of 30 minutes or less (OR, 0.13; P < .001).

The odds were similar for those with 2-3 hours of sun exposure (OR, 0.21; P < .001) and for those with more than 3 hours of daily exposure (OR, 0.14; P < .001), versus less than 30 minutes.

Mr. Sebastian and his team also assessed the role of summer ambient levels of UV light and whether such exposure conferred a similar degree of protection. The risk for MS was lower among those who were exposed to higher summer ambient UV levels than among those exposed to lower levels (OR, 0.80; P = .046).

He noted, “Based on the results, individuals residing in Florida (28° N) would have 20% lower odds of MS, compared with an individual residing in New York (40° N).”

Interestingly, median rates of the use of sun protection were similar for the participants with MS and those without MS (OR, 0.95), suggesting that the use of sunscreen did not reduce the protective effect of sun exposure.

“We predicted that greater use of protection would limit effective sun exposure and would therefore increase MS risk,” Mr. Sebastian said, “but we don’t see that, and it’s probably because someone who uses sun protection likely gets more sun exposure anyway.”

“Our results suggest that you can use adequate sun protection and still get most of the benefit in terms of MS prevention, which is quite encouraging,” he added.

For those with MS, median serum 25(OH)D levels were higher (27.7 ng/mL vs. 23.7 ng/mL; P < .001), but Mr. Sebastian noted that this difference was likely attributable to the use of vitamin D supplementation after an MS diagnosis. An important limitation of the study was a lack of data on supplementation.
 

Stronger effect of frequent sun protection

Previous studies have shown a link between sun exposure and MS. A study published in 2018 compared 2,251 patients with MS with 4,028 control persons who did not have MS. The participants were in Canada, Italy, and Norway.

In that study, for most of the patients with MS, the age of onset was older than 18 years. In that study, there was a nearly 50% increased risk among those with the lowest degree of summer sun exposure in comparison with those who had the highest level of exposure (risk ratio, 1.47).

Contrary to the current study, that study did show an effect of the use of sun protection – those with the lowest degree of sun exposure during summer and winter and the highest use of sun protection had the highest risk for MS. They had a 76% increased risk, compared with those who had the highest degree of sun exposure and the least use of sun protection (RR, 1.76).

Sandra Magalhaes, PhD, of the University of New Brunswick, Fredericton, Canada, who was first author on that study, noted that the new study of pediatric MS adds valuable evidence on the issue.

“This study is important, as it adds to the etiological literature on MS implicating relevance of sun exposure,” Dr. Magalhaes said.

“We have a number of studies that have demonstrated an important effect of reduced levels of sun exposure and increased risk of MS. However, these studies focus on adult-onset MS populations; rather, the new study adds to the existing literature, as it also implicates sun exposure in etiology of pediatric-onset MS,” she said.

Notably, their previous work, unlike the current study, showed that, among those who experienced low levels of sun exposure, the risk for MS was higher for those who used sunscreen frequently.

“Overall, in their limited time outdoors, use of sunscreen may further increase risk of MS, which makes sense, since limited time outdoors in less sun, adding sun protection means [exposure to] even less sun.”

The findings of both studies support the bulk of research indicating that sun exposure is beneficial with regard to MS.

“There is a need for promoting balanced safe sun practices to reduce disease burden, especially in countries and cultures where children spend a lot of time indoors,” Dr. Magalhaes said. “Sun exposure has a number of important physiological roles, including vitamin D synthesis but also immune system functioning.”

Mr. Sebastian and Dr. Magalhaes have disclosed no relevant financial relationships.

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

Children who have higher levels of sun exposure appear to have a substantially lower risk of developing pediatric multiple sclerosis (MS) than children who are less exposed to the sun, research shows. The use of sunscreen does not appear to affect the risk.

“This is the first study, as far as we are aware, to investigate the effect of sun exposure in pediatric MS,” first author Prince Sebastian, of the ANU Medical School, Australian National University, Canberra, said during a presentation at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

“In order to reduce the incidence of MS, parents should be encouraged to allow their children to spend at least 30 minutes outdoors in the sun every day, while using adequate sun protection,” Mr. Sebastian said.

“This is especially important for children with a family history of MS,” he said. As the findings show, “you can use adequate sun protection and still get the benefit of sun exposure in terms of MS risk reduction.”

Low sun exposure, exposure to ultraviolet light, and vitamin D have been well established as modifiable risk factors for MS in adults. However, research is lacking on the effect of these factors upon patients younger than 18 years who have pediatric MS, a less common form of the disease. Pediatric MS constitutes about 5% of all MS cases.

To investigate the issue, Mr. Sebastian and colleagues evaluated data on 332 patients with pediatric MS who were between the ages of 4 and 22 years. The patients were enrolled at 16 MS centers around the United States. They were compared by sex and age with 534 control persons aged 3-22 years who did not have MS.

For the patients with MS, the median disease duration was 7.3 months, and 63% were female. The median age of the patients was 15.9 years.

Compared with those who did not have MS, patients with MS were significantly less likely to have been exposed to cigarette smoke (17.8% vs. 14.2%). They were significantly more likely to be overweight (23.8% vs. 14.2%), and the median anti-VCA level was higher (3.7 vs. 2.2).

Those who were exposed to the sun during the most recent summer for a duration of 30 minutes to 1 hour daily, as determined on the basis of self-report or parent report, had a 2.6-fold reduced risk of having MS, compared with those who spent less than 30 minutes outdoors daily (odds ratio, 0.39; P < .05), after adjusting for age, sex, birth season, the child’s skin color, the mother’s education, smoke exposure, being overweight, and Epstein-Barr virus infection.

Sun exposure for 1-2 hours daily was associated with a 7.4-fold reduced risk for MS, compared with exposure of 30 minutes or less (OR, 0.13; P < .001).

The odds were similar for those with 2-3 hours of sun exposure (OR, 0.21; P < .001) and for those with more than 3 hours of daily exposure (OR, 0.14; P < .001), versus less than 30 minutes.

Mr. Sebastian and his team also assessed the role of summer ambient levels of UV light and whether such exposure conferred a similar degree of protection. The risk for MS was lower among those who were exposed to higher summer ambient UV levels than among those exposed to lower levels (OR, 0.80; P = .046).

He noted, “Based on the results, individuals residing in Florida (28° N) would have 20% lower odds of MS, compared with an individual residing in New York (40° N).”

Interestingly, median rates of the use of sun protection were similar for the participants with MS and those without MS (OR, 0.95), suggesting that the use of sunscreen did not reduce the protective effect of sun exposure.

“We predicted that greater use of protection would limit effective sun exposure and would therefore increase MS risk,” Mr. Sebastian said, “but we don’t see that, and it’s probably because someone who uses sun protection likely gets more sun exposure anyway.”

“Our results suggest that you can use adequate sun protection and still get most of the benefit in terms of MS prevention, which is quite encouraging,” he added.

For those with MS, median serum 25(OH)D levels were higher (27.7 ng/mL vs. 23.7 ng/mL; P < .001), but Mr. Sebastian noted that this difference was likely attributable to the use of vitamin D supplementation after an MS diagnosis. An important limitation of the study was a lack of data on supplementation.
 

Stronger effect of frequent sun protection

Previous studies have shown a link between sun exposure and MS. A study published in 2018 compared 2,251 patients with MS with 4,028 control persons who did not have MS. The participants were in Canada, Italy, and Norway.

In that study, for most of the patients with MS, the age of onset was older than 18 years. In that study, there was a nearly 50% increased risk among those with the lowest degree of summer sun exposure in comparison with those who had the highest level of exposure (risk ratio, 1.47).

Contrary to the current study, that study did show an effect of the use of sun protection – those with the lowest degree of sun exposure during summer and winter and the highest use of sun protection had the highest risk for MS. They had a 76% increased risk, compared with those who had the highest degree of sun exposure and the least use of sun protection (RR, 1.76).

Sandra Magalhaes, PhD, of the University of New Brunswick, Fredericton, Canada, who was first author on that study, noted that the new study of pediatric MS adds valuable evidence on the issue.

“This study is important, as it adds to the etiological literature on MS implicating relevance of sun exposure,” Dr. Magalhaes said.

“We have a number of studies that have demonstrated an important effect of reduced levels of sun exposure and increased risk of MS. However, these studies focus on adult-onset MS populations; rather, the new study adds to the existing literature, as it also implicates sun exposure in etiology of pediatric-onset MS,” she said.

Notably, their previous work, unlike the current study, showed that, among those who experienced low levels of sun exposure, the risk for MS was higher for those who used sunscreen frequently.

“Overall, in their limited time outdoors, use of sunscreen may further increase risk of MS, which makes sense, since limited time outdoors in less sun, adding sun protection means [exposure to] even less sun.”

The findings of both studies support the bulk of research indicating that sun exposure is beneficial with regard to MS.

“There is a need for promoting balanced safe sun practices to reduce disease burden, especially in countries and cultures where children spend a lot of time indoors,” Dr. Magalhaes said. “Sun exposure has a number of important physiological roles, including vitamin D synthesis but also immune system functioning.”

Mr. Sebastian and Dr. Magalhaes have disclosed no relevant financial relationships.

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

Children who have higher levels of sun exposure appear to have a substantially lower risk of developing pediatric multiple sclerosis (MS) than children who are less exposed to the sun, research shows. The use of sunscreen does not appear to affect the risk.

“This is the first study, as far as we are aware, to investigate the effect of sun exposure in pediatric MS,” first author Prince Sebastian, of the ANU Medical School, Australian National University, Canberra, said during a presentation at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

“In order to reduce the incidence of MS, parents should be encouraged to allow their children to spend at least 30 minutes outdoors in the sun every day, while using adequate sun protection,” Mr. Sebastian said.

“This is especially important for children with a family history of MS,” he said. As the findings show, “you can use adequate sun protection and still get the benefit of sun exposure in terms of MS risk reduction.”

Low sun exposure, exposure to ultraviolet light, and vitamin D have been well established as modifiable risk factors for MS in adults. However, research is lacking on the effect of these factors upon patients younger than 18 years who have pediatric MS, a less common form of the disease. Pediatric MS constitutes about 5% of all MS cases.

To investigate the issue, Mr. Sebastian and colleagues evaluated data on 332 patients with pediatric MS who were between the ages of 4 and 22 years. The patients were enrolled at 16 MS centers around the United States. They were compared by sex and age with 534 control persons aged 3-22 years who did not have MS.

For the patients with MS, the median disease duration was 7.3 months, and 63% were female. The median age of the patients was 15.9 years.

Compared with those who did not have MS, patients with MS were significantly less likely to have been exposed to cigarette smoke (17.8% vs. 14.2%). They were significantly more likely to be overweight (23.8% vs. 14.2%), and the median anti-VCA level was higher (3.7 vs. 2.2).

Those who were exposed to the sun during the most recent summer for a duration of 30 minutes to 1 hour daily, as determined on the basis of self-report or parent report, had a 2.6-fold reduced risk of having MS, compared with those who spent less than 30 minutes outdoors daily (odds ratio, 0.39; P < .05), after adjusting for age, sex, birth season, the child’s skin color, the mother’s education, smoke exposure, being overweight, and Epstein-Barr virus infection.

Sun exposure for 1-2 hours daily was associated with a 7.4-fold reduced risk for MS, compared with exposure of 30 minutes or less (OR, 0.13; P < .001).

The odds were similar for those with 2-3 hours of sun exposure (OR, 0.21; P < .001) and for those with more than 3 hours of daily exposure (OR, 0.14; P < .001), versus less than 30 minutes.

Mr. Sebastian and his team also assessed the role of summer ambient levels of UV light and whether such exposure conferred a similar degree of protection. The risk for MS was lower among those who were exposed to higher summer ambient UV levels than among those exposed to lower levels (OR, 0.80; P = .046).

He noted, “Based on the results, individuals residing in Florida (28° N) would have 20% lower odds of MS, compared with an individual residing in New York (40° N).”

Interestingly, median rates of the use of sun protection were similar for the participants with MS and those without MS (OR, 0.95), suggesting that the use of sunscreen did not reduce the protective effect of sun exposure.

“We predicted that greater use of protection would limit effective sun exposure and would therefore increase MS risk,” Mr. Sebastian said, “but we don’t see that, and it’s probably because someone who uses sun protection likely gets more sun exposure anyway.”

“Our results suggest that you can use adequate sun protection and still get most of the benefit in terms of MS prevention, which is quite encouraging,” he added.

For those with MS, median serum 25(OH)D levels were higher (27.7 ng/mL vs. 23.7 ng/mL; P < .001), but Mr. Sebastian noted that this difference was likely attributable to the use of vitamin D supplementation after an MS diagnosis. An important limitation of the study was a lack of data on supplementation.
 

Stronger effect of frequent sun protection

Previous studies have shown a link between sun exposure and MS. A study published in 2018 compared 2,251 patients with MS with 4,028 control persons who did not have MS. The participants were in Canada, Italy, and Norway.

In that study, for most of the patients with MS, the age of onset was older than 18 years. In that study, there was a nearly 50% increased risk among those with the lowest degree of summer sun exposure in comparison with those who had the highest level of exposure (risk ratio, 1.47).

Contrary to the current study, that study did show an effect of the use of sun protection – those with the lowest degree of sun exposure during summer and winter and the highest use of sun protection had the highest risk for MS. They had a 76% increased risk, compared with those who had the highest degree of sun exposure and the least use of sun protection (RR, 1.76).

Sandra Magalhaes, PhD, of the University of New Brunswick, Fredericton, Canada, who was first author on that study, noted that the new study of pediatric MS adds valuable evidence on the issue.

“This study is important, as it adds to the etiological literature on MS implicating relevance of sun exposure,” Dr. Magalhaes said.

“We have a number of studies that have demonstrated an important effect of reduced levels of sun exposure and increased risk of MS. However, these studies focus on adult-onset MS populations; rather, the new study adds to the existing literature, as it also implicates sun exposure in etiology of pediatric-onset MS,” she said.

Notably, their previous work, unlike the current study, showed that, among those who experienced low levels of sun exposure, the risk for MS was higher for those who used sunscreen frequently.

“Overall, in their limited time outdoors, use of sunscreen may further increase risk of MS, which makes sense, since limited time outdoors in less sun, adding sun protection means [exposure to] even less sun.”

The findings of both studies support the bulk of research indicating that sun exposure is beneficial with regard to MS.

“There is a need for promoting balanced safe sun practices to reduce disease burden, especially in countries and cultures where children spend a lot of time indoors,” Dr. Magalhaes said. “Sun exposure has a number of important physiological roles, including vitamin D synthesis but also immune system functioning.”

Mr. Sebastian and Dr. Magalhaes have disclosed no relevant financial relationships.

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

Erythropoietin (EPO), shown in early studies to potentially provide neuroprotection for patients with optic neuritis, failed to provide any significant neuroprotection in comparison with placebo in a phase 3 randomized controlled trial.

“EPO conveyed neither functional nor structural neuroprotection in the visual pathways after optic neuritis as a clinically isolated syndrome,” said first author Wolf A. Lagreze, MD, of the University of Freiburg (Germany), in presenting the results at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

There are currently no treatments that provide neuroprotection for patients with optic neuritis, which can result in the degeneration of retinal ganglion cells, the axons of which form the optic nerve.

Although methylprednisolone, the standard treatment, can be of benefit, it has no effect in preventing neurodegeneration or subsequent vision impairment.

Importantly, optic neuritis, which can be a first sign of multiple sclerosis (MS), is considered an ideal model for an acute inflammatory attack on the nervous system and resulting neurodegeneration. Therefore, any treatment that provides neuroprotection for patients with optic neuritis could have potentially exciting broader implications.
 

The TONE trial

Preclinical studies have shown that EPO provides a small, potential degree of neuroprotection. To further evaluate EPO in this setting, Dr. Lagreze and colleagues conducted the TONE trial (Treatment of Optic Neuritis With Erythropoietin) in Germany between 2014 and 2017, in which they enrolled 108 patients with optic neuritis.

Inclusion criteria were having only unilateral optic neuritis as a clinically isolated syndrome that presented within 10 days of the first symptoms and having moderate to severe loss of visual acuity.

Persons with known MS were excluded; however, patients who were diagnosed with MS at the beginning of the study during the workup evaluation were included. Hence, about 20% of patients did have newly diagnosed MS, Dr. Lagreze noted.

The participants were randomly assigned in double-blind 1:1 ratio to receive treatment with either 33,000 IU EPO or placebo intravenously for 3 days as an adjunct to high-dose intravenous methylprednisolone (1,000 mg/day).

The final analysis included 52 patients who received EPO and 51 patients who received placebo. There were no significant differences between the groups in the first primary outcome of retinal nerve fiber layer atrophy, assessed with optic coherence tomography at week 26 (P = .76).

Likewise, no significant difference between groups was observed in the second primary outcome of low-contrast visual acuity at week 26, assessed using the 2.5% Sloan chart score of the affected eye (P = .38).

In addition, there were no significant differences between the groups in the rates of optic neuritis relapse.

In terms of safety measures, one patient in the EPO group developed sinus venous thrombosis, which was treated with anticoagulants and resolved without complications.
 

Reduced conversion to MS?

Interestingly, after 6 months, significantly fewer patients in the EPO arm (36%) had converted from clinically isolated syndrome to MS, compared with 57% in the placebo arm (P = .032). The difference became apparent as early as week 4.

Although those findings suggest that EPO provided some neuroprotection, there are notable caveats, Philippe Albrecht, MD, of the department of neurology at the University Hospital Dusseldorf (Germany), and a coauthor on the study, said.

“The significant separation of EPO and placebo group regarding MS conversion was observed very early on in the course and did not change thereafter,” Dr. Albrecht noted.

“One would expect a true disease-modifying effect of EPO on MS conversion to take longer to develop, and this early separation may very well have been due to an imbalance in the treatment groups, [for example] regarding MRI imaging findings such as gadolinium enhancement at baseline,” he said.

Dr. Lagreze said that it was a surprise to see no benefit from the drug, and a closer look at certain subgroups may still be worthwhile. Factors that could have a bearing on results include a shorter time interval for inclusion, having no concomitant use of steroids, and longer duration of treatment with EPO.

“If I could do the study again, I would do the treatment for longer than 3 days – that was based on experiences in previous EPO trials,” he said. “I would also love to do the trial without the concomitant methylprednisolone, but that is not possible from an ethical point of view.”
 

Trial nevertheless important

Commenting on the study, E. Anne Yeh, MD, of the division of neurology at the Hospital for Sick Children, Toronto, agreed that a challenge in evaluating therapies for optic neuritis is the potential for confounding from existing therapies that patients need to take.

“This agent could not be evaluated alone for its protective effect in comparison to no treatment at all,” she said.

In addition, improved metrics for gauging outcomes are needed to better determine the true effects, she added.

“The development of newer vision-related outcome metrics is important for future studies, and many are hard at work on both structural and functional metrics that may help us to understand the benefits of any protective therapies in a more nuanced manner than we are currently able to,” she said.

However, results of any kind – negative or positive – are valuable in improving understanding, Dr. Yeh underscored.

“Negative results can be disappointing in any trial, especially one in which alternative therapeutic pathways are being sought,” Dr. Yeh said. “I want to emphasize, however, that the fact that we are even considering and completing trials in this area is important.”

Dr. Yeh noted that she is currently involved in a trial that is evaluating the diabetes drug metformin for its remyelinating potential. “We hope to have some pilot data on MS in a few years,” she said.

Dr. Lagreze, Dr. Albrecht, and Dr. Yeh have disclosed no relevant financial relationships.

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

Erythropoietin (EPO), shown in early studies to potentially provide neuroprotection for patients with optic neuritis, failed to provide any significant neuroprotection in comparison with placebo in a phase 3 randomized controlled trial.

“EPO conveyed neither functional nor structural neuroprotection in the visual pathways after optic neuritis as a clinically isolated syndrome,” said first author Wolf A. Lagreze, MD, of the University of Freiburg (Germany), in presenting the results at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

There are currently no treatments that provide neuroprotection for patients with optic neuritis, which can result in the degeneration of retinal ganglion cells, the axons of which form the optic nerve.

Although methylprednisolone, the standard treatment, can be of benefit, it has no effect in preventing neurodegeneration or subsequent vision impairment.

Importantly, optic neuritis, which can be a first sign of multiple sclerosis (MS), is considered an ideal model for an acute inflammatory attack on the nervous system and resulting neurodegeneration. Therefore, any treatment that provides neuroprotection for patients with optic neuritis could have potentially exciting broader implications.
 

The TONE trial

Preclinical studies have shown that EPO provides a small, potential degree of neuroprotection. To further evaluate EPO in this setting, Dr. Lagreze and colleagues conducted the TONE trial (Treatment of Optic Neuritis With Erythropoietin) in Germany between 2014 and 2017, in which they enrolled 108 patients with optic neuritis.

Inclusion criteria were having only unilateral optic neuritis as a clinically isolated syndrome that presented within 10 days of the first symptoms and having moderate to severe loss of visual acuity.

Persons with known MS were excluded; however, patients who were diagnosed with MS at the beginning of the study during the workup evaluation were included. Hence, about 20% of patients did have newly diagnosed MS, Dr. Lagreze noted.

The participants were randomly assigned in double-blind 1:1 ratio to receive treatment with either 33,000 IU EPO or placebo intravenously for 3 days as an adjunct to high-dose intravenous methylprednisolone (1,000 mg/day).

The final analysis included 52 patients who received EPO and 51 patients who received placebo. There were no significant differences between the groups in the first primary outcome of retinal nerve fiber layer atrophy, assessed with optic coherence tomography at week 26 (P = .76).

Likewise, no significant difference between groups was observed in the second primary outcome of low-contrast visual acuity at week 26, assessed using the 2.5% Sloan chart score of the affected eye (P = .38).

In addition, there were no significant differences between the groups in the rates of optic neuritis relapse.

In terms of safety measures, one patient in the EPO group developed sinus venous thrombosis, which was treated with anticoagulants and resolved without complications.
 

Reduced conversion to MS?

Interestingly, after 6 months, significantly fewer patients in the EPO arm (36%) had converted from clinically isolated syndrome to MS, compared with 57% in the placebo arm (P = .032). The difference became apparent as early as week 4.

Although those findings suggest that EPO provided some neuroprotection, there are notable caveats, Philippe Albrecht, MD, of the department of neurology at the University Hospital Dusseldorf (Germany), and a coauthor on the study, said.

“The significant separation of EPO and placebo group regarding MS conversion was observed very early on in the course and did not change thereafter,” Dr. Albrecht noted.

“One would expect a true disease-modifying effect of EPO on MS conversion to take longer to develop, and this early separation may very well have been due to an imbalance in the treatment groups, [for example] regarding MRI imaging findings such as gadolinium enhancement at baseline,” he said.

Dr. Lagreze said that it was a surprise to see no benefit from the drug, and a closer look at certain subgroups may still be worthwhile. Factors that could have a bearing on results include a shorter time interval for inclusion, having no concomitant use of steroids, and longer duration of treatment with EPO.

“If I could do the study again, I would do the treatment for longer than 3 days – that was based on experiences in previous EPO trials,” he said. “I would also love to do the trial without the concomitant methylprednisolone, but that is not possible from an ethical point of view.”
 

Trial nevertheless important

Commenting on the study, E. Anne Yeh, MD, of the division of neurology at the Hospital for Sick Children, Toronto, agreed that a challenge in evaluating therapies for optic neuritis is the potential for confounding from existing therapies that patients need to take.

“This agent could not be evaluated alone for its protective effect in comparison to no treatment at all,” she said.

In addition, improved metrics for gauging outcomes are needed to better determine the true effects, she added.

“The development of newer vision-related outcome metrics is important for future studies, and many are hard at work on both structural and functional metrics that may help us to understand the benefits of any protective therapies in a more nuanced manner than we are currently able to,” she said.

However, results of any kind – negative or positive – are valuable in improving understanding, Dr. Yeh underscored.

“Negative results can be disappointing in any trial, especially one in which alternative therapeutic pathways are being sought,” Dr. Yeh said. “I want to emphasize, however, that the fact that we are even considering and completing trials in this area is important.”

Dr. Yeh noted that she is currently involved in a trial that is evaluating the diabetes drug metformin for its remyelinating potential. “We hope to have some pilot data on MS in a few years,” she said.

Dr. Lagreze, Dr. Albrecht, and Dr. Yeh have disclosed no relevant financial relationships.

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

Erythropoietin (EPO), shown in early studies to potentially provide neuroprotection for patients with optic neuritis, failed to provide any significant neuroprotection in comparison with placebo in a phase 3 randomized controlled trial.

“EPO conveyed neither functional nor structural neuroprotection in the visual pathways after optic neuritis as a clinically isolated syndrome,” said first author Wolf A. Lagreze, MD, of the University of Freiburg (Germany), in presenting the results at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

There are currently no treatments that provide neuroprotection for patients with optic neuritis, which can result in the degeneration of retinal ganglion cells, the axons of which form the optic nerve.

Although methylprednisolone, the standard treatment, can be of benefit, it has no effect in preventing neurodegeneration or subsequent vision impairment.

Importantly, optic neuritis, which can be a first sign of multiple sclerosis (MS), is considered an ideal model for an acute inflammatory attack on the nervous system and resulting neurodegeneration. Therefore, any treatment that provides neuroprotection for patients with optic neuritis could have potentially exciting broader implications.
 

The TONE trial

Preclinical studies have shown that EPO provides a small, potential degree of neuroprotection. To further evaluate EPO in this setting, Dr. Lagreze and colleagues conducted the TONE trial (Treatment of Optic Neuritis With Erythropoietin) in Germany between 2014 and 2017, in which they enrolled 108 patients with optic neuritis.

Inclusion criteria were having only unilateral optic neuritis as a clinically isolated syndrome that presented within 10 days of the first symptoms and having moderate to severe loss of visual acuity.

Persons with known MS were excluded; however, patients who were diagnosed with MS at the beginning of the study during the workup evaluation were included. Hence, about 20% of patients did have newly diagnosed MS, Dr. Lagreze noted.

The participants were randomly assigned in double-blind 1:1 ratio to receive treatment with either 33,000 IU EPO or placebo intravenously for 3 days as an adjunct to high-dose intravenous methylprednisolone (1,000 mg/day).

The final analysis included 52 patients who received EPO and 51 patients who received placebo. There were no significant differences between the groups in the first primary outcome of retinal nerve fiber layer atrophy, assessed with optic coherence tomography at week 26 (P = .76).

Likewise, no significant difference between groups was observed in the second primary outcome of low-contrast visual acuity at week 26, assessed using the 2.5% Sloan chart score of the affected eye (P = .38).

In addition, there were no significant differences between the groups in the rates of optic neuritis relapse.

In terms of safety measures, one patient in the EPO group developed sinus venous thrombosis, which was treated with anticoagulants and resolved without complications.
 

Reduced conversion to MS?

Interestingly, after 6 months, significantly fewer patients in the EPO arm (36%) had converted from clinically isolated syndrome to MS, compared with 57% in the placebo arm (P = .032). The difference became apparent as early as week 4.

Although those findings suggest that EPO provided some neuroprotection, there are notable caveats, Philippe Albrecht, MD, of the department of neurology at the University Hospital Dusseldorf (Germany), and a coauthor on the study, said.

“The significant separation of EPO and placebo group regarding MS conversion was observed very early on in the course and did not change thereafter,” Dr. Albrecht noted.

“One would expect a true disease-modifying effect of EPO on MS conversion to take longer to develop, and this early separation may very well have been due to an imbalance in the treatment groups, [for example] regarding MRI imaging findings such as gadolinium enhancement at baseline,” he said.

Dr. Lagreze said that it was a surprise to see no benefit from the drug, and a closer look at certain subgroups may still be worthwhile. Factors that could have a bearing on results include a shorter time interval for inclusion, having no concomitant use of steroids, and longer duration of treatment with EPO.

“If I could do the study again, I would do the treatment for longer than 3 days – that was based on experiences in previous EPO trials,” he said. “I would also love to do the trial without the concomitant methylprednisolone, but that is not possible from an ethical point of view.”
 

Trial nevertheless important

Commenting on the study, E. Anne Yeh, MD, of the division of neurology at the Hospital for Sick Children, Toronto, agreed that a challenge in evaluating therapies for optic neuritis is the potential for confounding from existing therapies that patients need to take.

“This agent could not be evaluated alone for its protective effect in comparison to no treatment at all,” she said.

In addition, improved metrics for gauging outcomes are needed to better determine the true effects, she added.

“The development of newer vision-related outcome metrics is important for future studies, and many are hard at work on both structural and functional metrics that may help us to understand the benefits of any protective therapies in a more nuanced manner than we are currently able to,” she said.

However, results of any kind – negative or positive – are valuable in improving understanding, Dr. Yeh underscored.

“Negative results can be disappointing in any trial, especially one in which alternative therapeutic pathways are being sought,” Dr. Yeh said. “I want to emphasize, however, that the fact that we are even considering and completing trials in this area is important.”

Dr. Yeh noted that she is currently involved in a trial that is evaluating the diabetes drug metformin for its remyelinating potential. “We hope to have some pilot data on MS in a few years,” she said.

Dr. Lagreze, Dr. Albrecht, and Dr. Yeh have disclosed no relevant financial relationships.

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

Veterans who have suffered a traumatic brain injury (TBI) are significantly more likely to develop insomnia and other sleep problems years later compared to their counterparts who have not suffered a brain injury, a new study shows.

Results of a large longitudinal study show that those with TBI were about 40% more likely to develop insomnia, sleep apnea, excessive daytime sleepiness, or another sleep disorder in later years, after adjusting for demographics and medical and psychiatric conditions.

Interestingly, the association with sleep disorders was strongest among those with mild TBI versus a more severe brain injury.

The study showed that the risk for sleep disorders increased up to 14 years after a brain injury, an indicator that “clinicians should really pay attention to sleep disorders in TBI patients both in the short term and the long term,” study investigator Yue Leng, MD, PhD, assistant professor, department of psychiatry and behavioral sciences, University of California, San Francisco, told this news organization.

The study was published online March 3 in Neurology.
 

First long-term look

TBI is common among veterans, who may have sleep complaints or psychiatric symptoms, but previous studies into the consequences of TBI have examined the short- vs. long-term impact, said Dr. Leng.

To examine the longitudinal association between TBI and sleep disorders, the investigators examined data on 98,709 Veterans Health Administration patients diagnosed with TBI and an age-matched group of the same number of veterans who had not received such a diagnosis. The mean age of the participants was 49 years at baseline, and 11.7% were women. Of the TBI cases, 49.6% were mild.

Researchers used an exposure survey and diagnostic codes to establish TBI and its severity.

Patients with TBI were more likely to be male and were much more likely to have a psychiatric condition, such as a mood disorder (22.4% vs. 9.3%), anxiety (10.5% vs. 4.4%), posttraumatic stress disorder (19.5% vs. 4.4%), or substance abuse (11.4% vs. 5.2%). They were also more likely to smoke or use tobacco (13.5% vs. 8.7%).

Researchers assessed a number of sleep disorders, including insomnia, hypersomnia disorders, narcolepsy, sleep-related breathing disorders, and sleep-related movement disorders.

During a follow-up period that averaged 5 years but ranged up to 14 years, 23.4% of veterans with TBI and 15.8% of those without TBI developed a sleep disorder.

After adjusting for age, sex, race, education, and income, those who had suffered a TBI were 50% more likely to develop any sleep disorder, compared with those who had not had a TBI (hazard ratio, 1.50; 95% confidence interval, 1.47-1.53.)

After controlling for medical conditions that included diabetes, hypertension, myocardial infarction, and cerebrovascular disease, as well as psychiatric disorders such as mood disorders, anxiety, PTSD, substance use disorder, and tobacco use, the HR for developing a sleep disorder was 1.41 (95% CI, 1.37-1.44).

The association with TBI was stronger for some sleep disorders. Adjusted HRs were 1.50 (95% CI, 1.45-1.55) for insomnia, 1.50 (95% CI, 1.39-1.61) for hypersomnia, 1.33 (95% CI, 1.16-1.52) for sleep-related movement disorders, and 1.28 (95% CI, 1.24-1.32) for sleep apnea.

It’s unclear what causes postinjury sleep problems, but it could be that TBI induces structural brain damage, or it could affect melatonin secretion or wake-promoting neurons.

Damage to arousal-promoting neurons could help explain the reason the link between TBI and sleep disorders was strongest for insomnia and hypersomnia, although the exact mechanism is unclear, said Dr. Leng.
 

Greater risk with mild TBI

Overall, the association was stronger for mild TBI than for moderate to severe TBI. This, said Dr. Leng, might be because of differences in the brain injury mechanism.

Mild TBI often involves repetitive concussive or subconcussive injuries, such as sports injuries or blast injury among active-duty military personnel. This type of injury is more likely to cause diffuse axonal injury and inflammation, whereas moderate or severe TBI is often attributable to a direct blow with more focal but severe damage, explained Dr. Leng.

She noted that veterans with mild TBI were more likely to have a psychiatric condition, but because the study controlled for such conditions, this doesn’t fully explain the stronger association between mild TBI and sleep disorders.

Further studies are needed to sort out the exact mechanisms, she said.

The association between TBI and risk for sleep disorders was reduced somewhat but was still moderate in an analysis that excluded patients who developed a sleep disorder within 2 years of a brain injury.

This analysis, said Dr. Leng, helped ensure that the sleep disorder developed after the brain injury.

The researchers could not examine the trajectory of sleep problems, so it’s not clear whether sleep problems worsen or get better over time, said Dr. Leng.

Because PTSD also leads to sleep problems, the researchers thought that having both PTSD and TBI might increase the risk for sleep problems. “But actually we found the association was pretty similar in those with, and without, PTSD, so that was kind of contrary to our hypothesis,” she said.

The new results underline the need for more screening for sleep disorders among patients with TBI, both in the short term and the long term, said Dr. Leng. “Clinicians should ask TBI patients about their sleep, and they should follow that up,” she said.

She added that long-term sleep disorders can affect a patient’s health and can lead to psychiatric problems and neurodegenerative diseases.

Depending on the type of sleep disorder, there are a number of possible treatments. For example, for patients with sleep apnea, continuous positive airway pressure treatment may be considered.
 

‘Outstanding’ research

Commenting for this news organization, Frank Conidi, MD, director, Florida Center for Headache and Sports Neurology; CEO, Brainsport, Team Neurologist, the Florida Panthers of the National Hockey League; and past president, Florida Society of Neurology, said the study is “by far” the largest to investigate the correlation between sleep disorders and head trauma.

The design and outcome measures “were well thought out,” and the researchers “did an outstanding job in sorting through and analyzing the data,” said Dr. Conidi.

He added that he was particularly impressed with how the researchers addressed PTSD, which is highly prevalent among veterans with head trauma and is known to affect sleep.

The new results “solidify what those of us who see individuals with TBI have observed over the years: that there is a higher incidence of all types of sleep disorders” in individuals with a TBI, said Dr. Conidi.

However, he questioned the study’s use of guidelines to classify the various types of head trauma. These guidelines, he said, “are based on loss of consciousness, which we have started to move away from when classifying TBI.”

In addition, Dr. Conidi said he “would have loved to have seen” some correlation with neuroimaging studies, such as those used to assess subdural hematoma, epidural hematoma, subarachnoid hemorrhage, and diffuse axonal injury, but that this “could be an impetus for future studies.”

In “a perfect world,” all patients with a TBI would undergo a polysomnography study in a sleep laboratory, but insurance companies now rarely cover such studies and have attempted to have clinicians shift to home sleep studies, said Dr. Conidi. “These are marginal at best for screening for sleep disorders,” he noted.

At his centers, every TBI patient is screened for sleep disorders and, whenever possible, undergoes formal evaluation in the sleep lab, he added.

The study was supported by the U.S. Army Medical Research and Material Command and the U.S. Department of Veterans Affairs. Dr. Leng and Dr. Conidi have disclosed no relevant financial relationships.

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

Veterans who have suffered a traumatic brain injury (TBI) are significantly more likely to develop insomnia and other sleep problems years later compared to their counterparts who have not suffered a brain injury, a new study shows.

Results of a large longitudinal study show that those with TBI were about 40% more likely to develop insomnia, sleep apnea, excessive daytime sleepiness, or another sleep disorder in later years, after adjusting for demographics and medical and psychiatric conditions.

Interestingly, the association with sleep disorders was strongest among those with mild TBI versus a more severe brain injury.

The study showed that the risk for sleep disorders increased up to 14 years after a brain injury, an indicator that “clinicians should really pay attention to sleep disorders in TBI patients both in the short term and the long term,” study investigator Yue Leng, MD, PhD, assistant professor, department of psychiatry and behavioral sciences, University of California, San Francisco, told this news organization.

The study was published online March 3 in Neurology.
 

First long-term look

TBI is common among veterans, who may have sleep complaints or psychiatric symptoms, but previous studies into the consequences of TBI have examined the short- vs. long-term impact, said Dr. Leng.

To examine the longitudinal association between TBI and sleep disorders, the investigators examined data on 98,709 Veterans Health Administration patients diagnosed with TBI and an age-matched group of the same number of veterans who had not received such a diagnosis. The mean age of the participants was 49 years at baseline, and 11.7% were women. Of the TBI cases, 49.6% were mild.

Researchers used an exposure survey and diagnostic codes to establish TBI and its severity.

Patients with TBI were more likely to be male and were much more likely to have a psychiatric condition, such as a mood disorder (22.4% vs. 9.3%), anxiety (10.5% vs. 4.4%), posttraumatic stress disorder (19.5% vs. 4.4%), or substance abuse (11.4% vs. 5.2%). They were also more likely to smoke or use tobacco (13.5% vs. 8.7%).

Researchers assessed a number of sleep disorders, including insomnia, hypersomnia disorders, narcolepsy, sleep-related breathing disorders, and sleep-related movement disorders.

During a follow-up period that averaged 5 years but ranged up to 14 years, 23.4% of veterans with TBI and 15.8% of those without TBI developed a sleep disorder.

After adjusting for age, sex, race, education, and income, those who had suffered a TBI were 50% more likely to develop any sleep disorder, compared with those who had not had a TBI (hazard ratio, 1.50; 95% confidence interval, 1.47-1.53.)

After controlling for medical conditions that included diabetes, hypertension, myocardial infarction, and cerebrovascular disease, as well as psychiatric disorders such as mood disorders, anxiety, PTSD, substance use disorder, and tobacco use, the HR for developing a sleep disorder was 1.41 (95% CI, 1.37-1.44).

The association with TBI was stronger for some sleep disorders. Adjusted HRs were 1.50 (95% CI, 1.45-1.55) for insomnia, 1.50 (95% CI, 1.39-1.61) for hypersomnia, 1.33 (95% CI, 1.16-1.52) for sleep-related movement disorders, and 1.28 (95% CI, 1.24-1.32) for sleep apnea.

It’s unclear what causes postinjury sleep problems, but it could be that TBI induces structural brain damage, or it could affect melatonin secretion or wake-promoting neurons.

Damage to arousal-promoting neurons could help explain the reason the link between TBI and sleep disorders was strongest for insomnia and hypersomnia, although the exact mechanism is unclear, said Dr. Leng.
 

Greater risk with mild TBI

Overall, the association was stronger for mild TBI than for moderate to severe TBI. This, said Dr. Leng, might be because of differences in the brain injury mechanism.

Mild TBI often involves repetitive concussive or subconcussive injuries, such as sports injuries or blast injury among active-duty military personnel. This type of injury is more likely to cause diffuse axonal injury and inflammation, whereas moderate or severe TBI is often attributable to a direct blow with more focal but severe damage, explained Dr. Leng.

She noted that veterans with mild TBI were more likely to have a psychiatric condition, but because the study controlled for such conditions, this doesn’t fully explain the stronger association between mild TBI and sleep disorders.

Further studies are needed to sort out the exact mechanisms, she said.

The association between TBI and risk for sleep disorders was reduced somewhat but was still moderate in an analysis that excluded patients who developed a sleep disorder within 2 years of a brain injury.

This analysis, said Dr. Leng, helped ensure that the sleep disorder developed after the brain injury.

The researchers could not examine the trajectory of sleep problems, so it’s not clear whether sleep problems worsen or get better over time, said Dr. Leng.

Because PTSD also leads to sleep problems, the researchers thought that having both PTSD and TBI might increase the risk for sleep problems. “But actually we found the association was pretty similar in those with, and without, PTSD, so that was kind of contrary to our hypothesis,” she said.

The new results underline the need for more screening for sleep disorders among patients with TBI, both in the short term and the long term, said Dr. Leng. “Clinicians should ask TBI patients about their sleep, and they should follow that up,” she said.

She added that long-term sleep disorders can affect a patient’s health and can lead to psychiatric problems and neurodegenerative diseases.

Depending on the type of sleep disorder, there are a number of possible treatments. For example, for patients with sleep apnea, continuous positive airway pressure treatment may be considered.
 

‘Outstanding’ research

Commenting for this news organization, Frank Conidi, MD, director, Florida Center for Headache and Sports Neurology; CEO, Brainsport, Team Neurologist, the Florida Panthers of the National Hockey League; and past president, Florida Society of Neurology, said the study is “by far” the largest to investigate the correlation between sleep disorders and head trauma.

The design and outcome measures “were well thought out,” and the researchers “did an outstanding job in sorting through and analyzing the data,” said Dr. Conidi.

He added that he was particularly impressed with how the researchers addressed PTSD, which is highly prevalent among veterans with head trauma and is known to affect sleep.

The new results “solidify what those of us who see individuals with TBI have observed over the years: that there is a higher incidence of all types of sleep disorders” in individuals with a TBI, said Dr. Conidi.

However, he questioned the study’s use of guidelines to classify the various types of head trauma. These guidelines, he said, “are based on loss of consciousness, which we have started to move away from when classifying TBI.”

In addition, Dr. Conidi said he “would have loved to have seen” some correlation with neuroimaging studies, such as those used to assess subdural hematoma, epidural hematoma, subarachnoid hemorrhage, and diffuse axonal injury, but that this “could be an impetus for future studies.”

In “a perfect world,” all patients with a TBI would undergo a polysomnography study in a sleep laboratory, but insurance companies now rarely cover such studies and have attempted to have clinicians shift to home sleep studies, said Dr. Conidi. “These are marginal at best for screening for sleep disorders,” he noted.

At his centers, every TBI patient is screened for sleep disorders and, whenever possible, undergoes formal evaluation in the sleep lab, he added.

The study was supported by the U.S. Army Medical Research and Material Command and the U.S. Department of Veterans Affairs. Dr. Leng and Dr. Conidi have disclosed no relevant financial relationships.

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

Veterans who have suffered a traumatic brain injury (TBI) are significantly more likely to develop insomnia and other sleep problems years later compared to their counterparts who have not suffered a brain injury, a new study shows.

Results of a large longitudinal study show that those with TBI were about 40% more likely to develop insomnia, sleep apnea, excessive daytime sleepiness, or another sleep disorder in later years, after adjusting for demographics and medical and psychiatric conditions.

Interestingly, the association with sleep disorders was strongest among those with mild TBI versus a more severe brain injury.

The study showed that the risk for sleep disorders increased up to 14 years after a brain injury, an indicator that “clinicians should really pay attention to sleep disorders in TBI patients both in the short term and the long term,” study investigator Yue Leng, MD, PhD, assistant professor, department of psychiatry and behavioral sciences, University of California, San Francisco, told this news organization.

The study was published online March 3 in Neurology.
 

First long-term look

TBI is common among veterans, who may have sleep complaints or psychiatric symptoms, but previous studies into the consequences of TBI have examined the short- vs. long-term impact, said Dr. Leng.

To examine the longitudinal association between TBI and sleep disorders, the investigators examined data on 98,709 Veterans Health Administration patients diagnosed with TBI and an age-matched group of the same number of veterans who had not received such a diagnosis. The mean age of the participants was 49 years at baseline, and 11.7% were women. Of the TBI cases, 49.6% were mild.

Researchers used an exposure survey and diagnostic codes to establish TBI and its severity.

Patients with TBI were more likely to be male and were much more likely to have a psychiatric condition, such as a mood disorder (22.4% vs. 9.3%), anxiety (10.5% vs. 4.4%), posttraumatic stress disorder (19.5% vs. 4.4%), or substance abuse (11.4% vs. 5.2%). They were also more likely to smoke or use tobacco (13.5% vs. 8.7%).

Researchers assessed a number of sleep disorders, including insomnia, hypersomnia disorders, narcolepsy, sleep-related breathing disorders, and sleep-related movement disorders.

During a follow-up period that averaged 5 years but ranged up to 14 years, 23.4% of veterans with TBI and 15.8% of those without TBI developed a sleep disorder.

After adjusting for age, sex, race, education, and income, those who had suffered a TBI were 50% more likely to develop any sleep disorder, compared with those who had not had a TBI (hazard ratio, 1.50; 95% confidence interval, 1.47-1.53.)

After controlling for medical conditions that included diabetes, hypertension, myocardial infarction, and cerebrovascular disease, as well as psychiatric disorders such as mood disorders, anxiety, PTSD, substance use disorder, and tobacco use, the HR for developing a sleep disorder was 1.41 (95% CI, 1.37-1.44).

The association with TBI was stronger for some sleep disorders. Adjusted HRs were 1.50 (95% CI, 1.45-1.55) for insomnia, 1.50 (95% CI, 1.39-1.61) for hypersomnia, 1.33 (95% CI, 1.16-1.52) for sleep-related movement disorders, and 1.28 (95% CI, 1.24-1.32) for sleep apnea.

It’s unclear what causes postinjury sleep problems, but it could be that TBI induces structural brain damage, or it could affect melatonin secretion or wake-promoting neurons.

Damage to arousal-promoting neurons could help explain the reason the link between TBI and sleep disorders was strongest for insomnia and hypersomnia, although the exact mechanism is unclear, said Dr. Leng.
 

Greater risk with mild TBI

Overall, the association was stronger for mild TBI than for moderate to severe TBI. This, said Dr. Leng, might be because of differences in the brain injury mechanism.

Mild TBI often involves repetitive concussive or subconcussive injuries, such as sports injuries or blast injury among active-duty military personnel. This type of injury is more likely to cause diffuse axonal injury and inflammation, whereas moderate or severe TBI is often attributable to a direct blow with more focal but severe damage, explained Dr. Leng.

She noted that veterans with mild TBI were more likely to have a psychiatric condition, but because the study controlled for such conditions, this doesn’t fully explain the stronger association between mild TBI and sleep disorders.

Further studies are needed to sort out the exact mechanisms, she said.

The association between TBI and risk for sleep disorders was reduced somewhat but was still moderate in an analysis that excluded patients who developed a sleep disorder within 2 years of a brain injury.

This analysis, said Dr. Leng, helped ensure that the sleep disorder developed after the brain injury.

The researchers could not examine the trajectory of sleep problems, so it’s not clear whether sleep problems worsen or get better over time, said Dr. Leng.

Because PTSD also leads to sleep problems, the researchers thought that having both PTSD and TBI might increase the risk for sleep problems. “But actually we found the association was pretty similar in those with, and without, PTSD, so that was kind of contrary to our hypothesis,” she said.

The new results underline the need for more screening for sleep disorders among patients with TBI, both in the short term and the long term, said Dr. Leng. “Clinicians should ask TBI patients about their sleep, and they should follow that up,” she said.

She added that long-term sleep disorders can affect a patient’s health and can lead to psychiatric problems and neurodegenerative diseases.

Depending on the type of sleep disorder, there are a number of possible treatments. For example, for patients with sleep apnea, continuous positive airway pressure treatment may be considered.
 

‘Outstanding’ research

Commenting for this news organization, Frank Conidi, MD, director, Florida Center for Headache and Sports Neurology; CEO, Brainsport, Team Neurologist, the Florida Panthers of the National Hockey League; and past president, Florida Society of Neurology, said the study is “by far” the largest to investigate the correlation between sleep disorders and head trauma.

The design and outcome measures “were well thought out,” and the researchers “did an outstanding job in sorting through and analyzing the data,” said Dr. Conidi.

He added that he was particularly impressed with how the researchers addressed PTSD, which is highly prevalent among veterans with head trauma and is known to affect sleep.

The new results “solidify what those of us who see individuals with TBI have observed over the years: that there is a higher incidence of all types of sleep disorders” in individuals with a TBI, said Dr. Conidi.

However, he questioned the study’s use of guidelines to classify the various types of head trauma. These guidelines, he said, “are based on loss of consciousness, which we have started to move away from when classifying TBI.”

In addition, Dr. Conidi said he “would have loved to have seen” some correlation with neuroimaging studies, such as those used to assess subdural hematoma, epidural hematoma, subarachnoid hemorrhage, and diffuse axonal injury, but that this “could be an impetus for future studies.”

In “a perfect world,” all patients with a TBI would undergo a polysomnography study in a sleep laboratory, but insurance companies now rarely cover such studies and have attempted to have clinicians shift to home sleep studies, said Dr. Conidi. “These are marginal at best for screening for sleep disorders,” he noted.

At his centers, every TBI patient is screened for sleep disorders and, whenever possible, undergoes formal evaluation in the sleep lab, he added.

The study was supported by the U.S. Army Medical Research and Material Command and the U.S. Department of Veterans Affairs. Dr. Leng and Dr. Conidi have disclosed no relevant financial relationships.

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

Edward H. Livingston, MD, has resigned as deputy editor of JAMA after he and the journal faced significant backlash over a February 2021 podcast that questioned the existence of structural racism.

JAMA editor in chief Howard Bauchner, MD, apologized to JAMA staff and stakeholders and asked for and received Dr. Livingston’s resignation, according to a statement from AMA CEO James Madara.

More than 2,000 people have signed a petition on Change.org calling for an investigation at JAMA over the podcast, called “Structural Racism for Doctors: What Is It?”

It appears they are now getting their wish. Dr. Bauchner announced that the journal’s oversight committee is investigating how the podcast and a tweet promoting the episode were developed, reviewed, and ultimately posted.

“This investigation and report of its findings will be thorough and completed rapidly,” Dr. Bauchner said.

Dr. Livingston, the host of the podcast, has been heavily criticized across social media. During the podcast, Dr. Livingston, who is White, said: “Structural racism is an unfortunate term. Personally, I think taking racism out of the conversation will help. Many of us are offended by the concept that we are racist.”

The audio of the podcast has been deleted from JAMA’s website. In its place is audio of a statement from Dr. Bauchner. In his statement, which he released last week, he said the comments in the podcast, which also featured Mitch Katz, MD, were “inaccurate, offensive, hurtful, and inconsistent with the standards of JAMA.”

Dr. Katz is an editor at JAMA Internal Medicine and CEO of NYC Health + Hospitals in New York.

Also deleted was a JAMA tweet promoting the podcast episode. The tweet said: “No physician is racist, so how can there be structural racism in health care? An explanation of the idea by doctors for doctors in this user-friendly podcast.”

The incident was met with anger and confusion in the medical community.

Herbert C. Smitherman, MD, vice dean of diversity and community affairs at Wayne State University, Detroit, noted after hearing the podcast that it was a symptom of a much larger problem.

“At its core, this podcast had racist tendencies. Those attitudes are why you don’t have as many articles by Black and Brown people in JAMA,” he said. “People’s attitudes, whether conscious or unconscious, are what drive the policies and practices which create the structural racism.”

Dr. Katz responded to the backlash last week with the following statement: “Systemic racism exists in our country. The disparate effects of the pandemic have made this painfully clear in New York City and across the country.

“As clinicians, we must understand how these structures and policies have a direct impact on the health outcomes of the patients and communities we serve. It is woefully naive to say that no physician is a racist just because the Civil Rights Act of 1964 forbade it, or that we should avoid the term ‘systematic racism’ because it makes people uncomfortable. We must and can do better.”

JAMA, an independent arm of the AMA, is taking other steps to address concerns. Its executive publisher, Thomas Easley, held an employee town hall this week, and said JAMA acknowledges that “structural racism is real, pernicious, and pervasive in health care.” The journal is also starting an “end-to-end review” of all editorial processes across all JAMA publications. Finally, the journal will also create a new associate editor’s position who will provide “insight and counsel” on racism and structural racism in health care.

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

Edward H. Livingston, MD, has resigned as deputy editor of JAMA after he and the journal faced significant backlash over a February 2021 podcast that questioned the existence of structural racism.

JAMA editor in chief Howard Bauchner, MD, apologized to JAMA staff and stakeholders and asked for and received Dr. Livingston’s resignation, according to a statement from AMA CEO James Madara.

More than 2,000 people have signed a petition on Change.org calling for an investigation at JAMA over the podcast, called “Structural Racism for Doctors: What Is It?”

It appears they are now getting their wish. Dr. Bauchner announced that the journal’s oversight committee is investigating how the podcast and a tweet promoting the episode were developed, reviewed, and ultimately posted.

“This investigation and report of its findings will be thorough and completed rapidly,” Dr. Bauchner said.

Dr. Livingston, the host of the podcast, has been heavily criticized across social media. During the podcast, Dr. Livingston, who is White, said: “Structural racism is an unfortunate term. Personally, I think taking racism out of the conversation will help. Many of us are offended by the concept that we are racist.”

The audio of the podcast has been deleted from JAMA’s website. In its place is audio of a statement from Dr. Bauchner. In his statement, which he released last week, he said the comments in the podcast, which also featured Mitch Katz, MD, were “inaccurate, offensive, hurtful, and inconsistent with the standards of JAMA.”

Dr. Katz is an editor at JAMA Internal Medicine and CEO of NYC Health + Hospitals in New York.

Also deleted was a JAMA tweet promoting the podcast episode. The tweet said: “No physician is racist, so how can there be structural racism in health care? An explanation of the idea by doctors for doctors in this user-friendly podcast.”

The incident was met with anger and confusion in the medical community.

Herbert C. Smitherman, MD, vice dean of diversity and community affairs at Wayne State University, Detroit, noted after hearing the podcast that it was a symptom of a much larger problem.

“At its core, this podcast had racist tendencies. Those attitudes are why you don’t have as many articles by Black and Brown people in JAMA,” he said. “People’s attitudes, whether conscious or unconscious, are what drive the policies and practices which create the structural racism.”

Dr. Katz responded to the backlash last week with the following statement: “Systemic racism exists in our country. The disparate effects of the pandemic have made this painfully clear in New York City and across the country.

“As clinicians, we must understand how these structures and policies have a direct impact on the health outcomes of the patients and communities we serve. It is woefully naive to say that no physician is a racist just because the Civil Rights Act of 1964 forbade it, or that we should avoid the term ‘systematic racism’ because it makes people uncomfortable. We must and can do better.”

JAMA, an independent arm of the AMA, is taking other steps to address concerns. Its executive publisher, Thomas Easley, held an employee town hall this week, and said JAMA acknowledges that “structural racism is real, pernicious, and pervasive in health care.” The journal is also starting an “end-to-end review” of all editorial processes across all JAMA publications. Finally, the journal will also create a new associate editor’s position who will provide “insight and counsel” on racism and structural racism in health care.

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

Edward H. Livingston, MD, has resigned as deputy editor of JAMA after he and the journal faced significant backlash over a February 2021 podcast that questioned the existence of structural racism.

JAMA editor in chief Howard Bauchner, MD, apologized to JAMA staff and stakeholders and asked for and received Dr. Livingston’s resignation, according to a statement from AMA CEO James Madara.

More than 2,000 people have signed a petition on Change.org calling for an investigation at JAMA over the podcast, called “Structural Racism for Doctors: What Is It?”

It appears they are now getting their wish. Dr. Bauchner announced that the journal’s oversight committee is investigating how the podcast and a tweet promoting the episode were developed, reviewed, and ultimately posted.

“This investigation and report of its findings will be thorough and completed rapidly,” Dr. Bauchner said.

Dr. Livingston, the host of the podcast, has been heavily criticized across social media. During the podcast, Dr. Livingston, who is White, said: “Structural racism is an unfortunate term. Personally, I think taking racism out of the conversation will help. Many of us are offended by the concept that we are racist.”

The audio of the podcast has been deleted from JAMA’s website. In its place is audio of a statement from Dr. Bauchner. In his statement, which he released last week, he said the comments in the podcast, which also featured Mitch Katz, MD, were “inaccurate, offensive, hurtful, and inconsistent with the standards of JAMA.”

Dr. Katz is an editor at JAMA Internal Medicine and CEO of NYC Health + Hospitals in New York.

Also deleted was a JAMA tweet promoting the podcast episode. The tweet said: “No physician is racist, so how can there be structural racism in health care? An explanation of the idea by doctors for doctors in this user-friendly podcast.”

The incident was met with anger and confusion in the medical community.

Herbert C. Smitherman, MD, vice dean of diversity and community affairs at Wayne State University, Detroit, noted after hearing the podcast that it was a symptom of a much larger problem.

“At its core, this podcast had racist tendencies. Those attitudes are why you don’t have as many articles by Black and Brown people in JAMA,” he said. “People’s attitudes, whether conscious or unconscious, are what drive the policies and practices which create the structural racism.”

Dr. Katz responded to the backlash last week with the following statement: “Systemic racism exists in our country. The disparate effects of the pandemic have made this painfully clear in New York City and across the country.

“As clinicians, we must understand how these structures and policies have a direct impact on the health outcomes of the patients and communities we serve. It is woefully naive to say that no physician is a racist just because the Civil Rights Act of 1964 forbade it, or that we should avoid the term ‘systematic racism’ because it makes people uncomfortable. We must and can do better.”

JAMA, an independent arm of the AMA, is taking other steps to address concerns. Its executive publisher, Thomas Easley, held an employee town hall this week, and said JAMA acknowledges that “structural racism is real, pernicious, and pervasive in health care.” The journal is also starting an “end-to-end review” of all editorial processes across all JAMA publications. Finally, the journal will also create a new associate editor’s position who will provide “insight and counsel” on racism and structural racism in health care.

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

Both high and low serum sodium levels are associated with adverse outcomes for hospitalized patients with COVID-19, new research suggests.

In the retrospective study of 488 patients hospitalized with COVID-19 at one of two London hospitals between February and May 2020, hypernatremia (defined as serum sodium level >145 mmol/L) at any time point during hospital stay was associated with a threefold increase in inpatient mortality.

Hyponatremia (serum sodium level <135 mmol/L) was associated with twice the likelihood of requiring advanced ventilatory support. In-hospital mortality was also increased among patients with hypovolemic hyponatremia.

“Serum sodium values could be used in clinical practice to identify patients with COVID-19 at high risk of poor outcomes who would benefit from more intensive monitoring and judicious rehydration,” Ploutarchos Tzoulis, MD, PhD, and colleagues wrote in their article, which was published online on Feb. 24, 2021, in the Journal of Clinical Endocrinology and Metabolism.

The findings will be presented at the upcoming news conference held by the Endocrine Society
 

Should sodium be included in a risk calculator for COVID-19?

Dr. Tzoulis, professor of endocrinology at the University College London Medical School, said in an interview that “sodium could be incorporated in risk calculators across other routine biomarkers, such as white cell count, lymphocytes, and CRP [C-reactive protein], in order to provide a tool for dynamic risk stratification throughout the clinical course of COVID-19 and assist clinical decision-making.”

Moreover, he said, “we should follow less conservative strategies in the rate and amount of fluid resuscitation in order to prevent hypernatremia, which is induced by negative fluid balance and can often be iatrogenic.”

Asked to comment, Steven Q. Simpson, MD, professor of medicine in the division of pulmonary, critical care, and sleep medicine at the University of Kansas, Kansas City, said that the article is missing key results that would assist in interpreting of the findings.

“Data regarding diuretic use and sparing of fluid administration are not in the paper. ... It is simply not possible to tell whether serum sodium is a ‘predictor’ ... or if it is a side effect of other issues or actions taken by physicians in patients who are progressing poorly.

“To say that sodium needs to be included in a risk calculator is to subtly suggest that there is some causal association with mortality, and that has quite clearly not been established,” stressed Dr. Simpson, who is president of the American College of Chest Physicians but was not speaking for the organization.

He added: “The data are interesting, but not actionable. It is common practice in critical care medicine to adjust water and salt intake to maintain serum sodium within the normal range, so the paper really doesn’t change any behavior.”

Dr. Tzoulis said in an interview that, despite not having electronic medical record data on diuretic use or fluid input and output, “our acute physicians and intensivists at both study sites have been adamant that they’ve not routinely used diuretics in COVID-19 patients. Diuretics have been sparingly used in our cohort, and also the frequency of pulmonary edema was reported as below 5%.”

Regarding volume of fluid intake, Dr. Tzoulis noted, “At our hospital sites, the strategy has been that of cautious fluid resuscitation. In fact, the amount of fluid given has been reported by our physicians and intensivists as ‘on purpose much more conservative than the usual one adopted in patients with community-acquired pneumonia at risk of respiratory failure.’ ”
 

Hyper- and hyponatremia linked to adverse COVID-19 outcomes

In the study, 5.3% of the 488 patients had hypernatremia at hospital presentation, and 24.6% had hyponatremia. Of note, only 19% of those with hyponatremia underwent laboratory workup to determine the etiology. Of those, three quarters had hypovolemic hyponatremia, determined on the basis of a urinary sodium cutoff of 30 mmol/L.

The total in-hospital mortality rate was 31.1%. There was a strong, although nonsignificant, trend toward higher mortality in association with sodium status at admission. Death rates were 28.4%, 30.8%, and 46.1% for those who were normonatremic, hyponatremic, and hypernatremic, respectively (P = .07). Baseline serum sodium levels didn’t differ between survivors (137 mmol/L) and nonsurvivors (138 mmol/L).

In multivariable analysis, the occurrence of hypernatremia at any point during the first 5 days in the hospital was among three independent risk factors for higher in-hospital mortality (adjusted hazard ratio, 2.74; P = .02). The other risk factors were older age and higher CRP level.

Overall, hyponatremia was not associated with death (P = .41).

During hospitalization, 37.9% of patients remained normonatremic; 36.9% experienced hyponatremia; 10.9% had hypernatremia; and 14.3% had both conditions at some point during their stay.

In-hospital mortality was 21% among those with normonatremia, compared with 56.6% for those with hypernatremia (odds ratio, 3.05; P = .0038) and 45.7% for those with both (OR, 2.25; P < .0001).

The 28.3% mortality rate in the overall group that experienced hyponatremia didn’t differ significantly from the 21.1% in the normonatremic group (OR, 1.34; P = .16). However, the death rate was 40.9% among the subgroup that developed hypovolemic hyponatremia, significantly higher than the normonatremic group (OR, 2.59, P = .0017).

The incidence of hyponatremia decreased from 24.6% at admission to 14.1% 5 days later, whereas the frequency of hypernatremia rose from 5.3% to 13.8%.
 

Key finding: Link between hospital-acquired hypernatremia and death

“The key novel finding of our study was that hospital-acquired hypernatremia, rather than hypernatremia at admission, was a predictor for in-hospital mortality, with the worst prognosis being reported in patients with the largest increase in serum sodium in the first 5 days of hospitalization,” noted Dr. Tzoulis and colleagues.

Hypernatremia was present in 29.6% of nonsurvivors, compared with 5.2% in survivors.

Among 120 patients with hyponatremia at admission, 31.7% received advanced respiratory support, compared with 17.5% and 7.7% of those with normonatremia or hypernatremia, respectively (OR, 2.18; P = .0011).

In contrast, there was no difference in the proportions needing ventilatory support between those with hypernatremia and those with normonatremia (16.7% vs. 12.4%; OR, 1.44; P = .39).

Acute kidney injury occurred in 181 patients (37.1%). It was not related to serum sodium concentration at any time point.

Dr. Tzoulis and Dr. Simpson disclosed no relevant financial relationships.

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

Both high and low serum sodium levels are associated with adverse outcomes for hospitalized patients with COVID-19, new research suggests.

In the retrospective study of 488 patients hospitalized with COVID-19 at one of two London hospitals between February and May 2020, hypernatremia (defined as serum sodium level >145 mmol/L) at any time point during hospital stay was associated with a threefold increase in inpatient mortality.

Hyponatremia (serum sodium level <135 mmol/L) was associated with twice the likelihood of requiring advanced ventilatory support. In-hospital mortality was also increased among patients with hypovolemic hyponatremia.

“Serum sodium values could be used in clinical practice to identify patients with COVID-19 at high risk of poor outcomes who would benefit from more intensive monitoring and judicious rehydration,” Ploutarchos Tzoulis, MD, PhD, and colleagues wrote in their article, which was published online on Feb. 24, 2021, in the Journal of Clinical Endocrinology and Metabolism.

The findings will be presented at the upcoming news conference held by the Endocrine Society
 

Should sodium be included in a risk calculator for COVID-19?

Dr. Tzoulis, professor of endocrinology at the University College London Medical School, said in an interview that “sodium could be incorporated in risk calculators across other routine biomarkers, such as white cell count, lymphocytes, and CRP [C-reactive protein], in order to provide a tool for dynamic risk stratification throughout the clinical course of COVID-19 and assist clinical decision-making.”

Moreover, he said, “we should follow less conservative strategies in the rate and amount of fluid resuscitation in order to prevent hypernatremia, which is induced by negative fluid balance and can often be iatrogenic.”

Asked to comment, Steven Q. Simpson, MD, professor of medicine in the division of pulmonary, critical care, and sleep medicine at the University of Kansas, Kansas City, said that the article is missing key results that would assist in interpreting of the findings.

“Data regarding diuretic use and sparing of fluid administration are not in the paper. ... It is simply not possible to tell whether serum sodium is a ‘predictor’ ... or if it is a side effect of other issues or actions taken by physicians in patients who are progressing poorly.

“To say that sodium needs to be included in a risk calculator is to subtly suggest that there is some causal association with mortality, and that has quite clearly not been established,” stressed Dr. Simpson, who is president of the American College of Chest Physicians but was not speaking for the organization.

He added: “The data are interesting, but not actionable. It is common practice in critical care medicine to adjust water and salt intake to maintain serum sodium within the normal range, so the paper really doesn’t change any behavior.”

Dr. Tzoulis said in an interview that, despite not having electronic medical record data on diuretic use or fluid input and output, “our acute physicians and intensivists at both study sites have been adamant that they’ve not routinely used diuretics in COVID-19 patients. Diuretics have been sparingly used in our cohort, and also the frequency of pulmonary edema was reported as below 5%.”

Regarding volume of fluid intake, Dr. Tzoulis noted, “At our hospital sites, the strategy has been that of cautious fluid resuscitation. In fact, the amount of fluid given has been reported by our physicians and intensivists as ‘on purpose much more conservative than the usual one adopted in patients with community-acquired pneumonia at risk of respiratory failure.’ ”
 

Hyper- and hyponatremia linked to adverse COVID-19 outcomes

In the study, 5.3% of the 488 patients had hypernatremia at hospital presentation, and 24.6% had hyponatremia. Of note, only 19% of those with hyponatremia underwent laboratory workup to determine the etiology. Of those, three quarters had hypovolemic hyponatremia, determined on the basis of a urinary sodium cutoff of 30 mmol/L.

The total in-hospital mortality rate was 31.1%. There was a strong, although nonsignificant, trend toward higher mortality in association with sodium status at admission. Death rates were 28.4%, 30.8%, and 46.1% for those who were normonatremic, hyponatremic, and hypernatremic, respectively (P = .07). Baseline serum sodium levels didn’t differ between survivors (137 mmol/L) and nonsurvivors (138 mmol/L).

In multivariable analysis, the occurrence of hypernatremia at any point during the first 5 days in the hospital was among three independent risk factors for higher in-hospital mortality (adjusted hazard ratio, 2.74; P = .02). The other risk factors were older age and higher CRP level.

Overall, hyponatremia was not associated with death (P = .41).

During hospitalization, 37.9% of patients remained normonatremic; 36.9% experienced hyponatremia; 10.9% had hypernatremia; and 14.3% had both conditions at some point during their stay.

In-hospital mortality was 21% among those with normonatremia, compared with 56.6% for those with hypernatremia (odds ratio, 3.05; P = .0038) and 45.7% for those with both (OR, 2.25; P < .0001).

The 28.3% mortality rate in the overall group that experienced hyponatremia didn’t differ significantly from the 21.1% in the normonatremic group (OR, 1.34; P = .16). However, the death rate was 40.9% among the subgroup that developed hypovolemic hyponatremia, significantly higher than the normonatremic group (OR, 2.59, P = .0017).

The incidence of hyponatremia decreased from 24.6% at admission to 14.1% 5 days later, whereas the frequency of hypernatremia rose from 5.3% to 13.8%.
 

Key finding: Link between hospital-acquired hypernatremia and death

“The key novel finding of our study was that hospital-acquired hypernatremia, rather than hypernatremia at admission, was a predictor for in-hospital mortality, with the worst prognosis being reported in patients with the largest increase in serum sodium in the first 5 days of hospitalization,” noted Dr. Tzoulis and colleagues.

Hypernatremia was present in 29.6% of nonsurvivors, compared with 5.2% in survivors.

Among 120 patients with hyponatremia at admission, 31.7% received advanced respiratory support, compared with 17.5% and 7.7% of those with normonatremia or hypernatremia, respectively (OR, 2.18; P = .0011).

In contrast, there was no difference in the proportions needing ventilatory support between those with hypernatremia and those with normonatremia (16.7% vs. 12.4%; OR, 1.44; P = .39).

Acute kidney injury occurred in 181 patients (37.1%). It was not related to serum sodium concentration at any time point.

Dr. Tzoulis and Dr. Simpson disclosed no relevant financial relationships.

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

Both high and low serum sodium levels are associated with adverse outcomes for hospitalized patients with COVID-19, new research suggests.

In the retrospective study of 488 patients hospitalized with COVID-19 at one of two London hospitals between February and May 2020, hypernatremia (defined as serum sodium level >145 mmol/L) at any time point during hospital stay was associated with a threefold increase in inpatient mortality.

Hyponatremia (serum sodium level <135 mmol/L) was associated with twice the likelihood of requiring advanced ventilatory support. In-hospital mortality was also increased among patients with hypovolemic hyponatremia.

“Serum sodium values could be used in clinical practice to identify patients with COVID-19 at high risk of poor outcomes who would benefit from more intensive monitoring and judicious rehydration,” Ploutarchos Tzoulis, MD, PhD, and colleagues wrote in their article, which was published online on Feb. 24, 2021, in the Journal of Clinical Endocrinology and Metabolism.

The findings will be presented at the upcoming news conference held by the Endocrine Society
 

Should sodium be included in a risk calculator for COVID-19?

Dr. Tzoulis, professor of endocrinology at the University College London Medical School, said in an interview that “sodium could be incorporated in risk calculators across other routine biomarkers, such as white cell count, lymphocytes, and CRP [C-reactive protein], in order to provide a tool for dynamic risk stratification throughout the clinical course of COVID-19 and assist clinical decision-making.”

Moreover, he said, “we should follow less conservative strategies in the rate and amount of fluid resuscitation in order to prevent hypernatremia, which is induced by negative fluid balance and can often be iatrogenic.”

Asked to comment, Steven Q. Simpson, MD, professor of medicine in the division of pulmonary, critical care, and sleep medicine at the University of Kansas, Kansas City, said that the article is missing key results that would assist in interpreting of the findings.

“Data regarding diuretic use and sparing of fluid administration are not in the paper. ... It is simply not possible to tell whether serum sodium is a ‘predictor’ ... or if it is a side effect of other issues or actions taken by physicians in patients who are progressing poorly.

“To say that sodium needs to be included in a risk calculator is to subtly suggest that there is some causal association with mortality, and that has quite clearly not been established,” stressed Dr. Simpson, who is president of the American College of Chest Physicians but was not speaking for the organization.

He added: “The data are interesting, but not actionable. It is common practice in critical care medicine to adjust water and salt intake to maintain serum sodium within the normal range, so the paper really doesn’t change any behavior.”

Dr. Tzoulis said in an interview that, despite not having electronic medical record data on diuretic use or fluid input and output, “our acute physicians and intensivists at both study sites have been adamant that they’ve not routinely used diuretics in COVID-19 patients. Diuretics have been sparingly used in our cohort, and also the frequency of pulmonary edema was reported as below 5%.”

Regarding volume of fluid intake, Dr. Tzoulis noted, “At our hospital sites, the strategy has been that of cautious fluid resuscitation. In fact, the amount of fluid given has been reported by our physicians and intensivists as ‘on purpose much more conservative than the usual one adopted in patients with community-acquired pneumonia at risk of respiratory failure.’ ”
 

Hyper- and hyponatremia linked to adverse COVID-19 outcomes

In the study, 5.3% of the 488 patients had hypernatremia at hospital presentation, and 24.6% had hyponatremia. Of note, only 19% of those with hyponatremia underwent laboratory workup to determine the etiology. Of those, three quarters had hypovolemic hyponatremia, determined on the basis of a urinary sodium cutoff of 30 mmol/L.

The total in-hospital mortality rate was 31.1%. There was a strong, although nonsignificant, trend toward higher mortality in association with sodium status at admission. Death rates were 28.4%, 30.8%, and 46.1% for those who were normonatremic, hyponatremic, and hypernatremic, respectively (P = .07). Baseline serum sodium levels didn’t differ between survivors (137 mmol/L) and nonsurvivors (138 mmol/L).

In multivariable analysis, the occurrence of hypernatremia at any point during the first 5 days in the hospital was among three independent risk factors for higher in-hospital mortality (adjusted hazard ratio, 2.74; P = .02). The other risk factors were older age and higher CRP level.

Overall, hyponatremia was not associated with death (P = .41).

During hospitalization, 37.9% of patients remained normonatremic; 36.9% experienced hyponatremia; 10.9% had hypernatremia; and 14.3% had both conditions at some point during their stay.

In-hospital mortality was 21% among those with normonatremia, compared with 56.6% for those with hypernatremia (odds ratio, 3.05; P = .0038) and 45.7% for those with both (OR, 2.25; P < .0001).

The 28.3% mortality rate in the overall group that experienced hyponatremia didn’t differ significantly from the 21.1% in the normonatremic group (OR, 1.34; P = .16). However, the death rate was 40.9% among the subgroup that developed hypovolemic hyponatremia, significantly higher than the normonatremic group (OR, 2.59, P = .0017).

The incidence of hyponatremia decreased from 24.6% at admission to 14.1% 5 days later, whereas the frequency of hypernatremia rose from 5.3% to 13.8%.
 

Key finding: Link between hospital-acquired hypernatremia and death

“The key novel finding of our study was that hospital-acquired hypernatremia, rather than hypernatremia at admission, was a predictor for in-hospital mortality, with the worst prognosis being reported in patients with the largest increase in serum sodium in the first 5 days of hospitalization,” noted Dr. Tzoulis and colleagues.

Hypernatremia was present in 29.6% of nonsurvivors, compared with 5.2% in survivors.

Among 120 patients with hyponatremia at admission, 31.7% received advanced respiratory support, compared with 17.5% and 7.7% of those with normonatremia or hypernatremia, respectively (OR, 2.18; P = .0011).

In contrast, there was no difference in the proportions needing ventilatory support between those with hypernatremia and those with normonatremia (16.7% vs. 12.4%; OR, 1.44; P = .39).

Acute kidney injury occurred in 181 patients (37.1%). It was not related to serum sodium concentration at any time point.

Dr. Tzoulis and Dr. Simpson disclosed no relevant financial relationships.

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

Seven weeks appears to be the ideal amount of time to delay surgery, when possible, after someone tests positive for COVID-19, researchers in the United Kingdom report.

BraunS/Getty Images

Risk for death was about 3.5 to 4 times higher in the first 6 weeks after surgery among more than 3,000 people with a preoperative COVID-19 diagnosis compared with patients without COVID-19. After 7 weeks, the 30-day mortality rate dropped to a baseline level.

The study was published online March 9 in Anaesthesia.

Surgery should be further delayed for people who remain symptomatic at 7 weeks post diagnosis, lead author Dmitri Nepogodiev, MBChB, said in an interview.

“In this group we recommend waiting until COVID-19 symptoms resolve, if possible. However, our study did not capture specific data on long COVID … so we are unable to make specific recommendations for this group,” said Dr. Nepogodiev, research fellow at the NIHR Global Health Research Unit on Global Surgery at the University of Birmingham (England).

“This should be an area for future research,” he added.

The international, multicenter, prospective cohort study is notable for its sheer size – more than 15,000 investigators reported outcomes for 140,231 surgical patients from 1,674 hospitals across 116 countries. In total, 2.2% of these patients tested positive for SARS-CoV-2 prior to surgery.

Surgery of any type performed in October 2020 was assessed. A greater proportion of patients with a preoperative COVID-19 diagnosis had emergency surgery, 44%, compared with 30% of people who never had a COVID-19 diagnosis.

Most patients were asymptomatic at the time of surgery, either because they never experienced COVID-19 symptoms or their symptoms resolved. The 30-day mortality rate was the primary outcome.
 

Death rates among surgical patients with preoperative COVID-19 diagnosis

Comparing the timing of surgery after COVID-19 diagnosis vs. 30-day mortality yielded the following results:

• 0 to 2 weeks – 9.1% mortality.
• 3 to 4 weeks – 6.9%.
• 5 to 6 weeks – 5.5%.
• 7 weeks or longer – 2.0%..

For comparison, the 30-day mortality rate for surgical patients without a preoperative COVID-19 diagnosis was 1.4%. A COVID-19 diagnosis more than 7 weeks before surgery did not make a significant difference on outcomes.
 

The ‘why’ remains unknown

The reasons for the association between a COVID-19 diagnosis and higher postoperative death rates remain unknown. However, Dr. Nepogodiev speculated that it could be related to “some degree of lung injury, even if patients are initially asymptomatic.”

Intubation and mechanical ventilation during surgery could exacerbate the existing lung injury, he said, thereby leading to more severe COVID-19.

In fact, Dr. Nepogodiev and colleagues found that postoperative pulmonary complications followed a pattern similar to the findings on death. They reported higher rates of pneumonia, acute respiratory distress syndrome, and unexpected reventilation in the first 6 weeks following a COVID-19 diagnosis. Again, at 7 weeks and beyond, the rates returned to be relatively the same as those for people who never had COVID-19.

“Waiting for 7 or more weeks may allow time for the initial COVID-19 injury to resolve,” Dr. Nepogodiev said.
 

‘An important study’

“This is an important study of postoperative mortality among patients recovered from COVID-19,” Adrian Diaz, MD, MPH, said in an interview when asked to comment.

The large cohort and numerous practice settings are among the strengths of the research, said Dr. Diaz, of the University of Michigan Institute for Healthcare Policy and Innovation in Ann Arbor. He was lead author of a June 2020 review article on elective surgery in the time of COVID-19, published in The American Journal of Surgery.

“As with nearly all studies of this nature, results must be interpreted on a case-by-case basis for individual patients. However, this study does add important information for patients and providers in helping them have an informed discussion on the timing of surgery,” said Dr. Diaz, a fellow in the Center for Healthcare Outcomes and Policy and a resident in general surgery at the Ohio State University, Columbus.

Dr. Nepogodiev and colleagues included both urgent and elective surgeries in the study. Dr. Diaz said this was a potential limitation because emergency operations “should never be delayed, by definition.” Lack of indications for the surgeries and information on cause of death were additional limitations.

Future research should evaluate any benefit in delaying surgery longer than 7 or more weeks, Dr. Diaz added, perhaps looking specifically at 10, 12, or 14 weeks, or considering outcomes as a continuous variable. This would help health care providers “garner more insight into risk and benefits of delaying surgery beyond 7 weeks.”

Dr. Nepogodiev and Dr. Diaz disclosed no relevant financial relationships. The study had multiple funding sources, including the National Institute for Health Research Global Health Research Unit, the Association of Upper Gastrointestinal Surgeons, the British Association of Surgical Oncology, and Medtronic.

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

Seven weeks appears to be the ideal amount of time to delay surgery, when possible, after someone tests positive for COVID-19, researchers in the United Kingdom report.

BraunS/Getty Images

Risk for death was about 3.5 to 4 times higher in the first 6 weeks after surgery among more than 3,000 people with a preoperative COVID-19 diagnosis compared with patients without COVID-19. After 7 weeks, the 30-day mortality rate dropped to a baseline level.

The study was published online March 9 in Anaesthesia.

Surgery should be further delayed for people who remain symptomatic at 7 weeks post diagnosis, lead author Dmitri Nepogodiev, MBChB, said in an interview.

“In this group we recommend waiting until COVID-19 symptoms resolve, if possible. However, our study did not capture specific data on long COVID … so we are unable to make specific recommendations for this group,” said Dr. Nepogodiev, research fellow at the NIHR Global Health Research Unit on Global Surgery at the University of Birmingham (England).

“This should be an area for future research,” he added.

The international, multicenter, prospective cohort study is notable for its sheer size – more than 15,000 investigators reported outcomes for 140,231 surgical patients from 1,674 hospitals across 116 countries. In total, 2.2% of these patients tested positive for SARS-CoV-2 prior to surgery.

Surgery of any type performed in October 2020 was assessed. A greater proportion of patients with a preoperative COVID-19 diagnosis had emergency surgery, 44%, compared with 30% of people who never had a COVID-19 diagnosis.

Most patients were asymptomatic at the time of surgery, either because they never experienced COVID-19 symptoms or their symptoms resolved. The 30-day mortality rate was the primary outcome.
 

Death rates among surgical patients with preoperative COVID-19 diagnosis

Comparing the timing of surgery after COVID-19 diagnosis vs. 30-day mortality yielded the following results:

• 0 to 2 weeks – 9.1% mortality.
• 3 to 4 weeks – 6.9%.
• 5 to 6 weeks – 5.5%.
• 7 weeks or longer – 2.0%..

For comparison, the 30-day mortality rate for surgical patients without a preoperative COVID-19 diagnosis was 1.4%. A COVID-19 diagnosis more than 7 weeks before surgery did not make a significant difference on outcomes.
 

The ‘why’ remains unknown

The reasons for the association between a COVID-19 diagnosis and higher postoperative death rates remain unknown. However, Dr. Nepogodiev speculated that it could be related to “some degree of lung injury, even if patients are initially asymptomatic.”

Intubation and mechanical ventilation during surgery could exacerbate the existing lung injury, he said, thereby leading to more severe COVID-19.

In fact, Dr. Nepogodiev and colleagues found that postoperative pulmonary complications followed a pattern similar to the findings on death. They reported higher rates of pneumonia, acute respiratory distress syndrome, and unexpected reventilation in the first 6 weeks following a COVID-19 diagnosis. Again, at 7 weeks and beyond, the rates returned to be relatively the same as those for people who never had COVID-19.

“Waiting for 7 or more weeks may allow time for the initial COVID-19 injury to resolve,” Dr. Nepogodiev said.
 

‘An important study’

“This is an important study of postoperative mortality among patients recovered from COVID-19,” Adrian Diaz, MD, MPH, said in an interview when asked to comment.

The large cohort and numerous practice settings are among the strengths of the research, said Dr. Diaz, of the University of Michigan Institute for Healthcare Policy and Innovation in Ann Arbor. He was lead author of a June 2020 review article on elective surgery in the time of COVID-19, published in The American Journal of Surgery.

“As with nearly all studies of this nature, results must be interpreted on a case-by-case basis for individual patients. However, this study does add important information for patients and providers in helping them have an informed discussion on the timing of surgery,” said Dr. Diaz, a fellow in the Center for Healthcare Outcomes and Policy and a resident in general surgery at the Ohio State University, Columbus.

Dr. Nepogodiev and colleagues included both urgent and elective surgeries in the study. Dr. Diaz said this was a potential limitation because emergency operations “should never be delayed, by definition.” Lack of indications for the surgeries and information on cause of death were additional limitations.

Future research should evaluate any benefit in delaying surgery longer than 7 or more weeks, Dr. Diaz added, perhaps looking specifically at 10, 12, or 14 weeks, or considering outcomes as a continuous variable. This would help health care providers “garner more insight into risk and benefits of delaying surgery beyond 7 weeks.”

Dr. Nepogodiev and Dr. Diaz disclosed no relevant financial relationships. The study had multiple funding sources, including the National Institute for Health Research Global Health Research Unit, the Association of Upper Gastrointestinal Surgeons, the British Association of Surgical Oncology, and Medtronic.

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

Seven weeks appears to be the ideal amount of time to delay surgery, when possible, after someone tests positive for COVID-19, researchers in the United Kingdom report.

BraunS/Getty Images

Risk for death was about 3.5 to 4 times higher in the first 6 weeks after surgery among more than 3,000 people with a preoperative COVID-19 diagnosis compared with patients without COVID-19. After 7 weeks, the 30-day mortality rate dropped to a baseline level.

The study was published online March 9 in Anaesthesia.

Surgery should be further delayed for people who remain symptomatic at 7 weeks post diagnosis, lead author Dmitri Nepogodiev, MBChB, said in an interview.

“In this group we recommend waiting until COVID-19 symptoms resolve, if possible. However, our study did not capture specific data on long COVID … so we are unable to make specific recommendations for this group,” said Dr. Nepogodiev, research fellow at the NIHR Global Health Research Unit on Global Surgery at the University of Birmingham (England).

“This should be an area for future research,” he added.

The international, multicenter, prospective cohort study is notable for its sheer size – more than 15,000 investigators reported outcomes for 140,231 surgical patients from 1,674 hospitals across 116 countries. In total, 2.2% of these patients tested positive for SARS-CoV-2 prior to surgery.

Surgery of any type performed in October 2020 was assessed. A greater proportion of patients with a preoperative COVID-19 diagnosis had emergency surgery, 44%, compared with 30% of people who never had a COVID-19 diagnosis.

Most patients were asymptomatic at the time of surgery, either because they never experienced COVID-19 symptoms or their symptoms resolved. The 30-day mortality rate was the primary outcome.
 

Death rates among surgical patients with preoperative COVID-19 diagnosis

Comparing the timing of surgery after COVID-19 diagnosis vs. 30-day mortality yielded the following results:

• 0 to 2 weeks – 9.1% mortality.
• 3 to 4 weeks – 6.9%.
• 5 to 6 weeks – 5.5%.
• 7 weeks or longer – 2.0%..

For comparison, the 30-day mortality rate for surgical patients without a preoperative COVID-19 diagnosis was 1.4%. A COVID-19 diagnosis more than 7 weeks before surgery did not make a significant difference on outcomes.
 

The ‘why’ remains unknown

The reasons for the association between a COVID-19 diagnosis and higher postoperative death rates remain unknown. However, Dr. Nepogodiev speculated that it could be related to “some degree of lung injury, even if patients are initially asymptomatic.”

Intubation and mechanical ventilation during surgery could exacerbate the existing lung injury, he said, thereby leading to more severe COVID-19.

In fact, Dr. Nepogodiev and colleagues found that postoperative pulmonary complications followed a pattern similar to the findings on death. They reported higher rates of pneumonia, acute respiratory distress syndrome, and unexpected reventilation in the first 6 weeks following a COVID-19 diagnosis. Again, at 7 weeks and beyond, the rates returned to be relatively the same as those for people who never had COVID-19.

“Waiting for 7 or more weeks may allow time for the initial COVID-19 injury to resolve,” Dr. Nepogodiev said.
 

‘An important study’

“This is an important study of postoperative mortality among patients recovered from COVID-19,” Adrian Diaz, MD, MPH, said in an interview when asked to comment.

The large cohort and numerous practice settings are among the strengths of the research, said Dr. Diaz, of the University of Michigan Institute for Healthcare Policy and Innovation in Ann Arbor. He was lead author of a June 2020 review article on elective surgery in the time of COVID-19, published in The American Journal of Surgery.

“As with nearly all studies of this nature, results must be interpreted on a case-by-case basis for individual patients. However, this study does add important information for patients and providers in helping them have an informed discussion on the timing of surgery,” said Dr. Diaz, a fellow in the Center for Healthcare Outcomes and Policy and a resident in general surgery at the Ohio State University, Columbus.

Dr. Nepogodiev and colleagues included both urgent and elective surgeries in the study. Dr. Diaz said this was a potential limitation because emergency operations “should never be delayed, by definition.” Lack of indications for the surgeries and information on cause of death were additional limitations.

Future research should evaluate any benefit in delaying surgery longer than 7 or more weeks, Dr. Diaz added, perhaps looking specifically at 10, 12, or 14 weeks, or considering outcomes as a continuous variable. This would help health care providers “garner more insight into risk and benefits of delaying surgery beyond 7 weeks.”

Dr. Nepogodiev and Dr. Diaz disclosed no relevant financial relationships. The study had multiple funding sources, including the National Institute for Health Research Global Health Research Unit, the Association of Upper Gastrointestinal Surgeons, the British Association of Surgical Oncology, and Medtronic.

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

Palliative care for people with dementia is increasingly recognized as a way to improve quality of life and provide relief from the myriad physical and psychological symptoms of advancing neurodegenerative disease. But unlike in cancer, relatively few patients with terminal dementia receive referrals to palliative care.

A new literature review has found these referrals to be all over the map among patients with dementia – with many occurring very late in the disease process – and do not reflect any consistent criteria based on patient needs.

For their research, published March 2 in the Journal of the American Geriatrics Society, Li Mo, MD, of the University of Texas MD Anderson Cancer Center in Houston, and colleagues looked at nearly 60 studies dating back to the early 1990s that contained information on referrals to palliative care for patients with dementia. While a palliative care approach can be provided by nonspecialists, all the included studies dealt at least in part with specialist care.
 

Standardized criteria is lacking

The investigators found advanced or late-stage dementia to be the most common reason cited for referral, with three quarters of the studies recommending palliative care for late-stage or advanced dementia, generally without qualifying what symptoms or needs were present. Patients received palliative care across a range of settings, including nursing homes, hospitals, and their own homes, though many articles did not include information on where patients received care.

A fifth of the articles suggested that medical complications of dementia including falls, pneumonia, and ulcers should trigger referrals to palliative care, while another fifth cited poor prognosis, defined varyingly as having between 2 years and 6 months likely left to live. Poor nutrition status was identified in 10% of studies as meriting referral.

Only 20% of the studies identified patient needs – evidence of psychological distress or functional decline, for example – as criteria for referral, despite these being ubiquitous in dementia. The authors said they were surprised by this finding, which could possibly be explained, they wrote, by “the interest among geriatrician, neurologist, and primary care teams to provide good symptom management,” reflecting a de facto palliative care approach. “There is also significant stigma associated with a specialist palliative care referral,” the authors noted.

Curiously, the researchers noted, a new diagnosis of dementia in more than a quarter of the studies triggered referral, a finding that possibly reflected delayed diagnoses.

The findings revealed “heterogeneity in the literature in reasons for involving specialist palliative care, which may partly explain the variation in patterns of palliative care referral,” Dr. Mo and colleagues wrote, stressing that more standardized criteria are urgently needed to bring dementia in line with cancer in terms of providing timely palliative care.

Patients with advancing dementia have little chance to self-report symptoms, meaning that more attention to patient complaints earlier in the disease course, and greater sensitivity to patient distress, are required. By routinely screening symptoms, clinicians could use specific cutoffs “as triggers to initiate automatic timely palliative care referral,” the authors concluded, noting that more research was needed before these cutoffs, whether based on symptom intensity or other measures, could be calculated.

Dr. Mo and colleagues acknowledged as weaknesses of their study the fact that a third of the articles in the review were based on expert consensus, while others did not distinguish clearly between primary and specialist palliative care.
 

A starting point for further discussion

Asked to comment on the findings, Elizabeth Sampson, MD, a palliative care researcher at University College London, praised Dr. Mo and colleagues’ study as “starting to pull together the strands” of a systematic approach to referrals and access to palliative care in dementia.

Dr. Sampson’s group is leading a UK-government funded research effort that aims to develop cost-effective palliative care interventions in dementia, in part through a tool that uses caregiver reports to assess symptom burden and patient needs. The research program “is founded on a needs-based approach, which aims to look at people’s individual needs and responding to them in a proactive way,” she said.

One of the obstacles to timely palliative care in dementia, Dr. Sampson said, is weighing resource allocation against what can be wildly varying prognoses. “Hospices understand when someone has terminal cancer and [is] likely to die within a few weeks, but it’s not unheard of for someone in very advanced stages of dementia to live another year,” she said. “There are concerns that a rapid increase in people with dementia being moved to palliative care could overwhelm already limited hospice capacity. We would argue that the best approach is to get palliative care out to where people with dementia live, which is usually the care home.”

Dr. Mo and colleagues’ study received funding from the National Institutes of Health, and its authors disclosed no financial conflicts of interest. Dr. Sampson’s work is supported by the UK’s Economic and Social Research Council and National Institute for Health Research. She disclosed no conflicts of interest.

Palliative care for people with dementia is increasingly recognized as a way to improve quality of life and provide relief from the myriad physical and psychological symptoms of advancing neurodegenerative disease. But unlike in cancer, relatively few patients with terminal dementia receive referrals to palliative care.

A new literature review has found these referrals to be all over the map among patients with dementia – with many occurring very late in the disease process – and do not reflect any consistent criteria based on patient needs.

For their research, published March 2 in the Journal of the American Geriatrics Society, Li Mo, MD, of the University of Texas MD Anderson Cancer Center in Houston, and colleagues looked at nearly 60 studies dating back to the early 1990s that contained information on referrals to palliative care for patients with dementia. While a palliative care approach can be provided by nonspecialists, all the included studies dealt at least in part with specialist care.
 

Standardized criteria is lacking

The investigators found advanced or late-stage dementia to be the most common reason cited for referral, with three quarters of the studies recommending palliative care for late-stage or advanced dementia, generally without qualifying what symptoms or needs were present. Patients received palliative care across a range of settings, including nursing homes, hospitals, and their own homes, though many articles did not include information on where patients received care.

A fifth of the articles suggested that medical complications of dementia including falls, pneumonia, and ulcers should trigger referrals to palliative care, while another fifth cited poor prognosis, defined varyingly as having between 2 years and 6 months likely left to live. Poor nutrition status was identified in 10% of studies as meriting referral.

Only 20% of the studies identified patient needs – evidence of psychological distress or functional decline, for example – as criteria for referral, despite these being ubiquitous in dementia. The authors said they were surprised by this finding, which could possibly be explained, they wrote, by “the interest among geriatrician, neurologist, and primary care teams to provide good symptom management,” reflecting a de facto palliative care approach. “There is also significant stigma associated with a specialist palliative care referral,” the authors noted.

Curiously, the researchers noted, a new diagnosis of dementia in more than a quarter of the studies triggered referral, a finding that possibly reflected delayed diagnoses.

The findings revealed “heterogeneity in the literature in reasons for involving specialist palliative care, which may partly explain the variation in patterns of palliative care referral,” Dr. Mo and colleagues wrote, stressing that more standardized criteria are urgently needed to bring dementia in line with cancer in terms of providing timely palliative care.

Patients with advancing dementia have little chance to self-report symptoms, meaning that more attention to patient complaints earlier in the disease course, and greater sensitivity to patient distress, are required. By routinely screening symptoms, clinicians could use specific cutoffs “as triggers to initiate automatic timely palliative care referral,” the authors concluded, noting that more research was needed before these cutoffs, whether based on symptom intensity or other measures, could be calculated.

Dr. Mo and colleagues acknowledged as weaknesses of their study the fact that a third of the articles in the review were based on expert consensus, while others did not distinguish clearly between primary and specialist palliative care.
 

A starting point for further discussion

Asked to comment on the findings, Elizabeth Sampson, MD, a palliative care researcher at University College London, praised Dr. Mo and colleagues’ study as “starting to pull together the strands” of a systematic approach to referrals and access to palliative care in dementia.

Dr. Sampson’s group is leading a UK-government funded research effort that aims to develop cost-effective palliative care interventions in dementia, in part through a tool that uses caregiver reports to assess symptom burden and patient needs. The research program “is founded on a needs-based approach, which aims to look at people’s individual needs and responding to them in a proactive way,” she said.

One of the obstacles to timely palliative care in dementia, Dr. Sampson said, is weighing resource allocation against what can be wildly varying prognoses. “Hospices understand when someone has terminal cancer and [is] likely to die within a few weeks, but it’s not unheard of for someone in very advanced stages of dementia to live another year,” she said. “There are concerns that a rapid increase in people with dementia being moved to palliative care could overwhelm already limited hospice capacity. We would argue that the best approach is to get palliative care out to where people with dementia live, which is usually the care home.”

Dr. Mo and colleagues’ study received funding from the National Institutes of Health, and its authors disclosed no financial conflicts of interest. Dr. Sampson’s work is supported by the UK’s Economic and Social Research Council and National Institute for Health Research. She disclosed no conflicts of interest.

Palliative care for people with dementia is increasingly recognized as a way to improve quality of life and provide relief from the myriad physical and psychological symptoms of advancing neurodegenerative disease. But unlike in cancer, relatively few patients with terminal dementia receive referrals to palliative care.

A new literature review has found these referrals to be all over the map among patients with dementia – with many occurring very late in the disease process – and do not reflect any consistent criteria based on patient needs.

For their research, published March 2 in the Journal of the American Geriatrics Society, Li Mo, MD, of the University of Texas MD Anderson Cancer Center in Houston, and colleagues looked at nearly 60 studies dating back to the early 1990s that contained information on referrals to palliative care for patients with dementia. While a palliative care approach can be provided by nonspecialists, all the included studies dealt at least in part with specialist care.
 

Standardized criteria is lacking

The investigators found advanced or late-stage dementia to be the most common reason cited for referral, with three quarters of the studies recommending palliative care for late-stage or advanced dementia, generally without qualifying what symptoms or needs were present. Patients received palliative care across a range of settings, including nursing homes, hospitals, and their own homes, though many articles did not include information on where patients received care.

A fifth of the articles suggested that medical complications of dementia including falls, pneumonia, and ulcers should trigger referrals to palliative care, while another fifth cited poor prognosis, defined varyingly as having between 2 years and 6 months likely left to live. Poor nutrition status was identified in 10% of studies as meriting referral.

Only 20% of the studies identified patient needs – evidence of psychological distress or functional decline, for example – as criteria for referral, despite these being ubiquitous in dementia. The authors said they were surprised by this finding, which could possibly be explained, they wrote, by “the interest among geriatrician, neurologist, and primary care teams to provide good symptom management,” reflecting a de facto palliative care approach. “There is also significant stigma associated with a specialist palliative care referral,” the authors noted.

Curiously, the researchers noted, a new diagnosis of dementia in more than a quarter of the studies triggered referral, a finding that possibly reflected delayed diagnoses.

The findings revealed “heterogeneity in the literature in reasons for involving specialist palliative care, which may partly explain the variation in patterns of palliative care referral,” Dr. Mo and colleagues wrote, stressing that more standardized criteria are urgently needed to bring dementia in line with cancer in terms of providing timely palliative care.

Patients with advancing dementia have little chance to self-report symptoms, meaning that more attention to patient complaints earlier in the disease course, and greater sensitivity to patient distress, are required. By routinely screening symptoms, clinicians could use specific cutoffs “as triggers to initiate automatic timely palliative care referral,” the authors concluded, noting that more research was needed before these cutoffs, whether based on symptom intensity or other measures, could be calculated.

Dr. Mo and colleagues acknowledged as weaknesses of their study the fact that a third of the articles in the review were based on expert consensus, while others did not distinguish clearly between primary and specialist palliative care.
 

A starting point for further discussion

Asked to comment on the findings, Elizabeth Sampson, MD, a palliative care researcher at University College London, praised Dr. Mo and colleagues’ study as “starting to pull together the strands” of a systematic approach to referrals and access to palliative care in dementia.

Dr. Sampson’s group is leading a UK-government funded research effort that aims to develop cost-effective palliative care interventions in dementia, in part through a tool that uses caregiver reports to assess symptom burden and patient needs. The research program “is founded on a needs-based approach, which aims to look at people’s individual needs and responding to them in a proactive way,” she said.

One of the obstacles to timely palliative care in dementia, Dr. Sampson said, is weighing resource allocation against what can be wildly varying prognoses. “Hospices understand when someone has terminal cancer and [is] likely to die within a few weeks, but it’s not unheard of for someone in very advanced stages of dementia to live another year,” she said. “There are concerns that a rapid increase in people with dementia being moved to palliative care could overwhelm already limited hospice capacity. We would argue that the best approach is to get palliative care out to where people with dementia live, which is usually the care home.”

Dr. Mo and colleagues’ study received funding from the National Institutes of Health, and its authors disclosed no financial conflicts of interest. Dr. Sampson’s work is supported by the UK’s Economic and Social Research Council and National Institute for Health Research. She disclosed no conflicts of interest.

Multiple sclerosis (MS) affects Whites, African Americans, and Hispanics differently, a new study finds, and there are big gaps in how they respond to disease-modifying therapies (DMTs).

“Hispanics and African Americans develop a more severe disease course and accumulate more MS-related disability over time despite similar sociodemographic backgrounds and similar patterns of DMT use throughout their disease, suggesting that socioeconomic status and access to health care may not be the main determinants of health,” said neurologist Carlos Pérez, MD, of the University of Texas Health Science Center, Houston. He spoke at the annual meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis and in a follow-up interview.

“In addition,” Dr. Pérez said, “therapeutic responses to individual DMTs, as well as tolerance and side-effect profiles, are also variable among racial/ethnic groups.”

The researchers tracked 150 patients with MS at the University of Texas Health Science Center – 50 Whites, 50 African American, and 50 Hispanic – who were age and gender matched. The average age of the subjects was 45, and 74% of those in each group were women.

While educational levels between the groups were similar, African Americans had a much higher rate of lost employment because of disability (38%) than Hispanics (19%) and Whites (15%, P = .02). Fifty-seven patients (38%) needed escalation of therapy, and 63% were African American.

About 30% of subjects switched DMTs because of intolerance/adverse events, and 47% of those were African American. Interferons most commonly caused adverse effects in African Americans (61%), and Whites were the most likely to not tolerate glatiramer acetate (39%) than Hispanics (8%) and African Americans (13%).

What might be behind the disparities? “It is possible that genetic factors may play a greater role than previously thought. A recent study reported that Hispanic and African American patients with MS have higher levels of peripheral blood plasmablasts, which may provide indirect evidence for potential biological mechanisms underlying racial and clinical disparities in MS,” Dr. Pérez said. “These mechanisms appear to involve higher degrees of inflammation in the central nervous system. This may explain why African Americans may respond better to higher-efficacy therapies initially, when inflammatory processes predominate MS-related pathology, rather than at later stages of the disease when inflammation plays a less prominent role. Neurologists should consider higher-efficacy DMT as first line. We have begun to do this in our practice.”

Dr. Pérez said the findings offer other lessons. “Neurologists should consider that Caucasian patients tolerate glatiramer acetate less frequently, compared with other racial groups, and potentially consider using alternative DMTs unless the benefits outweigh the risks, such as during pregnancy.”

He also noted that African Americans treated with oral DMTs at baseline were more likely to develop worsening disability over time. “This argues in favor of infusion therapies as first-line treatment,” he said, adding that more Hispanics with MS were not on treatment – or discontinued treatment – compared with Whites and African Americans.
 

Close patient monitoring is key

Atlanta-area neurologist Mitzi Joi Williams, MD, who was asked to comment on the study findings, said in an interview that it “adds to the body of real-world evidence to assist understanding of MS in minority populations.”

She noted that African American patients who started on infusions appeared to be more stable. “There are a great deal of questions surrounding starting patients on injectables versus higher-efficacy therapy initially to prevent disability and this may lend credence to the need for closer examination of initial therapy for these patients. It is important to closely monitor patients and consider a switch in DMT if there is any clinical or radiologic progression, especially for African American and Hispanic patients since there is a great deal of data to suggest they may have more aggressive disease.”

Moving forward, more research like this is needed, she said. “Patients did all have insurance and were largely educated, but there could be other social determinants of health – i.e., transportation, lapses in insurance, or technology barriers – that may have led to worse outcomes.”

No study funding was reported, and Dr. Pérez reported no disclosures. Dr. Williams disclosed research support from EMD Serono, Genentech, and Novartis and advisory committee/consultant relationships with AbbVie, Biogen Idec, Bristol-Myers Squibb, EMD Serono, Genentech, Novartis, and Sanofi Genzyme.

Multiple sclerosis (MS) affects Whites, African Americans, and Hispanics differently, a new study finds, and there are big gaps in how they respond to disease-modifying therapies (DMTs).

“Hispanics and African Americans develop a more severe disease course and accumulate more MS-related disability over time despite similar sociodemographic backgrounds and similar patterns of DMT use throughout their disease, suggesting that socioeconomic status and access to health care may not be the main determinants of health,” said neurologist Carlos Pérez, MD, of the University of Texas Health Science Center, Houston. He spoke at the annual meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis and in a follow-up interview.

“In addition,” Dr. Pérez said, “therapeutic responses to individual DMTs, as well as tolerance and side-effect profiles, are also variable among racial/ethnic groups.”

The researchers tracked 150 patients with MS at the University of Texas Health Science Center – 50 Whites, 50 African American, and 50 Hispanic – who were age and gender matched. The average age of the subjects was 45, and 74% of those in each group were women.

While educational levels between the groups were similar, African Americans had a much higher rate of lost employment because of disability (38%) than Hispanics (19%) and Whites (15%, P = .02). Fifty-seven patients (38%) needed escalation of therapy, and 63% were African American.

About 30% of subjects switched DMTs because of intolerance/adverse events, and 47% of those were African American. Interferons most commonly caused adverse effects in African Americans (61%), and Whites were the most likely to not tolerate glatiramer acetate (39%) than Hispanics (8%) and African Americans (13%).

What might be behind the disparities? “It is possible that genetic factors may play a greater role than previously thought. A recent study reported that Hispanic and African American patients with MS have higher levels of peripheral blood plasmablasts, which may provide indirect evidence for potential biological mechanisms underlying racial and clinical disparities in MS,” Dr. Pérez said. “These mechanisms appear to involve higher degrees of inflammation in the central nervous system. This may explain why African Americans may respond better to higher-efficacy therapies initially, when inflammatory processes predominate MS-related pathology, rather than at later stages of the disease when inflammation plays a less prominent role. Neurologists should consider higher-efficacy DMT as first line. We have begun to do this in our practice.”

Dr. Pérez said the findings offer other lessons. “Neurologists should consider that Caucasian patients tolerate glatiramer acetate less frequently, compared with other racial groups, and potentially consider using alternative DMTs unless the benefits outweigh the risks, such as during pregnancy.”

He also noted that African Americans treated with oral DMTs at baseline were more likely to develop worsening disability over time. “This argues in favor of infusion therapies as first-line treatment,” he said, adding that more Hispanics with MS were not on treatment – or discontinued treatment – compared with Whites and African Americans.
 

Close patient monitoring is key

Atlanta-area neurologist Mitzi Joi Williams, MD, who was asked to comment on the study findings, said in an interview that it “adds to the body of real-world evidence to assist understanding of MS in minority populations.”

She noted that African American patients who started on infusions appeared to be more stable. “There are a great deal of questions surrounding starting patients on injectables versus higher-efficacy therapy initially to prevent disability and this may lend credence to the need for closer examination of initial therapy for these patients. It is important to closely monitor patients and consider a switch in DMT if there is any clinical or radiologic progression, especially for African American and Hispanic patients since there is a great deal of data to suggest they may have more aggressive disease.”

Moving forward, more research like this is needed, she said. “Patients did all have insurance and were largely educated, but there could be other social determinants of health – i.e., transportation, lapses in insurance, or technology barriers – that may have led to worse outcomes.”

No study funding was reported, and Dr. Pérez reported no disclosures. Dr. Williams disclosed research support from EMD Serono, Genentech, and Novartis and advisory committee/consultant relationships with AbbVie, Biogen Idec, Bristol-Myers Squibb, EMD Serono, Genentech, Novartis, and Sanofi Genzyme.

Multiple sclerosis (MS) affects Whites, African Americans, and Hispanics differently, a new study finds, and there are big gaps in how they respond to disease-modifying therapies (DMTs).

“Hispanics and African Americans develop a more severe disease course and accumulate more MS-related disability over time despite similar sociodemographic backgrounds and similar patterns of DMT use throughout their disease, suggesting that socioeconomic status and access to health care may not be the main determinants of health,” said neurologist Carlos Pérez, MD, of the University of Texas Health Science Center, Houston. He spoke at the annual meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis and in a follow-up interview.

“In addition,” Dr. Pérez said, “therapeutic responses to individual DMTs, as well as tolerance and side-effect profiles, are also variable among racial/ethnic groups.”

The researchers tracked 150 patients with MS at the University of Texas Health Science Center – 50 Whites, 50 African American, and 50 Hispanic – who were age and gender matched. The average age of the subjects was 45, and 74% of those in each group were women.

While educational levels between the groups were similar, African Americans had a much higher rate of lost employment because of disability (38%) than Hispanics (19%) and Whites (15%, P = .02). Fifty-seven patients (38%) needed escalation of therapy, and 63% were African American.

About 30% of subjects switched DMTs because of intolerance/adverse events, and 47% of those were African American. Interferons most commonly caused adverse effects in African Americans (61%), and Whites were the most likely to not tolerate glatiramer acetate (39%) than Hispanics (8%) and African Americans (13%).

What might be behind the disparities? “It is possible that genetic factors may play a greater role than previously thought. A recent study reported that Hispanic and African American patients with MS have higher levels of peripheral blood plasmablasts, which may provide indirect evidence for potential biological mechanisms underlying racial and clinical disparities in MS,” Dr. Pérez said. “These mechanisms appear to involve higher degrees of inflammation in the central nervous system. This may explain why African Americans may respond better to higher-efficacy therapies initially, when inflammatory processes predominate MS-related pathology, rather than at later stages of the disease when inflammation plays a less prominent role. Neurologists should consider higher-efficacy DMT as first line. We have begun to do this in our practice.”

Dr. Pérez said the findings offer other lessons. “Neurologists should consider that Caucasian patients tolerate glatiramer acetate less frequently, compared with other racial groups, and potentially consider using alternative DMTs unless the benefits outweigh the risks, such as during pregnancy.”

He also noted that African Americans treated with oral DMTs at baseline were more likely to develop worsening disability over time. “This argues in favor of infusion therapies as first-line treatment,” he said, adding that more Hispanics with MS were not on treatment – or discontinued treatment – compared with Whites and African Americans.
 

Close patient monitoring is key

Atlanta-area neurologist Mitzi Joi Williams, MD, who was asked to comment on the study findings, said in an interview that it “adds to the body of real-world evidence to assist understanding of MS in minority populations.”

She noted that African American patients who started on infusions appeared to be more stable. “There are a great deal of questions surrounding starting patients on injectables versus higher-efficacy therapy initially to prevent disability and this may lend credence to the need for closer examination of initial therapy for these patients. It is important to closely monitor patients and consider a switch in DMT if there is any clinical or radiologic progression, especially for African American and Hispanic patients since there is a great deal of data to suggest they may have more aggressive disease.”

Moving forward, more research like this is needed, she said. “Patients did all have insurance and were largely educated, but there could be other social determinants of health – i.e., transportation, lapses in insurance, or technology barriers – that may have led to worse outcomes.”

No study funding was reported, and Dr. Pérez reported no disclosures. Dr. Williams disclosed research support from EMD Serono, Genentech, and Novartis and advisory committee/consultant relationships with AbbVie, Biogen Idec, Bristol-Myers Squibb, EMD Serono, Genentech, Novartis, and Sanofi Genzyme.