Federal Practitioner

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.

When I sat down to watch Oprah Winfrey’s interview with Meghan Markle on Sunday night, I didn’t know what to expect. As a psychiatrist dedicated to reducing the loss of life through suicide, I homed in on the aspect of the interview in which she discussed the depth of her suffering.

AkilinaWinner/Thinkstock

Meghan Markle is one of many celebrities to speak about their experience with suicidal crisis. Those disclosures provide opportunities to increase the public’s understanding of mental health and to deepen compassion for what others may be going through. They challenge our culturally normed assumptions: false beliefs – such as the idea that beauty, wealth, and success protect people from mental health struggles. We would do well to trust that the dichotomy between external appearances and internal experiences is always at play, and we never know what someone is going through. Human beings are both enormously resilient and vulnerable.

Suicide, while complex, is a health issue. Therefore, it is important that we all do our part in approaching mental health and suicide risk in a similar manner to other health issues.

We all have a dynamic and continuous interplay going on between life circumstances and our internal biological, genetic, and psychological makeup. The more honest and the more we learn about our own vulnerabilities and strengths, the more proactive we can be in protecting and optimizing our mental health. All individuals should be able to receive support and access to care to have their mental health needs addressed.

It’s important to note that distress leads many people to instinctually withdraw, just at a time when receiving support is even more important. In addition, cultures that traditionally emphasize self-sufficiency or stoicism may unintentionally create additional barriers to reaching out for help. Therefore, many people who experience suicidal thoughts do not disclose them to anyone. If someone does mention they are struggling, you can thank them for opening up and let them know you want to support them, and that you are there to help them find the help they need.

Dr. Moutier is chief medical officer of the American Foundation for Suicide Prevention. She reported no disclosures.

When I sat down to watch Oprah Winfrey’s interview with Meghan Markle on Sunday night, I didn’t know what to expect. As a psychiatrist dedicated to reducing the loss of life through suicide, I homed in on the aspect of the interview in which she discussed the depth of her suffering.

AkilinaWinner/Thinkstock

Meghan Markle is one of many celebrities to speak about their experience with suicidal crisis. Those disclosures provide opportunities to increase the public’s understanding of mental health and to deepen compassion for what others may be going through. They challenge our culturally normed assumptions: false beliefs – such as the idea that beauty, wealth, and success protect people from mental health struggles. We would do well to trust that the dichotomy between external appearances and internal experiences is always at play, and we never know what someone is going through. Human beings are both enormously resilient and vulnerable.

Suicide, while complex, is a health issue. Therefore, it is important that we all do our part in approaching mental health and suicide risk in a similar manner to other health issues.

We all have a dynamic and continuous interplay going on between life circumstances and our internal biological, genetic, and psychological makeup. The more honest and the more we learn about our own vulnerabilities and strengths, the more proactive we can be in protecting and optimizing our mental health. All individuals should be able to receive support and access to care to have their mental health needs addressed.

It’s important to note that distress leads many people to instinctually withdraw, just at a time when receiving support is even more important. In addition, cultures that traditionally emphasize self-sufficiency or stoicism may unintentionally create additional barriers to reaching out for help. Therefore, many people who experience suicidal thoughts do not disclose them to anyone. If someone does mention they are struggling, you can thank them for opening up and let them know you want to support them, and that you are there to help them find the help they need.

Dr. Moutier is chief medical officer of the American Foundation for Suicide Prevention. She reported no disclosures.

When I sat down to watch Oprah Winfrey’s interview with Meghan Markle on Sunday night, I didn’t know what to expect. As a psychiatrist dedicated to reducing the loss of life through suicide, I homed in on the aspect of the interview in which she discussed the depth of her suffering.

AkilinaWinner/Thinkstock

Meghan Markle is one of many celebrities to speak about their experience with suicidal crisis. Those disclosures provide opportunities to increase the public’s understanding of mental health and to deepen compassion for what others may be going through. They challenge our culturally normed assumptions: false beliefs – such as the idea that beauty, wealth, and success protect people from mental health struggles. We would do well to trust that the dichotomy between external appearances and internal experiences is always at play, and we never know what someone is going through. Human beings are both enormously resilient and vulnerable.

Suicide, while complex, is a health issue. Therefore, it is important that we all do our part in approaching mental health and suicide risk in a similar manner to other health issues.

We all have a dynamic and continuous interplay going on between life circumstances and our internal biological, genetic, and psychological makeup. The more honest and the more we learn about our own vulnerabilities and strengths, the more proactive we can be in protecting and optimizing our mental health. All individuals should be able to receive support and access to care to have their mental health needs addressed.

It’s important to note that distress leads many people to instinctually withdraw, just at a time when receiving support is even more important. In addition, cultures that traditionally emphasize self-sufficiency or stoicism may unintentionally create additional barriers to reaching out for help. Therefore, many people who experience suicidal thoughts do not disclose them to anyone. If someone does mention they are struggling, you can thank them for opening up and let them know you want to support them, and that you are there to help them find the help they need.

Dr. Moutier is chief medical officer of the American Foundation for Suicide Prevention. She reported no disclosures.

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 .

COVID-19 vaccines are safe and effective for patients taking osteoporosis medications, according to joint guidance from six endocrine and osteoporosis societies and foundations.

They noted, though, that some timing modifications with certain medications should be considered to help distinguish between adverse events from the medication versus the vaccine.

The American Society for Bone and Mineral Research “is an international organization, so we brought together our sister societies that have a vested interested in bone health. Vaccination is happening worldwide, and we wanted to present a united front and united recommendations about how to handle osteoporosis medications appropriately during vaccination,” said Suzanne Jan De Beur, MD, who is president of ASBMR and an associate professor of medicine at Johns Hopkins University, Baltimore.

There has been quite a lot of concern from the community about vaccine and medications, from both physicians and patients wondering whether treatments and vaccines should occur in a certain order, and whether there should be a time gap between the two, said Dr. Jan De Beur. “There was a dearth of information about the best practices for osteoporosis treatment management during vaccination, and we didn’t want people missing their opportunity for a vaccine, and we also didn’t want them unnecessarily delaying their osteoporosis treatment.”

There is no evidence that osteoporosis therapies affect the risk or severity of COVID-19 disease, nor do they appear to change the disease course. Osteoporosis itself does not appear associated with increased risk of infection or severe outcomes, so patients with osteoporosis do not need to be prioritized for vaccination based on that condition alone.

There is no evidence that osteoporosis therapies affect the safety or efficacy of vaccination, but given that vaccine availability is currently inconsistent, patients may need to make temporary changes to their osteoporosis regimens to ensure they can receive vaccine when it is available, such as ensuring a delay between medication and vaccination injections.

A key reason for a delay between injectable or infusion medications and a vaccine is to distinguish between adverse events that could occur, so that an adverse reaction to vaccine isn’t mistaken for an adverse reaction to a drug. Nevertheless, the real world is messy. Dr. Jan De Beur noted a recent patient who arrived at her clinic for an injectable treatment who had just received a COVID-19 vaccination that morning. “We decided to put the injection in the other arm, rather than reschedule the person and put them through the risk of coming back. We could distinguish between injection-site reactions, at least,” she said.

copyright DesignPics/Thinkstock

No changes should be made to general bone health therapies, such as calcium and vitamin D supplementation, weight-bearing exercises, and maintenance of a balanced diet.

The guidance includes some recommendations for specific osteoporosis medications.

• Oral bisphosphonates: Alendronate, risedronate, and ibandronate should be continued.
• Intravenous bisphosphonates: a 7-day interval (4-day minimum) is recommended between intravenous bisphosphonate (zoledronic acid and ibandronate) infusion and COVID-19 vaccination in order to distinguish potential autoimmune or inflammatory reactions that could be attributable to either intravenous bisphosphonate or the vaccine.
• Denosumab: There should be a 4- to 7-day delay between denosumab infusion and COVID-19 vaccination to account for injection-site reactions. Another option is to have denosumab injected into the contralateral arm or another site like the abdomen or upper thigh, if spacing the injections is not possible. In any case, denosumab injections should be performed within 7 months of the previous dose.
• Teriparatide and abaloparatide should be continued.
• Romosozumab: There should be a 4- to 7-day delay between a romosozumab injection and COVID-19 vaccine, or romosozumab can be injected in the abdomen (with the exception of a 2-inch area around the naval) or thigh if spacing is not possible.
• Raloxifene should be continued in patients receiving COVID-19 vaccination.

Guidance signatories include ASBMR, the American Association of Clinical Endocrinology, the Endocrine Society, the European Calcified Tissue Society, the National Osteoporosis Foundation, and the International Osteoporosis Foundation.

Dr. Jan De Beur has no relevant financial disclosures.

COVID-19 vaccines are safe and effective for patients taking osteoporosis medications, according to joint guidance from six endocrine and osteoporosis societies and foundations.

They noted, though, that some timing modifications with certain medications should be considered to help distinguish between adverse events from the medication versus the vaccine.

The American Society for Bone and Mineral Research “is an international organization, so we brought together our sister societies that have a vested interested in bone health. Vaccination is happening worldwide, and we wanted to present a united front and united recommendations about how to handle osteoporosis medications appropriately during vaccination,” said Suzanne Jan De Beur, MD, who is president of ASBMR and an associate professor of medicine at Johns Hopkins University, Baltimore.

There has been quite a lot of concern from the community about vaccine and medications, from both physicians and patients wondering whether treatments and vaccines should occur in a certain order, and whether there should be a time gap between the two, said Dr. Jan De Beur. “There was a dearth of information about the best practices for osteoporosis treatment management during vaccination, and we didn’t want people missing their opportunity for a vaccine, and we also didn’t want them unnecessarily delaying their osteoporosis treatment.”

There is no evidence that osteoporosis therapies affect the risk or severity of COVID-19 disease, nor do they appear to change the disease course. Osteoporosis itself does not appear associated with increased risk of infection or severe outcomes, so patients with osteoporosis do not need to be prioritized for vaccination based on that condition alone.

There is no evidence that osteoporosis therapies affect the safety or efficacy of vaccination, but given that vaccine availability is currently inconsistent, patients may need to make temporary changes to their osteoporosis regimens to ensure they can receive vaccine when it is available, such as ensuring a delay between medication and vaccination injections.

A key reason for a delay between injectable or infusion medications and a vaccine is to distinguish between adverse events that could occur, so that an adverse reaction to vaccine isn’t mistaken for an adverse reaction to a drug. Nevertheless, the real world is messy. Dr. Jan De Beur noted a recent patient who arrived at her clinic for an injectable treatment who had just received a COVID-19 vaccination that morning. “We decided to put the injection in the other arm, rather than reschedule the person and put them through the risk of coming back. We could distinguish between injection-site reactions, at least,” she said.

copyright DesignPics/Thinkstock

No changes should be made to general bone health therapies, such as calcium and vitamin D supplementation, weight-bearing exercises, and maintenance of a balanced diet.

The guidance includes some recommendations for specific osteoporosis medications.

• Oral bisphosphonates: Alendronate, risedronate, and ibandronate should be continued.
• Intravenous bisphosphonates: a 7-day interval (4-day minimum) is recommended between intravenous bisphosphonate (zoledronic acid and ibandronate) infusion and COVID-19 vaccination in order to distinguish potential autoimmune or inflammatory reactions that could be attributable to either intravenous bisphosphonate or the vaccine.
• Denosumab: There should be a 4- to 7-day delay between denosumab infusion and COVID-19 vaccination to account for injection-site reactions. Another option is to have denosumab injected into the contralateral arm or another site like the abdomen or upper thigh, if spacing the injections is not possible. In any case, denosumab injections should be performed within 7 months of the previous dose.
• Teriparatide and abaloparatide should be continued.
• Romosozumab: There should be a 4- to 7-day delay between a romosozumab injection and COVID-19 vaccine, or romosozumab can be injected in the abdomen (with the exception of a 2-inch area around the naval) or thigh if spacing is not possible.
• Raloxifene should be continued in patients receiving COVID-19 vaccination.

Guidance signatories include ASBMR, the American Association of Clinical Endocrinology, the Endocrine Society, the European Calcified Tissue Society, the National Osteoporosis Foundation, and the International Osteoporosis Foundation.

Dr. Jan De Beur has no relevant financial disclosures.

COVID-19 vaccines are safe and effective for patients taking osteoporosis medications, according to joint guidance from six endocrine and osteoporosis societies and foundations.

They noted, though, that some timing modifications with certain medications should be considered to help distinguish between adverse events from the medication versus the vaccine.

The American Society for Bone and Mineral Research “is an international organization, so we brought together our sister societies that have a vested interested in bone health. Vaccination is happening worldwide, and we wanted to present a united front and united recommendations about how to handle osteoporosis medications appropriately during vaccination,” said Suzanne Jan De Beur, MD, who is president of ASBMR and an associate professor of medicine at Johns Hopkins University, Baltimore.

There has been quite a lot of concern from the community about vaccine and medications, from both physicians and patients wondering whether treatments and vaccines should occur in a certain order, and whether there should be a time gap between the two, said Dr. Jan De Beur. “There was a dearth of information about the best practices for osteoporosis treatment management during vaccination, and we didn’t want people missing their opportunity for a vaccine, and we also didn’t want them unnecessarily delaying their osteoporosis treatment.”

There is no evidence that osteoporosis therapies affect the risk or severity of COVID-19 disease, nor do they appear to change the disease course. Osteoporosis itself does not appear associated with increased risk of infection or severe outcomes, so patients with osteoporosis do not need to be prioritized for vaccination based on that condition alone.

There is no evidence that osteoporosis therapies affect the safety or efficacy of vaccination, but given that vaccine availability is currently inconsistent, patients may need to make temporary changes to their osteoporosis regimens to ensure they can receive vaccine when it is available, such as ensuring a delay between medication and vaccination injections.

A key reason for a delay between injectable or infusion medications and a vaccine is to distinguish between adverse events that could occur, so that an adverse reaction to vaccine isn’t mistaken for an adverse reaction to a drug. Nevertheless, the real world is messy. Dr. Jan De Beur noted a recent patient who arrived at her clinic for an injectable treatment who had just received a COVID-19 vaccination that morning. “We decided to put the injection in the other arm, rather than reschedule the person and put them through the risk of coming back. We could distinguish between injection-site reactions, at least,” she said.

copyright DesignPics/Thinkstock

No changes should be made to general bone health therapies, such as calcium and vitamin D supplementation, weight-bearing exercises, and maintenance of a balanced diet.

The guidance includes some recommendations for specific osteoporosis medications.

• Oral bisphosphonates: Alendronate, risedronate, and ibandronate should be continued.
• Intravenous bisphosphonates: a 7-day interval (4-day minimum) is recommended between intravenous bisphosphonate (zoledronic acid and ibandronate) infusion and COVID-19 vaccination in order to distinguish potential autoimmune or inflammatory reactions that could be attributable to either intravenous bisphosphonate or the vaccine.
• Denosumab: There should be a 4- to 7-day delay between denosumab infusion and COVID-19 vaccination to account for injection-site reactions. Another option is to have denosumab injected into the contralateral arm or another site like the abdomen or upper thigh, if spacing the injections is not possible. In any case, denosumab injections should be performed within 7 months of the previous dose.
• Teriparatide and abaloparatide should be continued.
• Romosozumab: There should be a 4- to 7-day delay between a romosozumab injection and COVID-19 vaccine, or romosozumab can be injected in the abdomen (with the exception of a 2-inch area around the naval) or thigh if spacing is not possible.
• Raloxifene should be continued in patients receiving COVID-19 vaccination.

Guidance signatories include ASBMR, the American Association of Clinical Endocrinology, the Endocrine Society, the European Calcified Tissue Society, the National Osteoporosis Foundation, and the International Osteoporosis Foundation.

Dr. Jan De Beur has no relevant financial disclosures.

HIV-positive patients who are adherent with antiretroviral medications are achieving undetectable or very low levels of HIV viremia and living longer. In response, clinical care is continually adapting to the dramatically altered natural history of disease.

Today, the cutting edge of clinical care overlaps with primary care. The clinical vanguard addresses the medical vulnerabilities of patients with HIV, seeking to eliminate preventable morbidity and premature death. Among this clinical vanguard is the screening for and prevention of anal cancer. With the increased longevity of people living with HIV and the nearly universal exposure to human papillomavirus (HPV), there is now potential for progression to mucosal cellular dysplasia and eventual malignancy.

We know that prevention is possible because of the example of cervical cancer, the etiology of which is exposure to oncogenic serotypes of HPV (16 and 18 are most common). Screenings for cervical cancer (regular clinical examinations and Pap smears) and treatments to eliminate high-grade dysplasia have decreased the incidence rate by over 50% since the 1970s. Vaccination against HPV has been available since 2006 and offers the prospect of preventing HPV-associated malignancies, including head and neck cancer, in future decades.

However, rates of anal cancer are increasing. The CDC estimates that about 4,700 new cases of HPV-associated anal cancers are diagnosed in women and about 2,300 are diagnosed in men each year in the United States. Anal cancer rates in individuals with HIV have increased in the era of effective antiretrovirals and greater longevity. The highest rates, at 95 per 100,000, are in HIV-positive men who have sex with men. Very similar rates were noted in a more recent study that found increased risk with advancing age and in those with an AIDS diagnosis.
 

All patients with HIV should be screened

The New York State AIDS Institute Clinical Guidelines Program recommends screening for anal dysplasia in all patients with HIV. A proactive approach similar to cervical cancer screening is appropriate and includes measures easily implemented by all clinicians.

• History: Assess for rectal symptoms, anal pain, discharge, and lumps.
• Physical exam: Assess for presence of perianal lesions; perform a thorough digital rectal exam.
• Anal Pap test for anal cytology: Insert a Dacron swab moistened with tap water about 3 inches into the anal canal, applying pressure to lateral anal walls and rotating the swab. Then remove and place the swab into liquid cytology solution, shake vigorously for a full 30 seconds, and assess for any dysplasia (high-grade squamous intraepithelial lesion, low-grade intraepithelial lesion, atypical squamous cells of undetermined significance), which would warrant further evaluation by high-resolution anoscopy (HRA).

High-resolution anoscopy

HRA for anal dysplasia corresponds to colposcopy for cervical dysplasia. The ability to treat and eliminate high-risk precursor lesions interrupts the progression to malignancy. The efficacy of this strategy is being evaluated in a National Institutes of Health prospective trial called the Anchor Study. The epidemiology of HPV; the clinical horror of witnessing the painful, preventable deaths of young patients with well-controlled HIV caused by anal cancer; and the example of controlling cervical cancer have motivated my practice to assure comprehensive care for our patients.

Unfortunately, establishing HRA in one’s practice is challenging. Barriers to practice include the expense of required equipment and the absence of consensus on specific products. In addition, hands-on precepting to ease newcomers to competence is not generally available. Considerable skill is required for complete visualization of the anal transformative zone in the folds of the anal canal, and recognizing high-risk lesions requires study and accumulated experience. The International Anal Neoplasia Society is a useful resource that also offers a training course. We are invited to train ourselves, and to rely on the eventual feedback of biopsy results and the forbearance of our early patients.

The expanding scope of our medical practices must shift to meet the evolving needs of the growing population of virologically suppressed patients who are living longer. HIV care involves curing life-threatening opportunistic infections, encouraging antiretroviral adherence, and providing comprehensive care – which now includes preventing anal cancer.

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

HIV-positive patients who are adherent with antiretroviral medications are achieving undetectable or very low levels of HIV viremia and living longer. In response, clinical care is continually adapting to the dramatically altered natural history of disease.

Today, the cutting edge of clinical care overlaps with primary care. The clinical vanguard addresses the medical vulnerabilities of patients with HIV, seeking to eliminate preventable morbidity and premature death. Among this clinical vanguard is the screening for and prevention of anal cancer. With the increased longevity of people living with HIV and the nearly universal exposure to human papillomavirus (HPV), there is now potential for progression to mucosal cellular dysplasia and eventual malignancy.

We know that prevention is possible because of the example of cervical cancer, the etiology of which is exposure to oncogenic serotypes of HPV (16 and 18 are most common). Screenings for cervical cancer (regular clinical examinations and Pap smears) and treatments to eliminate high-grade dysplasia have decreased the incidence rate by over 50% since the 1970s. Vaccination against HPV has been available since 2006 and offers the prospect of preventing HPV-associated malignancies, including head and neck cancer, in future decades.

However, rates of anal cancer are increasing. The CDC estimates that about 4,700 new cases of HPV-associated anal cancers are diagnosed in women and about 2,300 are diagnosed in men each year in the United States. Anal cancer rates in individuals with HIV have increased in the era of effective antiretrovirals and greater longevity. The highest rates, at 95 per 100,000, are in HIV-positive men who have sex with men. Very similar rates were noted in a more recent study that found increased risk with advancing age and in those with an AIDS diagnosis.
 

All patients with HIV should be screened

The New York State AIDS Institute Clinical Guidelines Program recommends screening for anal dysplasia in all patients with HIV. A proactive approach similar to cervical cancer screening is appropriate and includes measures easily implemented by all clinicians.

• History: Assess for rectal symptoms, anal pain, discharge, and lumps.
• Physical exam: Assess for presence of perianal lesions; perform a thorough digital rectal exam.
• Anal Pap test for anal cytology: Insert a Dacron swab moistened with tap water about 3 inches into the anal canal, applying pressure to lateral anal walls and rotating the swab. Then remove and place the swab into liquid cytology solution, shake vigorously for a full 30 seconds, and assess for any dysplasia (high-grade squamous intraepithelial lesion, low-grade intraepithelial lesion, atypical squamous cells of undetermined significance), which would warrant further evaluation by high-resolution anoscopy (HRA).

High-resolution anoscopy

HRA for anal dysplasia corresponds to colposcopy for cervical dysplasia. The ability to treat and eliminate high-risk precursor lesions interrupts the progression to malignancy. The efficacy of this strategy is being evaluated in a National Institutes of Health prospective trial called the Anchor Study. The epidemiology of HPV; the clinical horror of witnessing the painful, preventable deaths of young patients with well-controlled HIV caused by anal cancer; and the example of controlling cervical cancer have motivated my practice to assure comprehensive care for our patients.

Unfortunately, establishing HRA in one’s practice is challenging. Barriers to practice include the expense of required equipment and the absence of consensus on specific products. In addition, hands-on precepting to ease newcomers to competence is not generally available. Considerable skill is required for complete visualization of the anal transformative zone in the folds of the anal canal, and recognizing high-risk lesions requires study and accumulated experience. The International Anal Neoplasia Society is a useful resource that also offers a training course. We are invited to train ourselves, and to rely on the eventual feedback of biopsy results and the forbearance of our early patients.

The expanding scope of our medical practices must shift to meet the evolving needs of the growing population of virologically suppressed patients who are living longer. HIV care involves curing life-threatening opportunistic infections, encouraging antiretroviral adherence, and providing comprehensive care – which now includes preventing anal cancer.

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

HIV-positive patients who are adherent with antiretroviral medications are achieving undetectable or very low levels of HIV viremia and living longer. In response, clinical care is continually adapting to the dramatically altered natural history of disease.

Today, the cutting edge of clinical care overlaps with primary care. The clinical vanguard addresses the medical vulnerabilities of patients with HIV, seeking to eliminate preventable morbidity and premature death. Among this clinical vanguard is the screening for and prevention of anal cancer. With the increased longevity of people living with HIV and the nearly universal exposure to human papillomavirus (HPV), there is now potential for progression to mucosal cellular dysplasia and eventual malignancy.

We know that prevention is possible because of the example of cervical cancer, the etiology of which is exposure to oncogenic serotypes of HPV (16 and 18 are most common). Screenings for cervical cancer (regular clinical examinations and Pap smears) and treatments to eliminate high-grade dysplasia have decreased the incidence rate by over 50% since the 1970s. Vaccination against HPV has been available since 2006 and offers the prospect of preventing HPV-associated malignancies, including head and neck cancer, in future decades.

However, rates of anal cancer are increasing. The CDC estimates that about 4,700 new cases of HPV-associated anal cancers are diagnosed in women and about 2,300 are diagnosed in men each year in the United States. Anal cancer rates in individuals with HIV have increased in the era of effective antiretrovirals and greater longevity. The highest rates, at 95 per 100,000, are in HIV-positive men who have sex with men. Very similar rates were noted in a more recent study that found increased risk with advancing age and in those with an AIDS diagnosis.
 

All patients with HIV should be screened

The New York State AIDS Institute Clinical Guidelines Program recommends screening for anal dysplasia in all patients with HIV. A proactive approach similar to cervical cancer screening is appropriate and includes measures easily implemented by all clinicians.

• History: Assess for rectal symptoms, anal pain, discharge, and lumps.
• Physical exam: Assess for presence of perianal lesions; perform a thorough digital rectal exam.
• Anal Pap test for anal cytology: Insert a Dacron swab moistened with tap water about 3 inches into the anal canal, applying pressure to lateral anal walls and rotating the swab. Then remove and place the swab into liquid cytology solution, shake vigorously for a full 30 seconds, and assess for any dysplasia (high-grade squamous intraepithelial lesion, low-grade intraepithelial lesion, atypical squamous cells of undetermined significance), which would warrant further evaluation by high-resolution anoscopy (HRA).

High-resolution anoscopy

HRA for anal dysplasia corresponds to colposcopy for cervical dysplasia. The ability to treat and eliminate high-risk precursor lesions interrupts the progression to malignancy. The efficacy of this strategy is being evaluated in a National Institutes of Health prospective trial called the Anchor Study. The epidemiology of HPV; the clinical horror of witnessing the painful, preventable deaths of young patients with well-controlled HIV caused by anal cancer; and the example of controlling cervical cancer have motivated my practice to assure comprehensive care for our patients.

Unfortunately, establishing HRA in one’s practice is challenging. Barriers to practice include the expense of required equipment and the absence of consensus on specific products. In addition, hands-on precepting to ease newcomers to competence is not generally available. Considerable skill is required for complete visualization of the anal transformative zone in the folds of the anal canal, and recognizing high-risk lesions requires study and accumulated experience. The International Anal Neoplasia Society is a useful resource that also offers a training course. We are invited to train ourselves, and to rely on the eventual feedback of biopsy results and the forbearance of our early patients.

The expanding scope of our medical practices must shift to meet the evolving needs of the growing population of virologically suppressed patients who are living longer. HIV care involves curing life-threatening opportunistic infections, encouraging antiretroviral adherence, and providing comprehensive care – which now includes preventing anal cancer.

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.

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.

Being obese and pregnant raises the risk for cardiac complications in women with preexisting heart disease, new research suggests, highlighting the need for earlier interventions in this high-risk population.

The analysis of 790 pregnancies revealed that 23% of women with obesity, defined as body mass index greater than 30 kg/m2, had a cardiac event during pregnancy versus 14% of women with normal body weight (P = .006).

The difference was driven largely by an increase in heart failure (8% vs. 3%; P = .02), although arrhythmias also trended higher in obese women (14% vs. 10%; P = .19).

Nearly half of the women with obesity and a cardiac event presented in the postpartum period (47%).

In multivariate analysis, both obesity and Canadian Cardiac Disease in Pregnancy Study (CARPREG) II risk score were independent predictors of cardiac events (odds ratios for both, 1.7), the investigators, led by Birgit Pfaller, MD, University of Toronto, reported in the Journal of the American College of Cardiology.

Although obesity has been linked to worse pregnancy outcomes and higher cardiovascular risk after delivery in the general population, the authors noted that this is the first study to examine its effect on outcomes in women with heart disease.

“We wanted to look at this high-risk group of women that had preexisting heart disease, but in addition had obesity, to try and find out if there was a kind of double hit for these women – and that, in the end, is what we found. It’s not just simply having heart disease, not simply having obesity, but the combination that’s problematic,” senior author and cardiologist Candice Silversides, MD, University of Toronto, said in an interview.

The findings are concerning given the rising prevalence of obesity worldwide. National data from 2018 show that slightly more than half of women who gave birth in the United States were significantly overweight or obese before becoming pregnant.

Similarly, in the present analysis of 600 women in the CARPREG study who gave birth from 2004 to 2014, nearly 1 in 5 pregnancies (19%) occurred in women with obesity and 25% were in overweight women.

Obese women were significantly more likely than those without obesity to have coronary artery disease (6% vs. 2%), cardiomyopathies (19% vs. 8%) and left ventricular dysfunction (19% vs. 12%) and to be hypertensive or have a hypertensive disorder of pregnancy (13% vs. 3%).

Preeclampsia developed in 32 women during the index pregnancy and 69% of these women were obese or overweight. Cardiac event rates were similar in women with or without preeclampsia but trended higher in women with preeclampsia with versus without obesity (36% vs. 14%; P = .20).

The ill effects of obesity were also reflected in fetal and neonatal events. Overall, 43% of women with obesity and 33% of normal-weight women had at least one fetal event (P = .02), with higher rates of preterm birth (19% vs. 10%; P = .005) and respiratory distress syndrome (8% vs. 3%; P = .02) in women with obesity. Congenital cardiac malformations were present in 6% of women in both groups.

Taken together, the composite of cardiac events, preeclampsia, or fetal events was significantly more common in women with obesity than in normal-weight women (56% vs. 41%; P = .002).

“We’ve spent the last number of years trying to research and understand what the drivers of these adverse outcomes are in this high-risk pregnant cohort, but on a bigger picture the real issue is how do we start intervening in a meaningful way,” Dr. Silversides said.

Like many in the burgeoning field of cardio-obstetrics, the team proposed a multidisciplinary approach that stresses preconception counseling, educating pregnant women with heart disease and obesity about their risks, ensuring that dietary advice, weight-gain recommendations, and comorbidities are addressed as part of routine care, and providing postpartum surveillance.

Preconception screening “has been the recommendation for a long, long time; it’s just that it doesn’t always happen in reality,” she said. “Many pregnancies aren’t planned and not all women are filtered into preconception counseling. So sometimes you’ll do it at the first antenatal visit and try to ensure women are educated but optimally you want to do it well in advance of pregnancy.”

Part of that preconception counseling “should also include giving them appropriate advice for contraception, if what they want to do is avoid pregnancy,” added Dr. Silversides.

Garima Sharma, MD, Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University, Baltimore, and colleagues wrote in an accompanying editorial that the adverse events observed in this high-risk cohort have “important implications for cardio-obstetricians and should be incorporated in routine prepregnancy and antenatal counseling, monitoring, and risk stratification for women with existing cardiovascular disease.”

They pointed to a paucity of data incorporating maternal prepregnancy obesity and gestational weight gain in risk prediction and called for larger population-based studies on the additive impact of obesity severity on predicting adverse cardiac events in women with existing cardiovascular disease.

Randomized trials are also urgently needed to evaluate the effect of nutritional and behavioral interventions in pregnancy on short- and long-term outcomes in mother and child.

“As the obesity epidemic continues to grow and public health interventions promoting lifestyle changes for obesity management remain a major challenge, maternal obesity may prove to be the ‘Achilles’ heel’ of sustainable national efforts to reduce maternal mortality and improve health equity. This is a call to action,” Dr. Sharma and colleagues concluded.

The investigators noted that the study was conducted at a single center and used self-reported pregnancy weight collected at the first antenatal visit, which may have underestimated obesity rates. Other limitations are that weight changes over the course of pregnancy were not studied and there was a limited number of women with a body mass index of 40 or higher.

The study was supported by a grant from the Allan E. Tiffin Trust, Toronto General and Western Hospital Foundation, and by a donation from Mrs. Josephine Rogers, Toronto General Hospital. Dr. Silversides is supported by the Miles Nadal Chair in Pregnancy and Heart Disease. Dr. Sharma and colleagues disclosed no relevant financial relationships.

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

Being obese and pregnant raises the risk for cardiac complications in women with preexisting heart disease, new research suggests, highlighting the need for earlier interventions in this high-risk population.

The analysis of 790 pregnancies revealed that 23% of women with obesity, defined as body mass index greater than 30 kg/m2, had a cardiac event during pregnancy versus 14% of women with normal body weight (P = .006).

The difference was driven largely by an increase in heart failure (8% vs. 3%; P = .02), although arrhythmias also trended higher in obese women (14% vs. 10%; P = .19).

Nearly half of the women with obesity and a cardiac event presented in the postpartum period (47%).

In multivariate analysis, both obesity and Canadian Cardiac Disease in Pregnancy Study (CARPREG) II risk score were independent predictors of cardiac events (odds ratios for both, 1.7), the investigators, led by Birgit Pfaller, MD, University of Toronto, reported in the Journal of the American College of Cardiology.

Although obesity has been linked to worse pregnancy outcomes and higher cardiovascular risk after delivery in the general population, the authors noted that this is the first study to examine its effect on outcomes in women with heart disease.

“We wanted to look at this high-risk group of women that had preexisting heart disease, but in addition had obesity, to try and find out if there was a kind of double hit for these women – and that, in the end, is what we found. It’s not just simply having heart disease, not simply having obesity, but the combination that’s problematic,” senior author and cardiologist Candice Silversides, MD, University of Toronto, said in an interview.

The findings are concerning given the rising prevalence of obesity worldwide. National data from 2018 show that slightly more than half of women who gave birth in the United States were significantly overweight or obese before becoming pregnant.

Similarly, in the present analysis of 600 women in the CARPREG study who gave birth from 2004 to 2014, nearly 1 in 5 pregnancies (19%) occurred in women with obesity and 25% were in overweight women.

Obese women were significantly more likely than those without obesity to have coronary artery disease (6% vs. 2%), cardiomyopathies (19% vs. 8%) and left ventricular dysfunction (19% vs. 12%) and to be hypertensive or have a hypertensive disorder of pregnancy (13% vs. 3%).

Preeclampsia developed in 32 women during the index pregnancy and 69% of these women were obese or overweight. Cardiac event rates were similar in women with or without preeclampsia but trended higher in women with preeclampsia with versus without obesity (36% vs. 14%; P = .20).

The ill effects of obesity were also reflected in fetal and neonatal events. Overall, 43% of women with obesity and 33% of normal-weight women had at least one fetal event (P = .02), with higher rates of preterm birth (19% vs. 10%; P = .005) and respiratory distress syndrome (8% vs. 3%; P = .02) in women with obesity. Congenital cardiac malformations were present in 6% of women in both groups.

Taken together, the composite of cardiac events, preeclampsia, or fetal events was significantly more common in women with obesity than in normal-weight women (56% vs. 41%; P = .002).

“We’ve spent the last number of years trying to research and understand what the drivers of these adverse outcomes are in this high-risk pregnant cohort, but on a bigger picture the real issue is how do we start intervening in a meaningful way,” Dr. Silversides said.

Like many in the burgeoning field of cardio-obstetrics, the team proposed a multidisciplinary approach that stresses preconception counseling, educating pregnant women with heart disease and obesity about their risks, ensuring that dietary advice, weight-gain recommendations, and comorbidities are addressed as part of routine care, and providing postpartum surveillance.

Preconception screening “has been the recommendation for a long, long time; it’s just that it doesn’t always happen in reality,” she said. “Many pregnancies aren’t planned and not all women are filtered into preconception counseling. So sometimes you’ll do it at the first antenatal visit and try to ensure women are educated but optimally you want to do it well in advance of pregnancy.”

Part of that preconception counseling “should also include giving them appropriate advice for contraception, if what they want to do is avoid pregnancy,” added Dr. Silversides.

Garima Sharma, MD, Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University, Baltimore, and colleagues wrote in an accompanying editorial that the adverse events observed in this high-risk cohort have “important implications for cardio-obstetricians and should be incorporated in routine prepregnancy and antenatal counseling, monitoring, and risk stratification for women with existing cardiovascular disease.”

They pointed to a paucity of data incorporating maternal prepregnancy obesity and gestational weight gain in risk prediction and called for larger population-based studies on the additive impact of obesity severity on predicting adverse cardiac events in women with existing cardiovascular disease.

Randomized trials are also urgently needed to evaluate the effect of nutritional and behavioral interventions in pregnancy on short- and long-term outcomes in mother and child.

“As the obesity epidemic continues to grow and public health interventions promoting lifestyle changes for obesity management remain a major challenge, maternal obesity may prove to be the ‘Achilles’ heel’ of sustainable national efforts to reduce maternal mortality and improve health equity. This is a call to action,” Dr. Sharma and colleagues concluded.

The investigators noted that the study was conducted at a single center and used self-reported pregnancy weight collected at the first antenatal visit, which may have underestimated obesity rates. Other limitations are that weight changes over the course of pregnancy were not studied and there was a limited number of women with a body mass index of 40 or higher.

The study was supported by a grant from the Allan E. Tiffin Trust, Toronto General and Western Hospital Foundation, and by a donation from Mrs. Josephine Rogers, Toronto General Hospital. Dr. Silversides is supported by the Miles Nadal Chair in Pregnancy and Heart Disease. Dr. Sharma and colleagues disclosed no relevant financial relationships.

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

Being obese and pregnant raises the risk for cardiac complications in women with preexisting heart disease, new research suggests, highlighting the need for earlier interventions in this high-risk population.

The analysis of 790 pregnancies revealed that 23% of women with obesity, defined as body mass index greater than 30 kg/m2, had a cardiac event during pregnancy versus 14% of women with normal body weight (P = .006).

The difference was driven largely by an increase in heart failure (8% vs. 3%; P = .02), although arrhythmias also trended higher in obese women (14% vs. 10%; P = .19).

Nearly half of the women with obesity and a cardiac event presented in the postpartum period (47%).

In multivariate analysis, both obesity and Canadian Cardiac Disease in Pregnancy Study (CARPREG) II risk score were independent predictors of cardiac events (odds ratios for both, 1.7), the investigators, led by Birgit Pfaller, MD, University of Toronto, reported in the Journal of the American College of Cardiology.

Although obesity has been linked to worse pregnancy outcomes and higher cardiovascular risk after delivery in the general population, the authors noted that this is the first study to examine its effect on outcomes in women with heart disease.

“We wanted to look at this high-risk group of women that had preexisting heart disease, but in addition had obesity, to try and find out if there was a kind of double hit for these women – and that, in the end, is what we found. It’s not just simply having heart disease, not simply having obesity, but the combination that’s problematic,” senior author and cardiologist Candice Silversides, MD, University of Toronto, said in an interview.

The findings are concerning given the rising prevalence of obesity worldwide. National data from 2018 show that slightly more than half of women who gave birth in the United States were significantly overweight or obese before becoming pregnant.

Similarly, in the present analysis of 600 women in the CARPREG study who gave birth from 2004 to 2014, nearly 1 in 5 pregnancies (19%) occurred in women with obesity and 25% were in overweight women.

Obese women were significantly more likely than those without obesity to have coronary artery disease (6% vs. 2%), cardiomyopathies (19% vs. 8%) and left ventricular dysfunction (19% vs. 12%) and to be hypertensive or have a hypertensive disorder of pregnancy (13% vs. 3%).

Preeclampsia developed in 32 women during the index pregnancy and 69% of these women were obese or overweight. Cardiac event rates were similar in women with or without preeclampsia but trended higher in women with preeclampsia with versus without obesity (36% vs. 14%; P = .20).

The ill effects of obesity were also reflected in fetal and neonatal events. Overall, 43% of women with obesity and 33% of normal-weight women had at least one fetal event (P = .02), with higher rates of preterm birth (19% vs. 10%; P = .005) and respiratory distress syndrome (8% vs. 3%; P = .02) in women with obesity. Congenital cardiac malformations were present in 6% of women in both groups.

Taken together, the composite of cardiac events, preeclampsia, or fetal events was significantly more common in women with obesity than in normal-weight women (56% vs. 41%; P = .002).

“We’ve spent the last number of years trying to research and understand what the drivers of these adverse outcomes are in this high-risk pregnant cohort, but on a bigger picture the real issue is how do we start intervening in a meaningful way,” Dr. Silversides said.

Like many in the burgeoning field of cardio-obstetrics, the team proposed a multidisciplinary approach that stresses preconception counseling, educating pregnant women with heart disease and obesity about their risks, ensuring that dietary advice, weight-gain recommendations, and comorbidities are addressed as part of routine care, and providing postpartum surveillance.

Preconception screening “has been the recommendation for a long, long time; it’s just that it doesn’t always happen in reality,” she said. “Many pregnancies aren’t planned and not all women are filtered into preconception counseling. So sometimes you’ll do it at the first antenatal visit and try to ensure women are educated but optimally you want to do it well in advance of pregnancy.”

Part of that preconception counseling “should also include giving them appropriate advice for contraception, if what they want to do is avoid pregnancy,” added Dr. Silversides.

Garima Sharma, MD, Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University, Baltimore, and colleagues wrote in an accompanying editorial that the adverse events observed in this high-risk cohort have “important implications for cardio-obstetricians and should be incorporated in routine prepregnancy and antenatal counseling, monitoring, and risk stratification for women with existing cardiovascular disease.”

They pointed to a paucity of data incorporating maternal prepregnancy obesity and gestational weight gain in risk prediction and called for larger population-based studies on the additive impact of obesity severity on predicting adverse cardiac events in women with existing cardiovascular disease.

Randomized trials are also urgently needed to evaluate the effect of nutritional and behavioral interventions in pregnancy on short- and long-term outcomes in mother and child.

“As the obesity epidemic continues to grow and public health interventions promoting lifestyle changes for obesity management remain a major challenge, maternal obesity may prove to be the ‘Achilles’ heel’ of sustainable national efforts to reduce maternal mortality and improve health equity. This is a call to action,” Dr. Sharma and colleagues concluded.

The investigators noted that the study was conducted at a single center and used self-reported pregnancy weight collected at the first antenatal visit, which may have underestimated obesity rates. Other limitations are that weight changes over the course of pregnancy were not studied and there was a limited number of women with a body mass index of 40 or higher.

The study was supported by a grant from the Allan E. Tiffin Trust, Toronto General and Western Hospital Foundation, and by a donation from Mrs. Josephine Rogers, Toronto General Hospital. Dr. Silversides is supported by the Miles Nadal Chair in Pregnancy and Heart Disease. Dr. Sharma and colleagues disclosed no relevant financial relationships.

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

A “stunning” new analysis of global data on eating disorders show that they are far more prevalent and disabling than previously reported.

Investigators found the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 underestimated the prevalence of eating disorders by nearly 42 million cases, meaning these disorders are four times more common than previously reported.

“Our work highlights that eating disorders are far more prevalent and disabling than previously quantified,” lead author Damian F. Santomauro, PhD, University of Queensland and Center for Mental Health Research, Brisbane, Australia, said in an interview.

Policy implications

The GBD Study 2019 reports the prevalence and burden of anorexia nervosa and bulimia nervosa under the umbrella of “eating disorders.”

However, binge-eating disorder (BED) and other specified feeding or eating disorder (OSFED) are more common, the investigators noted.

By excluding BED and OSFED, 41.9 million cases of eating disorders were not represented in the study.

The researchers calculate that the GBD 2019 overlooked 17.3 million people with BED and 24.6 million people with OSFED.

copyright JGI/Thinkstock

Landmark article, clarion call for action

In an accompanying commentary, Jennifer J. Thomas, PhD, and Kendra R. Becker, PhD, with the Eating Disorders Clinical and Research Program, Massachusetts General Hospital, Boston, said that this “stunning” analysis highlights that eating disorders are four times more common than previously thought.

This “landmark” analysis also demonstrates that BED and OSFED are especially common with increasing age. It highlights the burden of eating disorders in men, “shattering the inaccurate but entrenched stereotype that eating disorders affect only thin, young, White women,” Dr. Thomas and Dr. Becker pointed out.

This article, they wrote, is a “clarion call” for BED and OSFED to be included in future versions of the GBD Study.

Going a step further, Dr. Thomas and Dr. Becker said the GBD Study should also include estimates of the prevalence of avoidant/restrictive food intake disorder, rumination disorder, and pica and that the investigators should obtain direct measures of the disability associated with all feeding and eating disorders included in the DSM-5.

“If they do, the reported global burden will be even greater, underscoring the clear need for increased funding to study, prevent, and treat these debilitating illnesses,” they concluded.

The study was funded by Queensland Health, the Australian National Health and Medical Research Council, and the Bill & Melinda Gates Foundation. The authors have disclosed no relevant financial relationships. Disclosures for the editorialists are listed with the original article.

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

A “stunning” new analysis of global data on eating disorders show that they are far more prevalent and disabling than previously reported.

Investigators found the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 underestimated the prevalence of eating disorders by nearly 42 million cases, meaning these disorders are four times more common than previously reported.

“Our work highlights that eating disorders are far more prevalent and disabling than previously quantified,” lead author Damian F. Santomauro, PhD, University of Queensland and Center for Mental Health Research, Brisbane, Australia, said in an interview.

Policy implications

The GBD Study 2019 reports the prevalence and burden of anorexia nervosa and bulimia nervosa under the umbrella of “eating disorders.”

However, binge-eating disorder (BED) and other specified feeding or eating disorder (OSFED) are more common, the investigators noted.

By excluding BED and OSFED, 41.9 million cases of eating disorders were not represented in the study.

The researchers calculate that the GBD 2019 overlooked 17.3 million people with BED and 24.6 million people with OSFED.

copyright JGI/Thinkstock

Landmark article, clarion call for action

In an accompanying commentary, Jennifer J. Thomas, PhD, and Kendra R. Becker, PhD, with the Eating Disorders Clinical and Research Program, Massachusetts General Hospital, Boston, said that this “stunning” analysis highlights that eating disorders are four times more common than previously thought.

This “landmark” analysis also demonstrates that BED and OSFED are especially common with increasing age. It highlights the burden of eating disorders in men, “shattering the inaccurate but entrenched stereotype that eating disorders affect only thin, young, White women,” Dr. Thomas and Dr. Becker pointed out.

This article, they wrote, is a “clarion call” for BED and OSFED to be included in future versions of the GBD Study.

Going a step further, Dr. Thomas and Dr. Becker said the GBD Study should also include estimates of the prevalence of avoidant/restrictive food intake disorder, rumination disorder, and pica and that the investigators should obtain direct measures of the disability associated with all feeding and eating disorders included in the DSM-5.

“If they do, the reported global burden will be even greater, underscoring the clear need for increased funding to study, prevent, and treat these debilitating illnesses,” they concluded.

The study was funded by Queensland Health, the Australian National Health and Medical Research Council, and the Bill & Melinda Gates Foundation. The authors have disclosed no relevant financial relationships. Disclosures for the editorialists are listed with the original article.

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

A “stunning” new analysis of global data on eating disorders show that they are far more prevalent and disabling than previously reported.

Investigators found the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 underestimated the prevalence of eating disorders by nearly 42 million cases, meaning these disorders are four times more common than previously reported.

“Our work highlights that eating disorders are far more prevalent and disabling than previously quantified,” lead author Damian F. Santomauro, PhD, University of Queensland and Center for Mental Health Research, Brisbane, Australia, said in an interview.

Policy implications

The GBD Study 2019 reports the prevalence and burden of anorexia nervosa and bulimia nervosa under the umbrella of “eating disorders.”

However, binge-eating disorder (BED) and other specified feeding or eating disorder (OSFED) are more common, the investigators noted.

By excluding BED and OSFED, 41.9 million cases of eating disorders were not represented in the study.

The researchers calculate that the GBD 2019 overlooked 17.3 million people with BED and 24.6 million people with OSFED.

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Landmark article, clarion call for action

In an accompanying commentary, Jennifer J. Thomas, PhD, and Kendra R. Becker, PhD, with the Eating Disorders Clinical and Research Program, Massachusetts General Hospital, Boston, said that this “stunning” analysis highlights that eating disorders are four times more common than previously thought.

This “landmark” analysis also demonstrates that BED and OSFED are especially common with increasing age. It highlights the burden of eating disorders in men, “shattering the inaccurate but entrenched stereotype that eating disorders affect only thin, young, White women,” Dr. Thomas and Dr. Becker pointed out.

This article, they wrote, is a “clarion call” for BED and OSFED to be included in future versions of the GBD Study.

Going a step further, Dr. Thomas and Dr. Becker said the GBD Study should also include estimates of the prevalence of avoidant/restrictive food intake disorder, rumination disorder, and pica and that the investigators should obtain direct measures of the disability associated with all feeding and eating disorders included in the DSM-5.

“If they do, the reported global burden will be even greater, underscoring the clear need for increased funding to study, prevent, and treat these debilitating illnesses,” they concluded.

The study was funded by Queensland Health, the Australian National Health and Medical Research Council, and the Bill & Melinda Gates Foundation. The authors have disclosed no relevant financial relationships. Disclosures for the editorialists are listed with the original article.

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.

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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%..